Grossman’s Cardiac Catheterization, Angiography, & Intervention
7th Edition

11
Coronary Angiography
Donald S. Baima
a The contribution of William Grossman to this chapter in prior editions is gratefully acknowledged.
Diagnostic coronary angiography (also called coronary arteriography) is now the principal component of cardiac catheterization, with an estimated 2,000,000 procedures (roughly 800 per 100,000 population) performed each year in the United States (1,2). The goal is to examine the entire coronary tree (both native vessels as well as any surgically constructed bypass grafts) while recording details of the coronary anatomy that include the following: the pattern of arterial distribution, anatomic or functional pathology (atherosclerosis, thrombosis, congenital anomalies, or focal coronary spasm), and the presence of intercoronary and intracoronary collateral connections. The procedure is typically performed in 30 minutes or less, under local anesthesia, on an outpatient basis, with a procedure-related major complication rate (death, stroke, myocardial infarction, see Chapter 3) of <0.1%. By performing a series of intracoronary contrast injections in carefully chosen angulated views using current high-resolution x-ray imaging (see Chapter 2), it is possible to define all portions of the coronary arterial circulation down to vessels as small as 0.3 mm, free of any artifacts owing to vessel overlap or foreshortening.
There is currently no other imaging technique that gives as detailed a view of the coronary circulation, although noninvasive techniques such as magnetic resonance angiography (MRA) and multidetector and electron-beam computed tomography (MDCT, EBCT) have improved their resolution and emerged as effective screening tests for coronary artery disease in the proximal coronary arteries, coronary anomalies, and patency of surgical bypass grafts (3,4). But for patients with compelling ischemic symptoms, what begins as a diagnostic procedure can quickly shift to a definitive therapy (percutaneous coronary intervention or PCI, see Chapters 22,23 and 24) performed through the same access site. Even so, coronary angiography is limited to examination of only the coronary lumen and not the endothelial surface, plaque content, vessel wall, or (except indirectly) coronary flow physiology. When those features are in question, coronary angiography may be supplemented by intravascular ultrasound, optical computerized tomography, angioscopy, or intracoronary pressure and flow measurements (see Chapters 18 and 19). Despite these limitations, selective coronary angiography still remains the clinical gold standard for evaluating coronary anatomy. The performance of high-quality coronary angiography to safely define each and every coronary stenosis in an optimal view is an important measure of an operator’s skill in cardiac catheterization and is the foundation on which the ability to perform successful coronary intervention is based.
CURRENT INDICATIONS
The various current indications for coronary angiography are summarized comprehensively in the most recent set of AHA/ACC guidelines on coronary angiography (2), available online at http://www.acc.org/clinical/topic/topic.htm. Although the details of these indications continue to evolve as new applications of catheter-based therapy are developed, they are still best summarized by the principle stated by F. Mason Sones—coronary arteriography is indicated when a problem is encountered whose resolution may be aided by the objective demonstration of the coronary anatomy, provided competent personnel and adequate facilities are available and the potential risks are acceptable to the patient and physician.
The most frequent indication is the further evaluation of patients in whom the diagnosis of coronary atherosclerosis is almost certain and in whom anatomic correction by means of coronary bypass surgery or PCI is contemplated. Angiographic evaluation of coronary anatomy in
P.188

such patients provides the crucial information needed to select the most appropriate treatment strategy—catheter intervention (see Chapters 22,23 and 24), bypass surgery, or medical therapy. Included in this category are patients with stable angina pectoris refractory to medical therapy.
Even asymptomatic patients with noninvasive evidence of myocardial ischemia also benefit from revascularization and are thus candidates for coronary angiography (5). In patients with unstable angina (new onset, progressive, or rest pain), intensive drug therapy (beta-blocker, calcium channel blocker, nitrate, heparin, aspirin, clopidogrel or a platelet glycoprotein IIb/IIIa receptor blocker) may be temporizing, but more than two thirds of such patients will come to angiography within 6 weeks of presentation anyway owing to ongoing clinical symptoms or a positive exercise test (6,7). In most cases, therefore, such patients are brought to early coronary angiography, with same-procedure PCI if their anatomy is suitable. Patients with acute myocardial infarction routinely undergo immediate coronary angiography followed by same-procedure primary angioplasty (8). However, the role of routine post-MI coronary angiography in the asymptomatic postinfarct patient who was managed medically or with thrombolysis has not been established (9). The most recent AHA/ACC guidelines for the role of coronary angiography in stable angina, unstable angina, and acute myocardial infarction are available on the Internet at http://www.acc.org/clinical/topic/topic.htm.
A second group of indications for coronary angiography consists of patients in whom the presence or absence of coronary artery disease is unclear (2). This includes patients with troublesome chest pain syndromes but ambiguous noninvasive test results, patients with unexplained heart failure or ventricular arrhythmias, survivors of out-of-hospital cardiac arrest (10), patients with suspected or proven variant angina (11), and patients with risk factors for coronary artery disease who are being evaluated for major abdominal, thoracic, or vascular surgery (12). This category also includes patients scheduled for correction of congenital or valvular pathology. Patients with congenital defects such as tetralogy of Fallot frequently have anomalies of coronary distribution that may lead to surgical complications if unrecognized (13), whereas patients older than age 45 years with valvular disease may have advanced coronary atherosclerosis without clinical symptoms. Although younger patients with valvular disease are commonly operated on without prior coronary angiograms, given the extraordinary low risk of diagnostic catheterization and the potential benefit of knowing the coronary anatomy, most surgical center personnel believe it is best to perform a preoperative diagnostic catheterization to identify (and then correct) significant coronary lesions, to provide the best and safest outcome during concurrent valve replacement (14).
Finally, coronary angiography is frequently performed when a patient develops recurrent angina after coronary intervention (to detect and treat restenosis, see Chapter 22) or after bypass surgery (to detect vein graft failure, which might require catheter intervention or reoperation). Routine follow-up angiography 6 months after catheter intervention is not indicated clinically, but may play an important role in the research evaluation of new technologies or drug therapies targeted at reducing restenosis (15).
HISTORY AND GENERAL ISSUES
The initial attempts to perform coronary angiography used nonselective injections of contrast medium into the aortic root to opacify both the left and right coronary arteries simultaneously as the angiographic images were recorded on serial conventional sheet films (16). To improve contrast delivery into the coronary ostia, some early investigators used transient circulatory arrest induced by the administration of acetylcholine or by elevation of intrabronchial pressure, followed by occlusion of the ascending aorta by gas-filled balloon and injection of the contrast bolus. Although nonselective aortic root injection is still used occasionally today to evaluate ostial lesions, anomalous coronary ostia, or coronary bypass grafts, intentional circulatory arrest is no longer practiced, and earlier nonselective techniques have largely been replaced by selective injection into each coronary ostium using specially designed catheters advanced from any of several arterial access points.
In most patients, successful coronary angiography can be performed by either the brachial cutdown or the percutaneous approach (from the femoral, brachial, or radial artery), leaving the choice of access site up to physician and patient. Data from the Society for Cardiac Angiography and Intervention in 1990 (17) show the percutaneous femoral approach was used in 83% of cases, with further increase in that percentage over the subsequent years. The brachial cutdown approach (Chapter 5) has decreased, but the percutaneous radial approach (Chapter 4) entry may offer a selective advantage in patients with severe peripheral vascular disease or known abdominal aortic aneurysm. It also allows immediate postprocedure ambulation. Regardless of the approach, however, it is important for the catheterization team to meet the patient before the actual procedure to evaluate the best access site, to gain an appreciation of the clinical questions that need to be answered by coronary angiography, to uncover any history of adverse reaction to medications or organic iodine compounds, and to explain the procedure and its risks in detail.
Coronary angiography was traditionally performed with hospitalization on the night after the procedure and sometimes the night prior to the scheduled procedure as well. In contrast, most patients now come in on the morning of their scheduled procedure, with no oral intake (except for medications and limited quantities of clear liquid) for 6 to 8 hours before catheterization. A preprocedure workup has usually been done on an outpatient basis some days before. A mild sedative premedication (such as
P.189

diazepam, 5 to 10 mg orally) may be given prior to the procedure, or intravenous conscious sedation may be administered as needed during the procedure itself. Outpatient coronary angiography for low- to moderate-risk patients began in the 1990s (2,18,19,20,21), and continues as the dominant practice. However, patients who have undergone a coronary intervention, those with major comorbidities (e.g., heart failure, valve disease, renal insufficiency, peripheral vascular disease), those who live more than a 1-hour drive from the cardiac catheterization facility, or those who have sustained a procedural complication are expected to stay overnight in the hospital following a diagnostic coronary angiogram. If the angiogram shows significant disease and PCI is appropriate, this may be done during the same procedure followed by an overnight hospital stay. Patients needing revascularization but not found to be suitable for PCI at the time of coronary angiography may go for a bypass surgical operation within 24 to 48 hours or may be discharged home to return for surgery, depending on clinical acuity and availability of surgical time. At least 2 hours of bed rest is required after a percutaneous femoral procedure unless a puncture sealing device is used (see Chapter 4) to allow earlier ambulation and discharge.
THE FEMORAL APPROACH
As described in Chapter 4, the femoral approach to left heart catheterization involves insertion of the catheter either directly over a guidewire or through an introducing sheath. Systemic anticoagulation (heparin, 3,000 to 5,000 units at the time of sheath introduction) is used in some laboratories (2), although others now omit heparin in brief diagnostic procedures. A series of preformed catheters are used, starting with a pigtail catheter for left ventriculography followed by separate catheters (either Judkins or Amplatz shapes) for cannulation of the left and right coronary arteries and any surgical bypass grafts. Coronary catheters are available in 5F, 6F, 7F, or 8F end-hole designs that may taper further near the tip. They may be constructed of either polyethylene (Cook Inc, Bloomington, IN) or polyurethane (Cordis, Miami, FL; and USCI, Billerica, MA) and contain either steel braid, nylon, or other reinforcing materials (Kevlar, carbon fiber) within the catheter wall to provide the excellent torque control needed for coronary cannulation. Current catheters may have a soft distal tip to minimize the risk of arterial dissection. In the 1970s, 8F catheters predominated because they provided excellent torque control and permitted rapid contrast delivery. In the 1980s, improvements in the design of 7F catheters allowed for a lumen diameter comparable to that in standard 8F catheters, making them the standard in most laboratories. Smaller (6F and even 5F) coronary angiographic catheters are now available that use technology similar to that used in guiding catheters to provide thinner catheter walls and larger lumens (6F lumens up to 0.064 inches), exceeding the lumen size once available in 8F diagnostic catheters (22). We now use such 6F catheters for all of our routine diagnostic procedures. Some of the catheters used for native coronary injection via the femoral or brachial approach are shown in Fig. 11.1.
Insertion and Flushing of the Coronary Catheter
The desired catheter is inserted into the femoral sheath and advanced to the level of the left mainstem bronchus over the guidewire. Alternatively, some operators prefer to advance the tip of the coronary angiography catheter around the arch and into the ascending aorta before the guidewire is removed. Although this may reduce snagging of the catheter tip on aortic wall plaques and irregularities, it places greater emphasis on the precision of initial catheter flushing. After removal of the guidewire, the catheter is attached to a specially designed manifold system that permits the maintenance of a closed system during pressure monitoring, catheter flushing, and contrast agent administration (Fig. 11.2). The catheter is immediately double-flushed—blood is withdrawn and discarded, after which heparinized saline flush is injected through the catheter lumen. Difficulty in blood withdrawal suggests apposition of the catheter tip to the aortic wall, which can be rectified by slight withdrawal or rotation of
P.190

the catheter until free blood aspiration is possible. The lumen of the introducing sheath should also be flushed immediately before and after each catheter insertion and every 5 minutes thereafter to prevent the encroachment of blood into the sheath. Alternatively, the side arm of the sheath may be connected to a 30 mL/hour continuous flow regulator (Intraflo II).
Figure 11.1 Types of catheters currently in wide use for selective native coronary angiography. Left to right. Amplatz right, Judkins right, Sones, Judkins left, and Amplatz left.
Figure 11.2 A. Four-port coronary manifold. This manifold provides a closed system with which blood can be withdrawn from the catheter and discarded. The catheter can be filled with either flush solution or contrast medium, and the catheter pressure can be observed, all under the control of a series of stopcocks. The fourth port is connected to an empty plastic bag and is used as a discard port (for blood from the double flush, air bubbles) so that the syringe need not be disconnected from the manifold at any time during the procedure. Attachment of the transducer directly to the manifold allows optimum pressure waveform fidelity (see Chap. 9), and the fluid-filled reference line allows zeroing of the transducer to midchest level. B. The Bracco-Squibb Acist device consists of a contrast filled power injector, controlled by a sterile pneumatic actuator to deliver contrast in amounts and rates up to the limits preprogrammed on the digital panel. A power flushing system and a pressure transducer are also included, duplicating many of the functions of the traditional four-port manifold.
Once the catheter has been flushed with saline solution, tip pressure should be displayed on the physiologic monitor at all times (except during actual contrast injections). Recording this baseline pressure before contrast administration serves as an important baseline reference point. Next, the catheter lumen should be gently filled with contrast agent under fluoroscopic visualization, avoiding selective contrast administration into small branches such as the lumbar arteries if filling is performed in the descending aorta. Filling with contrast results in slight attenuation of high-frequency components in the aortic pressure waveform, whose new shape should be carefully noted. Any subsequent alteration in that waveform during coronary angiography (see damping and ventricularization, below) may signify an ostial coronary stenosis or an unfavorable catheter position within the coronary artery. Once these measures are completed, the coronary angiographic catheter is advanced into the aortic root in preparation for selective engagement of the desired coronary ostium.
Damping and Ventricularization of the Pressure Waveform
A fall in overall catheter tip pressure (damping) or a fall in diastolic pressure only (ventricularization, Fig. 11.3) during catheter engagement in a coronary ostium indicates obstruction of the catheter tip or interference with coronary inflow. The catheter tip may have been inserted across a proximal coronary stenosis or may have an adverse catheter lie that places it against the coronary wall. If either
P.191

of these phenomena is observed, the catheter should be withdrawn into the aortic root immediately until the operator can analyze the situation further. The catheter may be re-engaged and a cautious small-volume contrast injection made to further clarify the situation. This may disclose a proximal occlusion of the vessel, against which the tip of the coronary catheter is resting, in which case a cine run should be performed to document this finding. The test injection may also indicate ostial stenosis with absent reflux into the aortic root or retention of the injected contrast in the proximal and mid vessel. Lack of reflux indicates that the catheter tip is severely restricting or occluding ostial inflow and mandates that only a gentle injection be performed followed by immediate removal of the catheter at the end of the cine run to restore antegrade flow. Actually, continuing to inject and film as the catheter is removed from the ostium may capture the few frames that show the ostial lesion clearly.
Figure 11.3 Pressure tracings as recorded during coronary angiography. Except for its earlier phase and slightly lower systolic pressure, catheter tip pressure should resemble the pressure waveform simultaneously monitored by way of the femoral side-arm sheath or other arterial monitor (e.g., radial artery). In the presence of an ostial stenosis or an unfavorable catheter position against the vessel wall, the waveform shows either ventricularization (in which systolic pressure is preserved but diastolic pressure is reduced) or frank damping (in which both systolic and diastolic pressures are reduced). In either case, the best approach is to withdraw the catheter immediately until the waveform returns to normal and to attempt to define the cause of the problem by nonselective injections in the sinus of Valsalva. Alternatively, a catheter equipped with side holes near the tip may be used to provide ongoing coronary perfusion.
Another approach to evaluating such ostial lesions is to perform a nonselective injection into the sinus of Valsalva in an appropriate view (that displays the ostium of the vessel in question with no overlap by the sinus of Valsalva). Or the standard end-hole diagnostic catheter may be exchanged for an end- and side-hole angioplasty guiding catheter to overcome damping by preserving antegrade flow into the side holes, through the lumen of the catheter, and into the coronary artery, even though the catheter tip may be obstructing entry of blood into the ostium itself (see discussion of cannulation of the right coronary ostium, below). Vigorous injection despite a damped or ventricularized pressure waveform should be avoided, however, since it predisposes to ventricular fibrillation or dissection of the proximal coronary artery with major ischemic sequelae. Such a dissection is manifest by tracking of contrast down the vessel over the course of the injection and failure of contrast to clear on fluoroscopy after the injection is terminated. Prompt consideration of repair by catheter-based intervention or bypass surgery should be considered if creation of such a dye stain is associated with impeded antegrade coronary flow and signs of myocardial ischemia.
Cannulation of the Left Coronary Ostium
Engagement of the left coronary ostium is usually quite easy with the Judkins technique. As Judkins himself has stated, “No points are earned for coronary catheterization—the catheters know where to go if not thwarted by the operator” (23). If a left Judkins catheter with a 4-cm curve (commonly referred to as a JL4) is simply allowed to remain en face as it is advanced down into the aortic root, it will engage the left coronary ostium without further manipulation in 80 to 90% of patients (Fig. 11.4). Engagement should take place with the arm of the catheter traversing the ascending aorta at an angle of approximately 45°, the tip of the catheter in a more or less horizontal orientation, and with no change in the pressure waveform recorded from the catheter tip.
Figure 11.4 Judkins technique for catheterization of the left and right coronary arteries as viewed in the left anterior oblique (LAO) projection. In a patient with a normal-size aortic arch, simple advancement of the JL4 catheter leads to intubation of the left coronary ostium (A–C). In a patient with an enlarged aortic root (D), the arm of the JL4 may be too short, causing the catheter tip to point upward or even flip back into its packaged shape (dotted catheter). A catheter with an appropriately longer arm (a JL5 or JL6) is required. To catheterize the right coronary ostium, the right Judkins catheter is advanced around the aortic arch with its tip directed leftward, as viewed in the LAO projection, until it reaches a position 2 to 3 cm above the level of the left coronary ostium (E). Clockwise rotation causes the catheter tip to drop into the aortic root and point anteriorly (F). Slight further rotation causes the catheter tip to enter the right coronary ostium (G).
P.192

In patients with a widened aortic root owing to aortic valve disease or long-standing hypertension, the 4-cm left Judkins curve may be too short to allow successful engagement: The catheter arm may lie nearly horizontally across the aortic root with the tip pointing vertically against the roof of the left main artery, or the catheter may even refold into its packaged shape during advancement into the aortic root (Fig. 11.4D). In this case, a left Judkins catheter with a larger (JL4.5, JL5, or even JL6) curve should be selected. In the long run, changing to a larger catheter under these circumstances may end up saving time compared with trying to make an unsuitable catheter work.
In the occasional patient with a short or narrow aortic root (usually a younger female, particularly if of short stature), even the 4-cm Judkins curve may be too long. When brought down into the aortic root, the catheter arm may lie nearly vertically with the tip pointing downward below the left coronary ostium. The left ostium may still be engaged despite this somewhat unfavorable situation by pushing the catheter down into the left sinus of Valsalva for approximately 10 seconds to tighten the tip angle and then withdrawing the catheter slowly. Having the patient take a deep breath during this maneuver also helps by pulling the heart into a more vertical position to assist in engagement of the left ostium. The most satisfactory approach, however, is to exchange for a JL3.5 catheter with a shorter curve.
On rare occasions, the left coronary ostium lies out of plane (typically high and posterior), as seen in the right anterior oblique (RAO) projection where the ostium is seen to be posterior to the catheter tip. In this case, limited counterclockwise rotation of the left Judkins catheter may help orient the catheter’s tip posteriorly and facilitate engagement. Too much rotation of this catheter, however, may result in a refolded catheter that requires guidewire reinsertion to straighten. In that case, it may be helpful to step up to the next larger Judkins curve. Alternately, some operators prefer to switch to a left Amplatz shape (Fig. 11.1; (available in progressively larger curves—1, 2, 3, 4). Amplatz catheters (24) are more tolerant of rotational maneuvering and allow easy engagement of left coronary ostia that lie out of the conventional Judkins plane, as well as subselective engagement of the left anterior descending and circumflex coronary arteries in patients with short left main coronary segments or separate left coronary ostia. The left Amplatz is advanced around the arch oriented toward the left coronary ostium (Fig. 11.5). The tip of the catheter usually comes to rest in the sinus of Valsalva below the coronary ostium. As the catheter is advanced farther, however, the Amplatz shape causes the tip of the catheter to ride up the wall of the sinus until it engages the ostium. At that point,
P.193

slight withdrawal of the catheter causes deeper engagement of the coronary ostium, whereas further slight advancement causes paradoxic retraction of the catheter tip.
Figure 11.5 Catheterization of the left coronary with an Amplatz catheter. The catheter should be advanced into the ascending aorta with its tip pointing downward so that the terminal catheter configuration resembles a diving duck. As the Amplatz catheter is advanced into the left sinus of Valsalva, its tip initially lies below the left coronary ostium (left). Further advancement causes the tip to ride up the aortic wall and enter the ostium (center). Slight withdrawal of the catheter causes the tip to seat more deeply in the ostium (right).
Cannulation of the Right Coronary Ostium
The Judkins technique for engaging the right coronary ostium requires slightly more catheter manipulation than cannulation of the left coronary ostium (16,23). After being flushed and filled with contrast in the descending aorta (with the catheter tip directed anteriorly to avoid injection into the intercostal arteries), the right Judkins catheter with a 4-cm curve (JR4) is brought around the aortic arch with the tip facing inward until it comes to lie against the right side of the aortic root with its tip aimed toward the left coronary ostium (Fig. 11.4). In a left anterior oblique (LAO) projection, the operator slowly and carefully rotates the catheter clockwise by nearly 180° to engage the right coronary artery. The tip of the right Judkins catheter tends to drop more deeply into the aortic root when the catheter is rotated, as the tertiary curve of the right Judkins shape aligns with the top of the aortic arch. To compensate for this effect, the operator must either begin the rotational maneuver with the tip 2 to 3 cm above the coronary ostium or withdraw the catheter slowly during rotation. Care must be taken to avoid overrotation of the catheter, which tends to cause the catheter tip to engage too deeply into the right coronary artery. To avoid this common technical error, the operator should be prepared to apply a small amount of counterclockwise torque immediately as the tip of the catheter enters the ostium. Catheters with smaller (3.5-cm) or larger (5- or 6-cm) Judkins curves or right Amplatz catheters (AR1 or AR2) may be of value if aortic root configuration and proximal right coronary anatomy make engagement difficult.
Sometimes, the right coronary ostium lies high and anterior above the commissure of the left and right aortic valve leaflets rather than in the middle of the right sinus. If it has not been possible to engage the right coronary with the approach described above, a nonselective injection should be performed into the right sinus of Valsalva. This will show the high-anterior origin and trigger a change to a left Amplatz (either AL0.75 or AL1) as required to make contact with the aortic wall at that ostium location.
Damping and ventricularization are far more common in the right coronary artery than in the left. The cause may be (a) the generally smaller caliber of the vessel (particularly in nondominant vessels; see below), (b) ostial spasm around the catheter tip, (c) selective engagement of the conus branch, or (d) true ostial stenosis. These problems in right coronary engagement can usually be elucidated by nonselective injections into the right sinus of Valsalva or cautious injections in the damped position with immediate postinjection withdrawal of the catheter. As mentioned above, a 6 or 7F angioplasty guiding catheter with side holes near the tip may be used to allow uninterrupted coronary perfusion between contrast injections, if necessitated by true ostial or proximal right coronary disease.
Cannulation of Saphenous Vein and Free Arterial Grafts
Despite the high initial rate of anginal relief following bypass surgery, 3 to 12% of saphenous vein grafts occlude within the first month. Additional veins occlude between 1 month and 1 year after surgery due to exaggerated neointimal hyperplasia. By far the dominant failure mode of saphenous vein graft failure beyond 1 year, however, is diffuse graft atherosclerosis, which accounts for a 50% graft closure rate by 7 years (25). Free arterial grafts (free radial or free internal mammary) are sometimes used instead of saphenous vein grafts, and these have an intermediate long-term patency between that of saphenous vein grafts and pedicled internal mammary grafts (see next page). An
P.194

increasing number of patients thus develop recurrent angina after prior bypass surgery owing to vein graft or progressive native vessel disease, and these patients account for more than 20% of the diagnostic procedures in our laboratory.
The proximal anastomosis of a vein graft or free arterial graft is usually placed on the right or left anterior aortic surface, several centimeters above the sinuses of Valsalva. Because many surgeons still resist the practice of placing radiopaque markers on the proximal graft (26), the operator must generally rely on the surgeon’s operative report or diagram, as well as knowledge of usual surgical practice in her or his own institution. The operative report always should be obtained before elective angiography on any patient with prior bypass surgery, but is absolutely essential on patients who underwent their operation at another medical center (where local preference may include practices like proximal anastomosis to the right posterior surface of the aorta, see below), or even proximal anastomosis to the descending aorta in patients with aortic root disease. It may thus be quite frustrating to embark on coronary angiography in a patient with prior bypass surgery without a detailed graft map, operative note, or prior detailed catheterization report/films in hand.
Most commonly, grafts to the left coronary arise from the left anterior surface of the aorta, with grafts to the circumflex system usually placed somewhat higher on the aorta than those to the left anterior descending or diagonal branches. Alternatively, some surgeons prefer to route grafts to the circumflex through the transverse sinus behind the heart, in which case the circumflex graft may originate from the posterior surface of the aorta. Grafts to the right coronary (or the distal portions of a dominant circumflex) usually originate from the right anterior surface of the aorta, above and somewhat behind the plane of the native right coronary ostium. We generally use the right Judkins (JR4) or Amplatz (AL1) catheter to engage anterior (i.e., left) coronary grafts. Special left coronary bypass, internal mammary, or hockey stick catheters may be required for left grafts that originate with an upward trajectory (Fig. 11.6). For downward-pointing right coronary grafts, we prefer a soft catheter with no primary curve (a multipurpose, Wexler, or JR3.5 short-tip catheter), which provides better alignment with the proximal portion of the graft and thus better opacification. The Wexler catheter can also be used for grafts originating from the left or posterior surface of the aorta. Since its tip remains in contact with the aortic wall, the shaft of this catheter can be rotated or the tip can be flexed to bring it into alignment with the proximal graft once the ostium has been engaged.
If no markers have been provided, the catheter tip should be oriented against the appropriate aortic wall and slowly advanced and then withdrawn until its tip catches in a graft ostium. The graft is injected in multiple projections that show its origin, shaft, distal anastomosis, and the native vessels beyond the anastomosis. This process must then be repeated until all graft sites have been identified. Grafts should not be written off as occluded unless a clear stump is demonstrated. If the myocardial territory supplied by a graft assumed to be occluded is still contracting, and there is no evident native or collateral blood supply to that territory, there may be a missed graft—the myocardium cannot function without a visible means of support! In that case, it may be valuable to perform an aortogram in an appropriate view to try to demonstrate flow in and locate the origin of such a missed graft. The emergence of effective therapies for focal lesions in vein grafts has placed a premium on being able to find and fix such diseased grafts before they occlude (Fig. 11.7; see Chapters 23,24 and 25).
Figure 11.6 Catheters used for bypass graft angiography. Although the right Judkins or Amplatz catheters can be used for many anterior takeoff vein grafts, the catheters shown here may be useful. Left to right. Wexler, multipurpose, hockey stick shape, and internal mammary.
Internal Mammary Cannulation
Based on their superior demonstrated 10-year patency, the pedicled left and right internal mammary arteries (IMAs, also known as internal thoracic arteries [ITAs]) have become the conduits of choice. The proximal end of this graft remains attached to the subclavian artery (supplying
P.195

the nutritional needs of the graft itself), as the vessel is freed up from its lower sternal attachments and anastomosed to the target coronary artery (usually the left anterior descending). More than 90% of current elective bypass procedures involve placement of at least one internal mammary graft.
Figure 11.7 A. Sample of saphenous vein graft angiography, showing an occluded graft to the circumflex, filled with thrombus (top left, open arrow). A drug-infusion catheter (Tracker, Target Therapeutics) was placed (bottom left, curved arrow) and used to administer Urokinase (50,000 IU/hour) overnight. The following morning (top right), the thrombus had been dissolved, revealing the underlying ulcerated culprit lesion. This was treated with a single Palmaz-Schatz coronary stent (bottom right), re-establishing full patency. B. Saphenous vein graft with origin localized by ring marker implanted at the time of surgery.
Successful cannulation (27) requires knowledge of the left subclavian and brachiocephalic trunk as well as the right subclavian arteries, as shown in. Fig. 11.8A. It is also important to understand some of the common anatomic variants in the internal mammary artery, including more proximal origin in the vertical portion of the subclavian, or origin as a common vessel with the thyrocervical trunk.
Although uncommon, these grafts can develop significant lesions, making it important to evaluate such grafts during any postbypass catheterization. In patients with early recurrence of angina (within the first 6 months after surgery), the most common lesion is located at the distal mammary-coronary anastomosis. It is usually due to local intimal hyperplasia rather than atherosclerosis and responds well to balloon angioplasty (see Chapter 22).
P.196

Flow-limiting kinks may also be present in the midgraft, and ostial lesions at the origin of the internal mammary from the subclavian may also occur. In patients years postbypass, significant lesions may develop in the native coronary artery beyond the internal mammary touchdown. In addition to establishing the patency of the internal mammary itself, it may also be important to look for large nonligated side branches that may divert flow from the coronary circulation and whose occlusion (in the occasional patient) may be required for angina relief (28). It is also important to look for stenoses in the subclavian artery before the takeoff of the internal mammary that may compromise the inflow to the graft and thereby cause myocardial ischemia (Fig. 11.9). Such lesions may require construction of a carotid-to-subclavian graft, or more commonly stent placement (29) to restore normal flow to the internal mammary and vertebral branches of the subclavian artery (see Chapters 14 and 26).
Figure 11.8 Internal mammary angiography. A. Aortic arch injection shows the left internal mammary artery (LIMA) originating from the left subclavian (LS), just opposite the thyrocervical trunk (TCT) and distal to the right vertebral artery (VERT). The right internal mammary artery (RIMA) originates from the right subclavian (RS) just distal to the bifurcation of the right carotid from the brachiocephalic trunk (BT). B. Schematic diagram shows the corresponding arch vessel origins. Note that the left subclavian originates just inside the patient’s leftmost edge of the wedge-shaped shadow cast by the upper-mediastinal structures in the left anterior oblique projection. Catheter manipulation in this projection facilitates advancement of a guidewire into the LS (step 1), facilitating selective cannulation of the LIMA during catheter withdrawal and slight counterclockwise rotation (step 2, see text). C. Variant in which internal mammary originates in common with thyrocervical trunk, resulting in poor opacification. An angioplasty guide wire was placed down the internal mammary through the 6F diagnostic catheter and used to advance the tip of the diagnostic catheter selectively down the IMA. From that position, sufficient opacification was obtained to demonstrate occlusion of the distal left anterior descending (LAD) beyond the anastomosis as the cause of the patient’s recurrent angina.
Although mammary grafts can be studied easily from the ipsilateral brachial approach, we prefer the femoral approach using a soft-tip preformed internal mammary catheter, which resembles a right Judkins catheter except for a tighter primary curve. This used to be a time-consuming (up to 20 minutes for some operators) process, but has been reduced to less than 3 minutes in our laboratory by adoption of a systematic strategy (see Fig. 11.8B; 27). In the LAO projection, cannulation of the left internal mammary artery begins by advancement of this catheter into the aortic arch until it lies just inside the left edge of the wedgelike density formed by the shadow of the upper mediastinum against the lung fields. With 1 to 2 cm of J guidewire protruding from its tip, the mammary catheter is rotated counterclockwise until it falls into the subclavian artery origin. From there, the wire can be advanced well out into the axillary artery. The mammary catheter is then advanced over the wire, into the midsubclavian, where the guidewire is then removed and the catheter is flushed and filled with
P.197

contrast. A low-osmolar contrast agent should be used to avoid causing CNS toxicity by reflux of hyperosmolar ionic contrast up the vertebral arteries. Switching to the straight AP projection, the catheter is rotated counterclockwise slightly (to make the tip point slightly anteriorly) as it is withdrawn slowly until the internal mammary is engaged. Intermittent gentle puffs of contrast will help localize the mammary origin during this withdrawal. Great care should be taken to avoid catheter tip trauma/dissection of the relatively delicate mammary vessel.
Figure 11.9 Left subclavian stenosis in a patient with recurrent angina in the distribution of the otherwise patent left internal mammary artery (left), treated by stenting (right).
If selective cannulation is difficult because of tortuosity or anatomic variations, a variety of superselective or nonselective techniques can be used to permit angiographic evaluation. Nonselective injections into the subclavian will generally allow adequate opacification to see that the internal mammary is open, but generally not to provide detailed information about the distal native vessel. Inflation of a blood pressure cuff on the ipsilateral arm may help reduce runoff through the axillary artery and improve opacification of the internal mammary in cases where selective cannulation is difficult. When selective cannulation proves difficult, we sometimes attach a Y connector to the hub of the diagnostic internal mammary catheter and advance a 0.014 soft-tipped coronary angioplasty guidewire into the mammary to serve as a support for catheter advancement.
Cannulation of the right internal mammary artery may be slightly more difficult because of the need to avoid the right carotid before entering the right subclavian itself. Again in the LAO projection, the upper mediastinal wedge is identified. The mammary catheter with protruding J wire is taken to the right edge of this shadow and rotated counterclockwise until it falls into the brachiocephalic trunk. The wire is then advanced toward the right subclavian artery. Predilection for the wire to advance into the right carotid artery may require removing the guidewire and performing a nonselective contrast injection in the brachiocephalic trunk to identify the origin of the subclavian branch. The RAO-caudal projection often gives the best spatial resolution of the right carotid and right subclavian origins, after which steerable Wholey guidewire (Mallinckrodt) can be used to cannulate the subclavian. Once the wire is firmly out of the subclavian artery, the mammary catheter is advanced as described above. For cannulation of the right internal mammary artery, however, the catheter is rotated slightly clockwise during withdrawal to point its tip anteriorly.
Gastroepiploic Graft Cannulation
Taken together, the left and right internal mammary arteries can be used to revascularize most lesions in the left anterior descending, proximal circumflex, and proximal right coronary arteries. Even with sequential distal anastomoses, however, the fact that there are only two internal mammary arteries means that most revascularization procedures still suffer the long-term limitations associated with the use of saphenous veins. Free segments of radial artery have also been used as bypass conduits, either from the ascending aorta (like a saphenous vein) or from the descending thoracic aorta (30) in some patients undergoing repeat bypass surgery. Although the radial artery may have slight benefit over the saphenous vein, it is prone to
P.198

spasm in the early postop period, and does not match the long-term patency record of the internal mammary artery (because it does not retain its blood supply and innervation when used as a free graft). The effort to perform all arterial bypass has brought back the right gastroepiploic artery (as an arterial pedicle graft) for anastomosis to the posterior descending or other vessels on the inferior surface of the heart (31,32). The right gastroepiploic normally supplies most of the greater curvature of the stomach, but can be dissected free from that organ and tunneled through the diaphragm to reach the inferior wall of the heart. Angiography of this vessel is possible using standard visceral angiographic catheters (e.g., Cobra) which are designed to enter visceral arteries such as the celiac axis (33). From there, the catheter can be advanced into the common hepatic (as opposed to the splenic) artery and then turned downward into the gastroduodenal artery (Fig. 11.10). A 0.025-inch Glidewire (Terumo) can then be used to cannulate the right gastroepiploic (as opposed to the superior pancreatoduodenal artery) if more selective injection is desired.
Figure 11.10 A. Gastroepiploic graft anatomy. The common hepatic artery (CHA) originates with the splenic artery (SA) from the celiac trunk (CT). The gastroduodenal artery (GDA) originates from the CHA, which then becomes the proper hepatic artery (PHA). The terminal branches of the GDA are the pancreatoduodenal (PD) and the right gastroepiploic artery (GEA), shown here undergoing angioplasty of a lesion at its anastomosis to the right coronary artery (RCA). (Diagram from Ishiki T, et al. Percutaneous angioplasty of stenosed gastroepiploic artery grafts. J Am Coll Cardiol 1993,21:727, 1993, with permission.) B. Free radial graft from the descending aorta to an obtuse marginal graft, cannulated using a Cobra visceral angiographic catheter. Localization of the graft ostium was aided by the presence of multiple surgical clips used to ligate small side branches of the radial artery at the time of bypass.
P.199

THE BRACHIAL OR RADIAL APPROACH
The technique of brachial artery cutdown was the first approach used for selective coronary angiography, as described in Chapter 5. Dr. F. Mason Sones, Jr., designed the original catheter for this approach—a thin-walled radiopaque woven Dacron catheter with a 2.67-mm (8F) shaft diameter (16,34), tapering to 5F external diameter at a point 5 cm from its tip. In addition to the open tip, current models include side holes that are arranged in opposed pairs within 7 mm of the distal end. As Sones stated, this provides a “flexible finger” that may be curved upward into the coronary orifices by pressure of the more rigid shaft against the aortic valve cusps. This enables the Sones catheter to be used for cannulation of both the left and right coronary arteries, as well as entry into the left ventricle for ventriculography. The standard Sones catheter is available in lengths of 80, 100, and 125 cm and 6 to 8F diameters. Most operators now use a different Sones-type coronary catheter constructed of polyurethane and made by Cordis Corporation. This catheter traverses a tortuous subclavian system with much greater facility and smoothness than does the woven Dacron catheter, and its enhanced torque control and reduced coefficient of friction ease engagement of the coronary ostia. See Fig. 11.1 for a variety of preshaped coronary catheters, which are also effective from the brachial approach (35). In general, similar techniques apply for use of standard Judkins and Amplatz shapes from the left brachial or radial arteries, as described above for the femoral approach. From the right brachial or radial arteries, smaller left Judkins curves or special catheter shapes are preferable (see Chapter 4).
When the Sones method is used from the right arm, catheter tip pressure should be monitored continuously once the catheter enters the brachial artery. Further passage of the catheter into the subclavian and brachiocephalic arteries should be accomplished under both pressure monitoring and fluoroscopic visualization. Occasionally, it may be difficult to pass the catheter from the subclavian artery to the aortic arch, but a simple maneuver by the patient—such as a deep inspiration, shrugging the shoulders, or turning the head to the left—often facilitates passage of the catheter into the ascending aorta. If passage of the catheter from the subclavian artery to the ascending aorta is not accomplished immediately and with complete ease, the operator should stop catheter manipulation and use a soft J-tipped 0.035-inch guidewire. Once the catheter is in the ascending aorta, the guidewire is removed and the catheter is aspirated, flushed, and reconnected to the rotating adapter of the manifold, either directly or by a short length of large-bore flexible connecting tubing.
With the Sones technique, selective engagement of the left coronary artery is accomplished as follows. In a left anterior oblique projection, the sinus of Valsalva containing the ostium of the left coronary artery lies to the left, and the sinus containing the ostium of the right coronary artery lies to the right. The noncoronary sinus lies posteriorly. The operator advances the catheter to the aortic valve and then continues to advance the catheter until its tip bends cephalad and points toward the left coronary ostium. When the catheter is properly positioned with its tip bent cephalad, slightly advancing or rotating the catheter usually results in selective engagement of the left coronary ostium, which is verified by a small injection of radiographic contrast agent. Occasionally, a deep breath taken by the patient will facilitate this selective engagement. Our usual approach, illustrated in the upper left panel of Fig. 11.11, involves forming a smooth shallow loop and gradually inching up to the ostium from below. If the distal 2 to 3 mm of the catheter tip bends downward during this inching up process, the tip may enter the left coronary artery, giving a cobra head appearance (see Fig. 11.11, top right) similar to that achieved with the left Amplatz catheter (see Fig. 11.5). For the high takeoff left coronary ostium, the catheter may have the appearance (as in Fig. 11.11, bottom) in which the catheter tip is lying across the ostium at right angles to the course of the left main coronary artery. During contrast injection in this
P.200

instance, coronary blood flow generally carries the contrast agent down the vessel, giving good opacification of the entire left coronary artery. Once the catheter tip has engaged the coronary ostium and no damping of pressure from the catheter tip is observed, cineangiography may be performed with selective injection of radiopaque material in a variety of views, as described below.
Figure 11.11 Selective catheterization of the left coronary artery using the Sones catheter. The standard approach involves forming a smooth shallow loop and gradually “inching up” to the ostium from below. If the distal 2 to 3 mm of the catheter tip bends downward during this inching-up process, the tip may enter the left coronary artery, giving a cobra head appearance (upper right). When the left coronary ostium originates high in the left sinus of Valsalva (high takeoff left coronary artery), the catheter may have the appearance seen in the bottom panel, where the tip is lying across the ostium at right angles to the course of the left main coronary artery. During coronary injection in this instance, coronary blood flow usually carries the contrast agent down the vessel, giving good opacification of the entire left coronary artery.
Selective engagement of the right coronary orifice may be accomplished as illustrated in steps 1 to 3 of Fig. 11.12. In the shallow LAO projection, the catheter is curved up toward the left coronary artery (step 1) and clockwise torque is applied. While the operator is gradually applying clockwise torque, a gentle to-and-fro motion of the catheter (the to-and-fro excursions are not more than 5 to 10 mm in length) helps to translate the applied torque to the catheter tip. When the tip starts moving in its clockwise sweep of the anterior wall of the aorta, the operator maintains (but does not increase) a clockwise torque on the catheter and simultaneously pulls the catheter back slightly (step 2, Fig. 11.12) because the right coronary ostium is lower than that of the left coronary artery. At this point, the catheter usually makes an abrupt turn into the right coronary ostium, at which time the operator must release all torque to prevent the catheter tip from continuing its sweep past the ostium. On occasion, the Sones catheter literally leaps into the right coronary artery and will be 4 to 5 cm down its lumen. If this occurs, the catheter should be gently withdrawn until its tip is stable just within the ostium.
Another technique for catheterizing the right coronary artery involves a more direct approach by way of the right coronary cusp. With the catheter in the right sinus, the operator should make a small curve on the tip, directed rightward. A small dose of contrast material in the right sinus of Valsalva will allow visualization of the right coronary orifice and thus facilitate selective engagement. Occasionally, a deep inspiration by the patient accompanied by gentle advancement of the catheter to the right of the aortic root results in selective engagement of the right coronary artery.
Figure 11.12 Selective catheterization of the right coronary artery using the Sones catheter. In the shallow left anterior oblique (LAO) projection, the catheter is curved upward and to the left (1) and clockwise torque is applied. While the operator is gradually applying clockwise torque, a gentle to-and-fro motion of the catheter helps to translate the applied torque to the catheter tip. When the tip starts moving in its clockwise sweep of the anterior wall of the aorta, the operator maintains (but does not increase) a clockwise torque tension on the catheter and simultaneously pulls the catheter back slightly (2), because the right coronary ostium is lower than that of the left coronary artery. At this point, the catheter usually makes an abrupt leap into the right coronary ostium (3), at which time the operator must release all torque to prevent the catheter tip from continuing its sweep and passing by the ostium. See text for details and alternative methods.
ADVERSE EFFECTS OF CORONARY ANGIOGRAPHY
Once the coronary vessels have been engaged, optimal selective angiography requires transient but nearly complete replacement of blood flow with the radiopaque contrast agent. A wide variety of iodine-containing agents are currently used for coronary angiography and have already been discussed in greater detail in Chapter 2. Older high-osmolar contrast agent had a number of potentially deleterious effects during coronary injection (see Chapters 2 and 3) that include the following: (a) transient (10- to 20-second) hemodynamic depression marked by arterial hypotension and elevation of the left ventricular end diastolic pressure, (b) electrocardiographic effects with T-wave inversion or peaking in the inferior leads (during right and left coronary injection, respectively), sinus slowing or arrest, and prolongation of the PR, QRS, and QT intervals (36,37), (c) significant arrhythmia (asystole or ventricular tachycardia/fibrillation) (38), (d) myocardial ischemia owing to interruption of oxygen delivery or inappropriate arteriolar vasodilatation (coronary “steal”), (e) allergic reaction (39), and (f) cumulative renal toxicity (40). Some (but not all) of these adverse effects are eliminated by use of a low-osmolar contrast agent, albeit at a modest increased expense (41).
P.201

Although newer low-osmolar contrast agents have less prominent side effects, patients undergoing coronary angiography should always be monitored continuously in terms of clinical status, surface electrocardiogram, and arterial pressure from the catheter tip. In patients with baseline left ventricular dysfunction or marked ischemic instability, we also like to perform a right heart catheterization, and display pulmonary artery pressure continuously on the same scale as the arterial pressure as an early indicator of procedural problems or progressive decompensation. A significant rise in pulmonary artery mean or diastolic pressure should prompt temporary suspension of angiography and initiation of treatment (e.g., intravenous furosemide, nitroglycerin, nitroprusside) before frank pulmonary edema develops. The venous sheath also provides a ready route for the rapid administration of fluid or medications through its side arm and allows rapid insertion of a temporary pacing electrode if needed. Prophylactic placement of temporary pacing electrodes in patients undergoing coronary angiography is not indicated (42), since most episodes of bradycardia or asystole are brief and are resolved promptly by having the patient give a forceful cough, which elevates central aortic pressure and probably helps wash residual contrast out of the myocardial capillary bed. Similarly, prophylactic drugs are not given routinely to prevent ventricular tachyarrhythmias, although appropriate drugs (lidocaine, amiodarone, atropine, epinephrine, and so on), a defibrillator, and airway management equipment are always kept at the ready and can be brought into play within seconds.
One of the most common adverse effects seen during coronary angiography is the provocation of myocardial ischemia, particularly in patients with unstable angina. In very unstable patients, we modify our usual practice of performing the left ventriculogram before coronary angiography (lest an adverse reaction to the ventriculogram compromise the more crucial coronary study). When myocardial ischemia does occur during coronary angiography, the best course of action is to remove the catheter from the coronary ostium and temporarily suspend injections until angina resolves. If this takes more than 30 seconds, we typically administer nitroglycerin (200 mg bolus, repeated at 30-second intervals up to a total of 1,000 mg) into either the involved coronary artery or the pulmonary artery catheter. If marked arterial hypertension is present and fails to respond to nitroglycerin, we may administer other vasodilators as needed to bring the blood pressure down. In patients with inappropriate tachycardia in the setting of angina and reasonable systolic left ventricular function, intravenous propranolol (1 mg every minute to a total dose of 0.1 to 0.15 mg/kg) or an infusion of a short-acting beta-blocking agent (esmolol) is frequently beneficial. Only rarely (in patients with severe three-vessel and/or left main coronary disease and those whose ischemia is associated with hypotension) is myocardial ischemia severe enough and refractory to the above management program to prompt placement of an intra-aortic counterpulsation balloon in the contralateral femoral artery before completion of coronary angiography (see Chapter 21). In any patient with prolonged or refractory ischemia during diagnostic coronary angiography, it may be worthwhile to perform limited re-examination of the coronary vessels to determine whether the angiographic procedure has caused a problem (spasm, dissection, thrombosis) that might require immediate treatment with additional vasodilators, coronary intervention, thrombolysis, or emergency bypass surgery.
Severe allergic reactions are uncommon during coronary angiography and are best prevented by 18 to 24 hours of premedication (prednisone 20 to 40 mg and cimetidine 300 mg every 6 hours; 32) and/or use of a nonionic contrast agent in patients with a history of prior allergic reaction to radiographic contrast (41). When a severe unexpected reaction does occur, it usually responds promptly to the intravenous administration of epinephrine (0.1 mg equals 1 mL of the 1:10,000 solution available on most emergency carts, repeated every 2 minutes until the blood pressure and/or wheezing improves). Larger bolus doses of epinephrine are to be avoided, because they may provoke marked tachycardia, hypertension, and arrhythmia.
Renal insufficiency may develop after coronary angiography, particularly in patients who are hypovolemic, who receive large volumes of contrast (more than 3 mL/kg), or who have had prior renal insufficiency, diabetes, or multiple myeloma (33). In these patients, every effort should be made to give adequate hydration preprocedure and postprocedure (see also Chapters 2 and 3). Use of low-osmolar or iso-osmolar contrast agents may be helpful in this situation, but their real benefit remains controversial (41).
INJECTION TECHNIQUE
As mentioned previously, high-quality coronary angiography requires selective injection of radiographic contrast at an adequate rate and volume to transiently replace the blood contained in the involved vessel with slight but continuous reflux into the aortic root. Too timid an injection allows intermittent entry of nonopaque blood into the coronary artery (producing contrast dilution or streaming, which makes interpretation of lesions difficult) and fails to visualize the coronary ostium and proximal coronary branches. However, too vigorous an injection may cause coronary dissection or excessive myocardial blushing, and too prolonged an injection may contribute to increased myocardial depression or bradycardia.
We train our fellows to adjust the rate and duration of manual contrast injection to match the observed filling pattern of the particular vessel being injected. Injection velocity should be built up gradually during the first second until the injection rate is adequate to completely replace antegrade blood flow into the coronary ostium (Fig. 11.13). The associated rate and volume required to
P.202

accomplish this goal have been measured (43) and were found to average 7 mL at 2.1 mL/second in the left and 4.8 mL at 1.7 mL/second in the right coronary. In patients with occlusion, much lower rates and volumes are required, and in patients with left ventricular hypertrophy (e.g., aortic stenosis, hypertrophic myopathy) much greater volumes and higher rates of injection may be required.
Figure 11.13 Suggested injection pattern for coronary angiography. To appropriately replace antegrade coronary blood flow with contrast medium throughout the cardiac cycle, the operator should build up the velocity of injection over 1 to 2 seconds until no unopacified blood is seen to enter the ostium and there is reflux of contrast medium into the aorta during systole and diastole. This injection is maintained until the entire coronary artery is filled with contrast medium. If the ostium has not been well seen, a brief extra push should be given to cause adequate reflux into the aortic root, and the injection should be terminated. Prolonged held inspiration with some degree of Valsalva maneuver is sometimes used during Sones angiography to reduce coronary flow and make it much easier to replace blood flow during manual contrast injection.
The injection should be maintained until the entire vessel is opacified. If there is any question about whether the body of the injection has provided adequate reflux to visualize the coronary ostium, an additional burst of contrast (extra reflux) should be given before the injection is terminated. The injection should then be terminated abruptly by turning the manifold stopcock back to monitor pressure, although cine filming should continue until opacification of distal vessels or late-filling branches is complete. The operator should monitor for excessive bradycardia or hypotension, review the video loop, and set up the gantry angles for the next injection. To avoid problems, each injection should begin with a completely full (and bubble-free) injection syringe, held with the handle slightly elevated so that any microbubbles will drift up toward the plunger. The injection syringe should be managed in such a way as to avoid mixtures of blood and contrast, because such mixtures may promote formation of thrombi (particularly when nonionic contrast agents are used).
Although manual contrast injection is the standard technique in coronary angiography, some operators favor use of a power injector (as used in left ventriculography or aortography) to perform coronary injections (44). The injector is preset for a rate to match the involved vessel (2 to 3 mL/second for the right and 3 to 4 mL/second for the left coronary) and activated by a foot switch for a sufficient time to fill the coronary with contrast (generally 2 to 3 seconds). This approach allows a single operator to perform injections and move the table and has proved safe in thousands of procedures. A special power injector has also been introduced (Acist, Bracco, Eden Prairie, MN) that can perform such power injections under rate control by finger pressure on a sterile control handle, reverting automatically to pressure monitoring when the injection is terminated. This may be of value when a single operator must perform injections and pan the table during diagnostic coronary angiography.
ANATOMY, ANGIOGRAPHIC VIEWS, AND QUANTITATION OF STENOSIS
Coronary Anatomy
The coronary angiographer must develop a detailed familiarity with normal coronary arterial anatomy and its common variants. For individuals just learning coronary anatomy, the main coronary trunks can be considered to lie in one of two orthogonal planes (Fig. 11.14). The anterior descending and posterior descending coronary arteries lie in the plane of the interventricular septum, whereas the right and circumflex coronary trunks lie in the plane of the atrioventricular valves. In the 60° left anterior oblique (LAO) projection, one is looking down the plane of the interventricular septum, with the plane of the AV valves seen en face; in the 30° right anterior oblique (RAO) projection, one is looking down the plane of the AV valves, with the plane of the interventricular septum seen en face. The major segments and branches have each been assigned a numerical identification in the BARI modification (45) of the CASS nomenclature (Fig. 11.15).
Right-Dominant Circulation
The right coronary artery gives rise to the conus branch (which supplies the right ventricular outflow tract) and one or more acute marginal branches (which supply the free wall of the right ventricle), whether or not the circulation is right dominant. In the 85% of patients who have a right-dominant coronary artery, it goes on to form the AV nodal artery, the posterior descending and the posterolateral left ventricular branches that supply the inferior aspect of the interventricular septum (see Fig. 11.14). The left main trunk branches after a short (but variable) distance into the left anterior descending and the circumflex coronary arteries. The left anterior descending artery gives rise to septal branches that curve down into the interventricular septum, as well as diagonal branches that wrap over the anterolateral free wall of the left ventricle.
Some patients have a twin left anterior descending system, in which one trunk (frequently intramyocardial) supplies the entire septum and the other trunk runs on the surface of the heart supplying all the diagonal branches. The
P.203

circumflex artery courses clockwise in the AV groove (viewed from the apex) as it gives rise to one or more obtuse marginal branches that supply the lateral free wall of the left ventricle, but does not reach the crux in patients with a right-dominant circulation. In some patients, a large intermedius or ramus medianus branch (neither a diagonal nor a marginal) may originate directly from the left main trunk, bisecting the angle between the left anterior descending and circumflex arteries, to create a trifurcation pattern of the left main coronary artery. Regardless of whether the patient is right or left dominant, the sinus node originates as a proximal branch of the right coronary in 60% of patients and as a left atrial branch of the circumflex in the remaining 40% of patients.
Figure 11.14 Representation of coronary anatomy relative to the interventricular and atrioventricular valve planes. Coronary branches are as indicated—L Main (left main), LAD (left anterior descending), D (diagonal), S (septal), CX (circumflex), OM (obtuse marginal), RCA (right coronary), CB (conus branch), SN (sinus node), AcM (acute marginal), PD (posterior descending), PL (posterolateral left ventricular).
Figure 11.15 The numerical coding system and official names of the coronary segments, as used in the Bypass Angioplasty Revascularization Investigation (BARI) study. Right coronary: 1, proximal; 2, middle; 3, distal; 4, posterior descending; 5, posteroatrioventricular; 6, first posterolateral; 7, second posterolateral; 8, third posterolateral; 9, inferior septals; 10, acute marginals. Left coronary: 11, left main; 12, proximal left anterior descending; 13, middle left anterior descending; 14, distal left anterior descending,;15, first diagonal (a, branch of first diagonal); 16, second diagonal,;17, septals (anterior septals); 18, proximal circumflex; 19, middle circumflex; 19a, distal circumflex; 20, 21, and 22, first, second, and third obtuse marginals; 23, left atrioventricular; 24, 25, and 26, first, second, and third posterolaterals (in left- or balanced-dominant system); 27, left posterior descending (in left-dominant system); 28, ramus (ramus intermedius); 29, third diagonal. (From The BARI Protocol. Protocol for the Bypass Angioplasty Revascularization Investigation. Circulation 1991;84:V1, with permission.)
Left-Dominant Circulation
In 8% of patients, the coronary circulation is left dominant; that is, the posterolateral left ventricular, posterior descending, and AV nodal arteries are all supplied by the terminal portion of the left circumflex coronary artery. In such patients, the right coronary artery is small and supplies only
P.204

the right atrium and right ventricle. It may be important to visualize, as a potential source of right-to-left collaterals, but the small diameter of a nondominant right coronary artery predisposes it to damping and catheter-induced spasm (see below, which make limited injections advisable.
Balanced-Dominant Circulation
In about 7% of hearts, there is a codominant or balanced system, in which the right coronary artery gives rise to the posterior descending artery and then terminates, and the circumflex artery gives rise to all the posterior left ventricular branches and perhaps also a parallel posterior descending branch that supplies part of the interventricular septum. In some patients, the supply to the inferior wall may be further fractionated among a short posterior descending branch of the right coronary (which supplies the inferobase), branches of the distal circumflex (which supply the midinferior wall), and branches of the acute marginal (which extend to supply the inferoapex).
Anatomic Variants
Although these basic concepts describe the general pattern of the coronary circulation, it must be noted that there is considerable patient-to-patient variability in the size and position of different coronary arterial branches (46). In 1 to 2% of patients, these coronary anatomic features are sufficiently divergent to qualify as coronary anomalies. Every operator must be thoroughly familiar with these anatomic anomalies and continually vigilant for their occurrence, lest failure to recognize an anomaly result in an incomplete and therefore inadequate examination. In a review of 126,595 cases from the Cleveland Clinic (47), the most common of these anomalies was separate ostia of the left anterior descending and left circumflex arteries (0.41%). When separate ostia of the left anterior descending and left circumflex are present, the catheter will generally sit with its tip in the left anterior descending, although there is generally adequate spillover to opacify the circumflex. If not, separate cannulation of the circumflex may be necessary, using the next-larger size left Judkins catheter (e.g., JL5 instead of JL4) or a left Amplatz catheter. A similar situation may exist in the right coronary artery, where the conus branch may have a separate ostium whose separate cannulation may be necessary to demonstrate important collaterals when reflux during the right coronary injection does not provide adequate reflux to opacify the conus.
The next most common anomaly is origin of the circumflex from the right coronary artery or right sinus of Valsalva (0.37%). This should be suspected when the left main is unusually long and a paucity of vessels to the lateral wall is identified. Careful review of the RAO left ventriculogram may show a dot of contrast just behind the aortic valve when the anomalous circumflex runs posterior to the aorta (48). If an anomalous circumflex is not filled adequately during right coronary injection, it must be cannulated separately (generally with an AL1 catheter). We have seen patients in whom the only coronary lesion was located in such an anomalous circumflex, and failure to identify and opacify this vessel would have led to failure to diagnose and treat the problem.
In another common variant, anomalous vessels (particularly the right coronary artery) may originate unusually high in the aortic root or out of the normal coronary plane (38; Fig. 11.16), making them easier to cannulate using left Amplatz rather than right Judkins catheters. The left coronary may originate from the right sinus of Valsalva (Fig. 11.17), either as a separate ostium (49) or as part of a single coronary (50). Origin of a coronary artery from the noncoronary sinus of Valsalva is rare but has been reported (47,51). The main effect of these coronary anomalies is to test the patience, knowledge, and resourcefulness of the angiographer. Other anomalies, however, may themselves cause myocardial ischemia (even in the absence of atherosclerotic stenosis) and are described later in the section on nonatherosclerotic coronary artery disease.
Angiographic Views
Accurate coronary diagnosis requires coronary injections in multiple views to be sure that all coronary segments are seen clearly without foreshortening or overlap. The angulation of each view is given in two terms. The first term denotes rotation, i.e., the term right anterior oblique (RAO) designates a view where the image intensifier is located over the patient’s right anterior chest wall, and left anterior oblique (LAO) designates a view where the image intensifier is located over the patient’s left anterior chest wall. The second term denotes skew, i.e., the amount of angulation toward the patient’s head (cranial) or foot (caudal). Although the full nomenclature of skew specifies first the source of the beam and then the location of the imaging device (e.g., caudocranial, to denote that the x-ray tube is toward the patient’s feet while the image intensifier is located toward the patient’s head), in practice this is simplified to give just the location of the imaging device. The term RAO caudocranial is thus stated as RAO-cranial.
When cradle systems were in use in the 1970s, these views were usually limited to different degrees of left or right anterior obliquity in the transverse plane, including the classic 60° LAO and 30° RAO projections (see Fig. 11.14). To allow concurrent cranial angulation of the x-ray beam, cradle systems were then modified by propping the patient’s shoulders up on a foam wedge—hence the name sit-up view—to provide compound LAO-cranial projection. In the 1980s, cradle systems were abandoned in favor of parallelogram or rigid U-arm systems supported by a rotating pedestal (see Chapter 2) that allow compound beam angulation in any combination of conventional transverse (LAO, RAO) with skew (cranial, caudal) angulation up to
P.205

45°. Although these views place increased demands on the generator and increase the scattered radiation, there is no doubt that they have improved our ability to define coronary anatomy (Fig. 11.18; 52,53,54).
Figure 11.16 Multidetector computed tomographic image of a patient with anomalous origin of the right coronary artery from the left sinus of Valsalva and a course between the aorta and pulmonary artery (RCA, right coronary artery; LAD, left anterior descending; LC, left circumflex; AO, aorta; RVOT, right ventricular outflow tract).
It is not necessary to perform all potential views in a given patient to constitute an adequate study. Rather, a series of screening views should be used as the foundation of the study, adjusted or supplemented by one or more additional views selected to more completely define suspicious areas. This requires the operator to interpret the coronary anatomy as each injection is made or by digital review—it is not acceptable to simply shoot a series of routine views and hope that the study will prove adequate when reviewed later. Although some laboratories rely on a technician to set up shots and pan the table during coronary angiography, I (DB) believe that each operator should know how to do this himself or herself to develop a good understanding of how the choice of gantry angulation influences the projected coronary anatomy. One valuable training tool in this respect is a simple wire model of the coronary anatomy, which is viewed as it is moved into different angles (Fig. 11.19; 55). A computer program that simulates the effect of changing angles on the projected coronary anatomy is provided on the companion DVD-ROM to this text book. Although there is no substitute for this type of hands-on learning, the discussion below is provided as a rough introduction.
Right Anterior Oblique Projections
For historic reasons relating to cradle systems, the screening views used in many laboratories were the straight LAO-RAO angulations. With the availability of more modern gantry systems, it became clear that certain cranial and caudal angulated views offer far better anatomic definition. Thus, we generally avoid the straight 30° RAO projection of the left coronary, because it suffers from overlap and foreshortening of both the left anterior descending and circumflex vessels (see Fig. 11.18). Instead, our initial view of choice is the RAO-caudal projection (0 to 10° RAO and 15 to 20° caudal), since it provides an excellent view of the left main bifurcation, the proximal left anterior descending artery, and the proximal to midcircumflex artery. The second view we perform is a shallow RAO-cranial projection (0 to 10° RAO and 25 to 40° cranial), which provides a superior view of the mid and distal left anterior descending artery, with clear visualization of the origins of the septal and diagonal branches. This shallow RAO cranial view is also quite good for examination of the distal right coronary artery or distal circumflex, since it effectively unstacks the posterior descending and posterolateral branches and projects them without foreshortening. It seldom, however, provides any useful information about the left main or circumflex coronary artery, because it causes them to be overlapped and foreshortened.
Left Anterior Oblique Projections
The conventional 60° LAO projection is limited by overlap and foreshortening of the left coronary artery, although it is very useful in the evaluation of the proximal and midright coronary artery. The LAO-cranial view, created by the addition of 15 to 30° of cranial angulation, elongates the left main and proximal left anterior descending arteries
P.206

while projecting the intermedius or first diagonal branch downward off the proximal circumflex. If radiographic penetration in this view is difficult, reducing the LAO angulation to 30 to 40° will usually allow the left anterior descending artery to fall into the lucent wedge between the right hemidiaphragm and the spine. Performing the angiographic run during a sustained maximal inspiration will usually pull the diaphragm down and improve x-ray penetration. The LAO-caudal view (40 to 60° LAO and 10 to 20° caudal) projects the left coronary artery upward from the left main in the appearance of a spider (hence the older term, spider view), and usually offers improved visualization of the left main, proximal left anterior descending (LAD), and proximal circumflex arteries. It is particularly valuable in patients whose heart has a horizontal lie, i.e., the origin of the left main artery projects at or below the proximal left anterior descending artery in the standard LAO projection. This view can often be enhanced by filming
P.207

during maximal expiration, which accentuates a horizontal cardiac position and allows a better look from below, although it stresses the radiographic capacity of most older installations.
Figure 11.17 Anomalous origin of the circumflex from the right coronary artery. Top left. Note the long left main and absence of a circumflex during injection of the left coronary artery. Top right. Review of the right anterior oblique (RAO) left ventriculogram shows the telltale dot behind the aortic root, created by an end-on look at the anomalous circumflex coursing behind the aorta. Center left. The anomalous circumflex (Cx) originates from the right sinus of Valsalva with severe stenosis (arrows) responsible for the patient’s unstable anginal syndrome. Center right. The RAO projection shows that the anomalous circumflex (arrow) has a separate ostium immediately posterior to the RCA origin, and then courses behind the aorta to reach the lateral wall of the left ventricle. Bottom left. In a different patient with an acute inferior wall myocardial infarction, a right sinus injection was performed after difficulty was encountered engaging the right coronary, and showed no right coronary ostium but faint filling of a vessel crossing the aorta. Bottom right. A left Amplatz catheter was used to cannulate the anomalous right coronary ostium originating from the left sinus of Valsalva (slightly anterior to the left coronary artery), revealing the RCA occlusion and thrombus (dotted arrow) responsible for the inferior MI, which then underwent primary angioplasty and stenting.
Figure 11.18 Geometry of angulated views. Conventional coronary angiography was performed previously using angulation only in the transverse plane (top), as demonstrated by the 60° left anterior oblique (LAO) and 30° right anterior oblique (RAO) views. Currently, improved x-ray equipment permits simultaneous cranial or caudal angulation in the sagittal plane. Each view is named based on the location of the image intensifier, rather than the older nomenclature specifying the location of both the x-ray tube and intensifier (i.e., cranial is equivalent to caudocranial).
Figure 11.19 Demonstration of angiographic projections using the author’s coronary model. LAO and RAO projections are photographed straight (i.e., with no cranial or caudal angulation) as well as with moderate cranial and moderate caudal angulation (see text for details).
Posteroanterior and Left Lateral Projections
The straight posteroanterior (PA, or “0-0”) and left lateral projections tend to be underused in the era of complex angulation. Because the left main coronary artery curves from a more leftward to an almost anterior direction along its length, the PA projection (sometimes referred to incorrectly as the AP projection) frequently provides the best view of the left main ostium. On the other hand, the shallow RAO-caudal view frequently provides a better look at the more distal left main artery. The left lateral projection is particularly useful in examining the proximal circumflex and the proximal and distal left anterior descending arteries, particularly when combined with slight (10 to 15°) cranial angulation. This projection also provides the best look at the anastomosis of a left internal mammary graft to the middistal left anterior descending and offers an excellent look at the midportion of the right coronary artery, free of the excessive motion seen when this portion of the vessel is viewed in the straight RAO projection. The left lateral projection also has the advantage of allowing easy radiographic penetration in most patients when it is performed with both of the patient’s hands positioned
P.208

behind the head, although it generates the highest degree of backscatter given the proximity of the beam entry point on the patient’s right side to the operator.
Over the past several years, operators in our laboratory have adopted a uniform sequence of these views, adjusting the exact angles slightly in each patient as dictated by test puffs of contrast. Beginning with the left coronary artery, these views include the following:
  • RAO-caudal to visualize the left main, proximal LAD, and proximal circumflex
  • RAO-cranial to visualize the mid and distal LAD without overlap of septal or diagonal branches
  • LAO-cranial to visualize the mid and distal LAD in an orthogonal projection
  • LAO-caudal to visualize the left main and proximal circumflex.
One or more supplemental views (PA, lateral-cranial, lateral-caudal) may then be taken to clarify any areas of uncertainty. The right coronary catheter is then placed, after which three screening views are obtained:
  • LAO to visualize the proximal right coronary artery (RCA)
  • RAO-cranial to visualize the posterior descending and posterolateral branches
  • Lateral to visualize the mid-RCA
Lesion Quantification
To quantify a coronary stenosis accurately, it must be seen in profile, free from artifact related to foreshortening or obfuscation by a crossing vessel. Multiple views are important, because many lesions have a markedly eccentric (elliptical rather than round) lumen (56). When seen across its major axis, the width of the lumen may appear nearly normal, but a clue to the presence of a severe degree of narrowing in the other axis may be marked lucency caused by thinning of the contrast column. Any such suspicious lesions must be examined in a variety of other projections to reveal their true severity and to distinguish the lucency caused by eccentric stenosis from a similar lucency that may be seen adjacent to an area of denser contrast (caused by tortuosity or overlapping vessels in the absence of any true abnormality at the site) through a perceptual artifact known as the Mach effect (57).
The ability of coronary angiography to quantify the degree of stenosis at different points in the coronary circulation is fundamentally limited by the fact that it consists of a “lumen-o-gram,” in which each stenosis can be evaluated only by comparison to an adjacent reference segment that is presumed to be free of disease. In fact, both intravascular ultrasound (56; see Chapter 19) and pathologic examination (58) show that even segments that appear smooth on angiography may harbor substantial plaque. It is thus important to have a sense of the normal caliber of the major coronary arteries (4.5 ± 0.5 mm for the left main, 3.7 ± 0.4 mm for the left anterior descending, 3.4 ± 0.5 mm for a nondominant versus 4.2 ± 0.6 mm for a dominant circumflex, and 3.9 ± 0.6 mm for a dominant versus 2.8 ± 0.5 mm for a nondominant right coronary artery (59). By comparing the diameter of a presumably disease-free segment of coronary artery to the size of the diagnostic catheter (6F equals 2 mm), the operator can identify vessels that fall below these normal size ranges and may thus be diffusely diseased.
In addition to the difficulty in finding a disease-free reference segment, a major problem in the interpretation of a coronary angiogram is deciding the severity of any given stenosis. Both animal data (60) and human data (61) show that a stenosis that reduces the lumen diameter by 50% (and hence cross-sectional area by 75%) is hemodynamically significant in that it reduces the normal threefold to fourfold flow reserve of a coronary bed (Fig. 11.20), whereas a 70% diameter stenosis (90% cross-sectional area) eliminates virtually any ability to increase flow above its resting level (see Chapter 18). Stenoses that reduce the lumen diameter by 90%, however, rarely exist without reducing antegrade flow (i.e., TIMI [Thrombolysis in Myocardial Infarction] grade 1 or 2, rather than TIMI grade 3 normal flow).
Instead of the subjective TIMI flow grading system, Gibson et al. (62) have created norms for the number of cine frames (at 30 frames per second [fps]) required for contrast to leave the catheter tip and reach standardized distal landmarks in each coronary artery (the LAD “mustache,” the first posterolateral branch of the right coronary). Contrast normally reaches these points in 20 frames for the RCA and 36 frames for the LAD, with TIMI 2 (partial) flow corresponding to more than a doubling of those frame counts. Of course, even more precise data about hemodynamic lesion significance can be determined by performance of flow or pressure gradient measurements, at rest and during arteriolar vasodilation (e.g., after adenosine administration) to calculate the coronary flow or fractional flow reserve (63). Lesions that permit a flow increase of more than twofold, or have a ratio of distal pressure to aortic pressure >0.75 in the setting of peak flow after adenosine injection, are generally considered to be hemodynamically insignificant. Angiographically borderline (40 to 60%) lesions for which there is no clear objective evidence of ischemia (i.e., exercise test, perfusion scan) should thus be interrogated further with intravascular ultrasound or pressure wire measurements before considering intervention (see Chapters 18 and 19).
In clinical practice, however, the degree of lesion stenosis is usually just estimated visually from the coronary angiogram. The operator must thus develop a sense of what constitutes a 50, 70, and 90% diameter stenosis (see Fig. 11.21). Although the process of visually estimating the degree of coronary stenosis may seem straightforward, it is subject to significant operator variability (the standard deviation for repeat estimates is ≤18%: 64) as well as a systematic
P.209

form of “stenosis inflation” that causes operators to estimate a diameter stenosis that is roughly 20% higher than that measured by quantitative coronary angiography (QCA; 65). A stenosis that measures 50% will thus typically be called 70%, whereas a stenosis that measures 70% will be called 90%.
Figure 11.20 Effect of coronary stenosis on myocardial blood flow and coronary vasodilator reserve. Top. Resting flow (open circles) is well maintained at approximately 1 mL/minute per gram of myocardium throughout the range of evaluated diameter stenosis. The ability to increase flow during vasodilator stimulus (closed circles), however, becomes impaired for stenosis >50% and is virtually abolished >70%. Bottom. The vasodilator reserve (dilated flow/resting flow), which has a normal value of 3 to 4 but is reduced with stenosis >50% and falls to 1 at >70%. (From Uren, et al., Relation between myocardial blood flow and the severity of coronary artery stenosis. N Engl J Med 1994;330:1782, with permission).
Tools are available to resolve this problem. The simplest is to project the coronary image on a wall-mounted viewing screen and to use inexpensive digital calipers (available from machinist supply houses) to measure the relative diameters of the stenotic and reference segments (66). Percent stenosis then can be calculated as 100 × [1-(stenosis diameter/reference diameter)] to provide a more accurate estimate of stenosis. This technique also reduces the standard deviation for diameter stenosis to 6 to 8% (64,66). Even greater precision can be obtained by using computer-assisted algorithms to perform automated edge detection on digitally acquired images to measure the coronary lumen with a standard deviation <5% (67,68). The amount of variation in diameter stenosis readings for one study (69) using these different methods concurrently is shown in Fig. 11.22.
Figure 11.21 Coronary stenoses of 50, 70, and 90% diameter reduction are shown in longitudinal and cross section. The corresponding reductions in cross-sectional area are indicated in parentheses.
The good news is that angiographers who have trained their eye in actual stenosis quantification (by using digital calipers or computer-assisted quantitative coronary angiography) can then actually give visual estimates much closer to true measurements. (70) This would allow angiographers to be more uniform in their visual estimates and move away from reporting physiologically impossible findings like a 95% stenosis with normal distal flow. Until there is a stenosis reading reform, so that those of us who call such lesions accurately (e.g., 70%) will not be accused of intervening on mild lesions, there will be no substitute to seeing the films yourself before making any clinical decisions!
It has also become important to evaluate lesion morphology more accurately from the coronary angiogram. Features such as eccentricity, ulceration, and thrombus may be associated with unstable clinical patterns (71,72), whereas features such as calcification, eccentricity, or thrombus may influence the choice of catheter intervention. Many of these features can be recognized from careful study of high-quality cineangiograms, although angiography is clearly not as sensitive to these features as intravascular ultrasound (73) or angioscopy (for thrombus or dissection; 74). Angiographers may also have trouble predicting the physiologic significance of a coronary lesion, in which case angiography may need to be supplemented by other techniques such as direct flow or distal pressure measurements (63). Finally, the absence of lesions narrowing the coronary lumen by >50% does not necessarily confer immunity from subsequent coronary events, since it is frequently a less severe stenotic lesion that
P.210

has the large lipid core and thin fibrous cap that may predispose to subsequent plaque rupture and the resulting coronary thrombosis (75). Despite these recognized limitations in quantification and morphology assessment, contrast coronary angiography remains the clinical standard by which lesions are evaluated and decisions are made regarding the need for (and best mode of providing) revascularization in the patient with ischemic heart disease.
Figure 11.22 In a series of 227 patients with single-vessel disease, visual estimates (right curve, average nearly 90%) were consistently higher than either caliper measurements (average near 80%) or computer-assisted quantitative angiography by either geometric or densitometric techniques (left curves, average near 70% diameter stenosis). (From Folland ED, Vogel RA, Hartigan P, et al. Relation between coronary artery stenosis assessed by visual, caliper, and computer methods and exercise capacity in patients with single-vessel coronary artery disease. Circulation 1994;89:2005, with permission).
Coronary Collaterals
In reviewing the coronary angiogram, one basic principle is that there should be evident blood supply to all portions of the left ventricle. Previously occluded vessel branches are usually manifest as truncated stumps, but a stump may not be evident if there has been a flush occlusion at the origin of the involved vessel. These occluded or severely stenotic vessels will frequently be seen to fill late in the injection by antegrade (so-called bridging) collaterals or collaterals that originate from the same (intracoronary) or an adjacent (intercoronary) vessel, which are reviewed in an excellent paper by Levin (76) and illustrated in Figs. 11.23,11.24 and 11.25. Finally, coronary occlusion may present in some patients simply as an angiographically arid area to which there is no evidence of either antegrade or collateral flow and no evident vascular stump. If such an area fails to show regional hypokinesis on the left ventriculogram, however, the operator should search carefully for blood supply by way of anomalous vessels or unopacified collaterals (i.e., a separate origin conus branch that was not opacified during the main right coronary injections), because the myocardium cannot continue to function normally with no visible means of support. Functioning collaterals, however, can maintain a coronary wedge pressure that averages nearly 40% of mean aortic pressure (77,78), thereby maintaining myocardial viability in the collateral-fed distribution. Along with other measures of retained or augmentable wall motion, redistributing defects on perfusion imaging, and positron emission tomographic (PET) evidence of ongoing glucose metabolism, the angiographic presence of collateral flow to an area in the distribution of an occluded coronary artery is one of the strongest evidences of ongoing myocardial viability and an important factor in determining the best revascularization strategy.
Although it is uncommon, what appears as a network of collaterals may be the vascular supply to an organized thrombus (in the left ventricle or left atrium) or a cardiac tumor. Those entities should be suspected when filling of an apparent collateral network is seen in the absence of occlusion or severe stenosis of the normal supply to a myocardial territory.
Figure 11.23 Ten collateral pathways observed in patients with right coronary (RC) obstruction (total occlusion or >90% stenosis). LAD, left anterior descending; C, circumflex; OM, obtuse marginal; PD, posterior descending; PLV, posterior left ventricular branch; AM, acute marginal branch of right coronary artery; AV, atrioventricular nodal; LC, left coronary. Numbers in parentheses represent numbers of cases in this series. (From Levin DC. Pathways and functional significance of the coronary collateral circulation. Circulation 1974;50:831. By permission of the American Heart Association, Inc.)
P.211

NONATHEROSCLEROTIC CORONARY ARTERY DISEASE
Although atherosclerotic stenosis is far and away the most common pathologic process responsible for myocardial ischemia, the angiographer must be aware of various other potential causes. These include certain congenital anomalies of coronary origin (46,79,80,81)—for example, an anomalous coronary that courses between the aorta and pulmonary artery (Fig. 11.16), in which flow may be compromised by deformation of the ostium or compression of the proximal vessel, potentially even causing sudden death. In patients with such anatomy and objective evidence of ischemia on medical therapy, bypass surgery or stenting of the anomalous segment may be considered (82).
Other abnormalities include coronary fistulae (Fig. 11.26), coronary aneurysms (83,84), and muscle bridges (Fig. 11.27; 85,86). Coronary fistulae, connections mostly from a coronary artery to the right ventricle, right atrium, pulmonary artery, or coronary sinus, are found in roughly 0.1% of patients coming to cardiac catheterization. When they are large (or in the setting of proximal coronary disease), these fistulae may cause chronic volume overload or myocardial ischemia and must be closed, using surgery or newer catheter techniques (embolization coils, covered stents; 87). Smaller, asymptomatic fistulae may close spontaneously, however, and can be managed conservatively (88). Muscle bridges are sections of a coronary artery (almost always the left anterior descending) that run under a strip of left ventricular muscle, which compresses the lumen during ventricular systole despite a normal appearance during diastole (85,86). Similar systolic compression of the first septal branch (saw-toothing) is also seen in many patients with hypertrophic cardiomyopathy (89). When one of these congenital anomalies is present in a patient with ischemic symptoms in whom catheterization has failed to demonstrate the expected finding of coronary atherosclerosis, the angiographer should be able to recognize it
P.212

as a potential cause of ischemia and recommend additional functional testing with an eye toward surgical or catheter-assisted repair (fistula coil embolization, muscle bridge stent placement).
Figure 11.24 Seven collateral pathways observed in patients with left coronary artery obstruction. Abbreviations and format are the same as in Figure 11.23. (From Levin DC: Pathways and functional significance of the coronary collateral circulation. Circulation 1974;50:831. By permission of the American Heart Association, Inc.)
The coronary arteries may also be affected by medium- vessel vasculitis (90), including polyarteritis nodosa and the mucocutaneous lymph node syndrome (Kawasaki disease). The latter is largely a childhood illness, in which coronary arteritis may lead to aneurysm, stenosis, or thrombosis that was often fatal (usually in the first month of the illness) before the use of high-dose gamma globulin to treat the acute illness. When coronary aneurysms are found in adults, it may thus be difficult to determine if they represent atherosclerotic damage to the vessel wall or the remainders of childhood Kawasaki disease (83). The treatment for the stenotic lesions (bypass or catheter-based intervention), however, are the same regardless of the etiology.
Although not an arteritis, cardiac allograft vasculopathy (91) is one of the most troublesome long-term complications of heart transplantation. The mechanism seems to be an immune-mediated diffuse vascular proliferative response involving distal as well as proximal coronary arteries, with superimposed focal lesions of the proximal vessels. The latter may be amenable to catheter-based revascularization. Patients who have received prior mantle radiation therapy for Hodgkin disease may be at risk for radiation-induced coronary stenosis (92), particularly of the left and right coronary ostia and the proximal left coronary artery, up to 20 years after completing their course of therapy. The pathology is most commonly fibrotic contraction of the vessel wall, rather than intimal proliferation or plaque formation.
Finally, some patients who come to catheterization have no demonstrable coronary abnormality to account for their clinically suspected ischemic heart disease. Although anginalike pain can be seen in patients with noncoronary cardiac abnormality (e.g., mitral valve prolapse, hypertrophic cardiomyopathy, aortic stenosis, myocarditis) or extracardiac conditions (esophageal dysmotility [93], cholecystitis), one must also consider the possibility of epicardial or microvascular coronary vasospastic disease (see below).
Figure 11.25 Angiographic appearance of some common collateral pathways. Top left. Bridging or vasa vasora collaterals in an occluded right coronary artery (RCA). Top right. Kugel collateral (sinus node to atrioventricular node, dotted arrow) supplying the distal RCA. Center left. Full-bore connection (dotted arrow) between the distal circumflex and the distal portion of an occluded RCA, in a patient with coexisting left anterior descending (LAD) occlusion (short arrow). Center right. Classic Vieussens (Raymond de Vieussens, 1641–1715) collateral connecting the conus branch of the RCA to the LAD in the same patient as shown in the previous example. Bottom left. Septal-to-septal collateral in severely stenotic LAD. Bottom right. Posterior descending septal branches connecting to septal branches of an occluded LAD.
P.213

Coronary Vasospasm
Vasospasm of an epicardial coronary artery typically presents as variant (or Prinzmetal) angina in which episodes of rest pain occur despite well-preserved effort tolerance at other times (94). An electrocardiogram recorded during an episode of spontaneous pain usually shows ST elevation in the territory supplied by the vasospastic artery. Absence of a significant coronary lesion in such a patient confirms the diagnosis of variant angina owing to focal coronary spasm (Fig. 11.28). In these patients, coronary angiography is performed mainly to look at the extent of underlying atherosclerosis (95). Provocative maneuvers to initiate spasm were once common to confirm the diagnosis and evaluate drug therapy (96). It is now used mostly when the diagnosis of variant angina is uncertain and a patient with troublesome chest pain fails to manifest sufficient disease to explain its cause.
Figure 11.26 Coronary artery fistula (arrow) between the midleft anterior descending coronary artery and the pulmonary artery, shown in the right anterior oblique view.
P.214

If provocative testing for coronary spasm is contemplated, the patient should be withdrawn from calcium channel blockers for at least 24 hours and long-acting nitrates for at least 12 hours before the study and should not be premedicated with either atropine or sublingual nitroglycerin. Ongoing therapy with any of these agents may render provocative tests falsely negative (96). Although various provocative tests have been used (methacholine, epinephrine and propranolol, hyperventilation and tris-buffer, cold pressor), the most commonly used provocative agent has been ergonovine or methylergonovine maleate (Methergine, Sandoz, East Hanover, NJ; 97,98,99). These agents are stimulants of the α-adrenergic and serotonin receptors in coronary vascular smooth muscle.
Figure 11.27 Muscle bridge. Moderately severe muscle bridge of the left anterior descending coronary artery (arrow) as seen in diastole (left) and systole (right).
Testing for coronary spasm should be performed only after baseline angiographic evaluation of both the left and
P.215

right coronary arteries. It should not be performed in patients with severe hypertension or severe anatomic cardiac pathology (left ventricular dysfunction, left main or multivessel disease, or aortic stenosis). As an example, our protocol for using methylergonovine calls for a total of 0.4 mg (400 mg equals 2 ampules) to be diluted to a total volume of 8 mL in a 10-mL syringe that is appropriately labeled. The provocative test consists of graded intravenous administration of 1 mL (0.05 mg), 2 mL (0.10 mg), and 5 mL (0.25 mg) of this mixture at 3- to 5-minute intervals. Parenteral nitroglycerin (100 to 200 mg/mL) must be premixed and loaded in a labeled syringe before the testing is begun. It is also advisable to have an intracoronary calcium channel blocker (verapamil 100 μg/mL, diltiazem 250 μg/mL) or nitroprusside (100 μg/mL) close at hand in case nitroglycerin-refractory spasm develops. Temporary pacing and defibrillator equipment should also be available to treat the bradyarrhythmias or tachyarrhythmias that sometimes accompany coronary spasm. At 1 minute before each ergonovine dose, the patient is interrogated about symptoms similar to those of her or his clinical complaint, and a 12-lead electrocardiogram is recorded. After each electrocardiogram, coronary angiography is performed, looking either at both arteries or only at the artery of highest clinical suspicion for vasospasm. In the absence of clinical symptoms, electrocardiographic changes, or focal coronary vasospasm, the next ergonovine dose is administered, and the cycle is repeated until the total dose of 0.4 mg has been given. The provocative test should be considered positive only if focal spasm (>70% diameter stenosis) occurs and is associated with clinical symptoms and/or electrocardiographic changes. Even if there are no symptoms or electrocardiographic changes, both coronary arteries should be opacified at the end of the provocative test, and any generalized vasoconstrictor effect should be terminated by administration of nitroglycerin to document the resolution of spasm and the extent of underlying atherosclerotic stenosis. Note that coronary artery spasm may occur in two vessels simultaneously (Fig. 11.29), and visualization of only one vessel may fail to adequately assess the magnitude of the vasospastic response.
Figure 11.28 True coronary spasm. Intense focal vasospasm of the left anterior descending coronary artery is shown in right anterior oblique projection in a patient with variant angina. Note the absence of a significant underlying atherosclerotic stenosis in the top view, the absence of vasoconstriction of other vessel segments, and the marked ST elevation in the anterior leads during the spontaneous vasospastic episode. (From Baim DS, Harrison DC. Nonatherosclerotic coronary heart disease. In: Hurst JW, ed. The Heart, 5th ed. New York: McGraw-Hill, 1985, with permission.)
Some operators have used an intracoronary methylergonovine administration protocol, in which a 4-minute intracoronary infusion (10 μg/minute in the right and 16 μg/min in the left coronary) is administered. Alternatively, discrete doses of 5 to 10 μg may be given into a coronary artery, waiting 3 minutes and imaging before a second dose is given (maximal total dose 50 μg per vessel). These intracoronary protocols may be advantageous in that they produce less systemic effect (hypertension, esophageal
P.216

spasm). The other intracoronary provocative test for coronary spasm uses acetylcholine (serial doses of 20-50-100 μg injected into the left coronary, and 20-50-80 μg injected into the right coronary). Some investigators have also used hyperventillation as a provocative test for spasm (100, Figure 11.29). The same caveats regarding ready availability of potent intracoronary vasodilators to treat spasm also apply to any of these prevocational protocols.
Figure 11.29 A 37-year-old man was admitted with chest pain and ST-segment elevation in the inferior leads. Emergency catheterization was performed for presumed acute myocardial infarction within 30 minutes of presentation (top left), but disclosed a dominant right coronary artery with only mild disease at a time when pain had resolved after nitrate and heparin therapy. Hyperventillation (30 breaths per minute for 5 minutes) was performed with reduction of PCO2 to 19 mm Hg and elevation of pH to 7.61, resulting in provocation of occlusive focal spasm of the distal right coronary artery with return of chest pain and ST-segment elevation (top right). Relief of vasospasm and marked general dilation of the RCA was produced by intracoronary administration of trinitroglycerin (TNG) 200μg (bottom left) and diltiazem 500μg (bottom right).
Several additional comments about ergonovine are in order. Ergonovine testing should be avoided in patients with severe atherosclerotic stenosis (≥80%), in whom spasm is not required to explain the clinical symptoms. In these patients, however, we frequently do repeat coronary angiography of the stenotic vessel after the intracoronary administration of 200 mg of nitroglycerin to exclude the possibility that spontaneous focal vasospasm is contributing to the appearance of severe atherosclerotic stenosis. Second, the operator should be aware that the positivity rate depends strongly on which patients are studied; the test is almost always positive in patients with known variant angina (if their disorder is active and medications have been withheld) and is positive in approximately one third of patients with clinically suspected variant angina, but it is positive in <5% of patients whose symptoms do not suggest variant angina (99). The Duke group (101) reported ergonovine testing in 3,447 patients without significant coronary disease or variant angina, with an overall positivity rate of 4% in such patients. There were two independent predictors of a positive test: mild to moderate disease on the angiogram (spasm often takes place at the point of such disease) and a history of smoking, whose presence increased the positivity rate to 10%.
Since finding spasm is so uncommon now that the syndrome is detected clinically in most patients and is treated so effectively by calcium channel blockers, the risk of ergonovine testing to evaluate patients with atypical symptoms and minimal fixed coronary disease is remarkably low. In the Duke study, significant complications occurred in only 11 patients (0.03%), including myocardial infarction in four patients and ventricular tachycardia or fibrillation (VT or VF) in seven patients (101). When provocative testing produces clinical symptoms but no angiographic evidence of vasospasm in either coronary artery, there may still be scintographic evidence of myocardial ischemia due to microvascular spasm. Both multivessel epicardial and microvascular spasm have been implicated in tako-tsubo syndrome where extreme emotional stress is followed by chest pain, ST elevation, and a particular pattern of apical hypokinesis extending beyond the usual single coronary territory. If there are no signs of myocardial ischemia, an alternative diagnosis such as esophageal dysmotility (93), which can also be provoked by methylergonovine, should be considered.
It is also important to distinguish the intense focal spasm seen in patients with variant angina from the normal mild (15 to 20%) diffuse coronary narrowing seen as a pharmacologic response to ergonovine in normal patients (102). True coronary spasm must also be distinguished from spasm induced by mechanical interventions such as rotational atherectomy (see Chapter 28) or catheter-tip spasm (Fig. 11.30). Catheter-tip spasm is most common in the right coronary artery, is not associated with clinical symptoms or electrocardiographic changes, and does not indicate variant angina (103). It should be recognized as such, however, and treated by withdrawal of the catheter, administration of nitroglycerin, and nonselective or cautious repeat selective opacification of the involved vessel to avoid mistaking catheter-tip spasm for an atherosclerotic lesion. Spasm should also be distinguished from a “pleating” artifact that may occur when a curved artery is straightened out by a stiff guidewire (Fig. 11.31), causing folds of the vessel wall to impinge on the lumen. Pleating is refractory to nitroglycerin but resolves immediately when the stiff guidewire is withdrawn (104).
Abnormal Coronary Vasodilator Reserve
Evidence has been accumulating that the patient group with angina and angiographically normal coronary arteries may contain a subgroup of patients who have myocardial ischemia on the basis of abnormal vasodilator reserve. Despite angiographic normality, intravascular
P.217

ultrasound examination may show normal vessel wall architecture, intimal thickening, or atheromatous plaque (84). In these patients, coronary blood flow (as described in Chapter 18) may fail to rise normally with pacing tachycardia or exercise, and the coronary vascular resistance is increased abnormally (105). Also, many of these patients show an abnormal rise in left ventricular end diastolic pressure following pacing tachycardia and show less lactate consumption than normal subjects in response to pacing tachycardia (106). A failure of small vessel coronary vasodilation, inappropriate vasoconstriction at the arteriolar level, or functional abnormalities of capillary endothelial cells in releasing endothelium-derived relaxing factor (EDRF) have been postulated to account for these findings. Many patients with so-called syndrome X respond at least partially to treatment with a calcium channel blocker. Disordered small vessel vasoconstriction has also been implicated in the tako-tsubo syndrome where patients with angiographically normal epicardial arteries may present with chest pain, anterior ST elevation, and a unique pattern of apical akinesis (107,108; see also Chapter 12).
Figure 11.30 Vasomotor changes not representing true coronary spasm. During right coronary catheterization with a Judkins catheter (top left), this patient developed severe catheter-tip spasm. Recatheterization 24 hours later with an Amplatz catheter (top right) showed neither catheter-tip spasm nor an atherosclerotic stenosis. Following ergonovine 0.4 mg, marked diffuse coronary narrowing was observed (bottom left) without angina or electrocardiographic changes. After the intracoronary administration of nitroglycerin 200 mcg (bottom right), there is marked diffuse vasodilation.
MISTAKES IN INTERPRETATION
An inexperienced operator often produces an incomplete or uninterpretable study, especially if she or he is using poor equipment. Such an operator is also likely to misinterpret the angiographic findings, with potentially serious clinical consequences. The following discussion summarizes some of the most common pitfalls that may lead the inexperienced coronary angiographer to mistaken conclusions.
Inadequate Number of Projections
There is no standard number of projections that will always provide complete information. Each major vessel must be viewed in an isolated fashion as it stands apart from other vessels. Usually, the angulated views discussed earlier in this chapter are necessary to visualize clearly the anatomy of the proximal left anterior descending and circumflex arteries.
Inadequate Injection of Contrast Material
The inexperienced operator or assistant has a tendency to hold back on the volume and force of injection into the coronary circulation. This results in inadequate or intermittent, pulsatile opacification of the coronary arterial tree as contrast flow fails short of peak coronary flow during diastole. Because there is inadequate mixing of contrast agent and blood, pockets of nonradiopaque blood in such inadequate injections may even give the appearance of arterial narrowing.
Superselective Injection
It is not uncommon to catheterize the left anterior descending or circumflex coronary artery superselectively, especially when the left main coronary artery is short and its bifurcation is early. To the inexperienced operator, this may give the impression of total occlusion of the nonvisualized vessel (e.g., if only the circumflex artery is opacified, the operator may conclude that the left anterior descending artery is occluded). If adequate filling of the noncannulated vessel cannot be achieved by reflux, selective cannulation of the LAD may be obtained by counterclockwise rotation or use of the next-smaller Judkins catheter (e.g., JL3.5), whereas selection cannulation of the circumflex may be obtained by clockwise rotation or use of the next-larger Judkins catheter (e.g., JL5). With the right coronary artery, superselective injection may occur if the catheter tip is too far down the vessel, leading to failure to visualize the conus and sinus node arteries. Because these are important sources of collateralization
P.218

of the left coronary system, important information may be missed (see Fig. 11.13). Adequate injection to give a continuous (nonpulsatile) reflux of contrast agent back into the sinus of Valsalva will help the operator to recognize vessels that originate proximally to the catheter tip and thus avoid the interpretation error of superselective injection.
Figure 11.31 Right coronary artery “pleating” artifact. Left. Baseline injection shows diffuse disease in this tortuous right coronary artery selected for rotational atherectomy. Center. shows straightening of the proximal vessel by the stiff type C wire, creating three areas of infolding of the vessel wall (arrows) as well as the appearance of ostial stenosis (curved arrow). Immediately on withdrawal of the guidewire, the artery returned to its baseline curvature and these defects resolved (arrows).
Selective cannulation of a coronary artery may also fail to detect significant ostial stenosis, particularly if the catheter tip lies beyond the lesion and adequate contrast reflux is not produced. If ostial stenosis is suspected (e.g., if there is partial ventricularization or damping), we have found it helpful to perform a final injection during withdrawal of the catheter from the ostium (Fig. 11.32).
Catheter-Induced Coronary Spasm
Coronary artery spasm may be related to the catheter itself, possibly caused by mechanical irritation and a myogenic reflex (see Fig. 11.30). It is seen most commonly when the right coronary artery is engaged selectively, although it may occur rarely in the left anterior descending artery as well. Although catheter-tip spasm can occur with either the brachial or femoral approach, it is probably more common with the right Judkins catheter, especially if the catheter tip enters the right coronary ostium at an angle and produces tenting of the proximal vessel. If coronary narrowing suggests the occurrence of spasm to the operator, sublingual, intravenous, or intracoronary nitroglycerin should be given and the injection repeated.
Congenital Variants of Coronary Origin and Distribution
This topic has been discussed earlier in this chapter, but it bears re-emphasis. Variation in origin and distribution of the coronary artery branches may confuse the operator and cause him or her to mistakenly diagnose coronary
P.219

occlusion. For example, a small right coronary artery that terminates in the AV groove well before the crux may be interpreted as an abnormal or occluded artery, whereas it is a normal finding in 7 to 10% of human hearts. Double ostia of the right coronary artery or origin of the circumflex artery from the right coronary artery may be similarly confusing and lead to misdiagnosis.
Figure 11.32 Masking of ostial stenosis during superselective cannulation. Ostial stenosis of previously stented vein graft is not apparent with the tip of the catheter well beyond the stenosis (top and center). Continued injection during catheter withdrawal (bottom) causes reflux into the aorta (solid arrow) and clearly shows significant ostial stenosis.
Myocardial Bridges
As discussed earlier, coronary arteries occasionally dip below the epicardial surface under small strips of myocardium. During systole, the segment of the artery surrounded by myocardium is narrowed and appears as a localized stenosis. These myocardial bridges occur most commonly in the distribution of the left anterior descending artery and its diagonal branches. The key to the recognition of these bridges is that the apparent localized stenosis returns to normal during diastole. Recent studies using the flow wire (see Chapter 18) show clear derangement in phasic flow dynamics in muscle bridge segments and their normalization by stent placement. Although some severe muscle bridges can thus cause true myocardial ischemia under certain circumstances, they are seen in at least 5% of normal angiograms obtained in patients with no evidence of ischemia in the LAD territory.
Total Occlusion
If a coronary artery or branch is totally occluded at its origin, it may not be visualized, and the occlusion may be missed. If the occlusion is flush with the parent vessel, no stump will be seen. Such occlusions are primarily recognized by visualization of the distal segment of the occluded vessel by means of collateral channels or by noting the absence of the usual vascularity seen in a particular portion of the heart.
REFERENCES
1. Bashore TM, et al. American College of Cardiology/Society for Cardiac Angiography and Interventions Clinical Expert Consensus Document on Cardiac Catheterization Laboratory Standards. A Report of the American College of Cardiology Task Force on Clinical Expert Consensus Documents. J Am Coll Cardiol 2001; 37:2170–2214.
2. Scanlon PJ, Faxon DP, Audet A, et al. AHA/ACC guidelines for coronary angiography. A report of the ACC/AHA Task force on practice guidelines. J Am Coll Cardiol 1999;33:1756.
3. Budoff MJ. Clinical utility of computed tomography and magnetic resonance techniques for noninvasive coronary angiography. J Am Coll Cardiol 2003;42:1867–1878.
4. Ropers D, et al. Visualization of coronary artery anomalies and their anatomic course by contrast-enhanced electron beam tomography and three dimensional reconstruction. Am J Cardiol 2001;87:193–197.
4a. Martuscelli E, et al. Evaluation of venous and arterial conduit patency by 16-slice spiral computed tomography. Circulation 2004;110:3234–38.
5. Davies RF, Goldberg AD, Forman S, et al. Asymptomatic Cardiac Ischemia Pilot (ACIP) study two-year follow-up: outcomes of patients randomized to initial strategies of medical therapy versus revascularization. Circulation 1997;95:2037.
6. The TIMI IIIB Investigators. Effects of tissue plasminogen activator and a comparison of early invasive and conservative strategies in unstable angina and non-Q wave myocardial infarction—results of the TIMI IIIB trial (Thrombolysis in Myocardial Ischemia). Circulation 1994;89:1545.
7. Miltenberg AJM, et al. Incidence and follow-up of Braunwald subgroups in unstable angina pectoris. J Am Coll Cardiol 1995; 25:1286.
8. Ryan TJ, Anderson JL, Antman EM, et al. ACC/AHA guidelines for the management of patients with acute myocardial infarction: executive summary. Circulation 1996;94:2341.
9. The TIMI Study Group. Comparison of invasive and conservative strategies after treatment with intravenous tissue plasminogen activator in acute myocardial infarction. N Engl J Med 1989;320: 618.
10. Spaulding CM, Joly L, Rosenberg A, et al. Immediate coronary angiography in survivors of out-of-hospital cardiac arrest. N Engl J Med 1997;336:1629.
11. Panza JA, Laurienzo JM, Curiel RV, et al. Investigation of the mechanism of chest pain in patients with angiographically normal coronary arteries using transesophageal dobutamine stress echocardiography. J Am Coll Cardiol 1997;29:293.
12. Eagle KA, et al. Guidelines for perioperative cardiovascular evaluation for noncardiac surgery (report of the ACC/AHA Task Force on Practice Guidelines). J Am Coll Cardiol 1996; 27:910.
13. Neufeld NH, Blieden LC. Coronary artery disease in children. Prog Cardiol 1975;4:119.
14. Roberts WC. No cardiac catheterization before cardiac valve replacement—a mistake. Am Heart J 1982;103:930.
15. Baim DS, Kuntz RE. Appropriate uses of angiographic follow-up in the evaluation of new technologies for coronary intervention. Circulation 1994;90:2560.
16. Conti CR. Coronary arteriography. Circulation 1977;55:227.
17. Noto TJ, Johnson LW, Krone R, et al. Cardiac catheterization 1990: a report of the registry of the Society for Cardiac Angiography and Interventions. Cathet Cardiovasc Diagn 1991;24:75.
18. Fierens E. Outpatient coronary arteriography. Cathet Cardiovasc Diagn 1984;10:27.
19. Maher PR, Young C, Magnusson PT. Efficacy and safety of outpatient cardiac catheterization. Cathet Cardiovasc Diagn 1987;13:304.
20. Lee JC, et al. Feasibility and cost-saving potential of outpatient cardiac catheterization. J Am Coll Cardiol 1990;15:378.
21. Talley JD. The cost of performing diagnostic cardiac catheterization. J Intervent Cardiol 1994;7:273.
22. Kohli RS, Vetrovec GW, Lewis SA, Cole S. Study of the performance of 5 French and 7 French catheters in coronary angiography: a functional comparison. Cathet Cardiovasc Diagn 1989;18:131.
23. Judkins MP. Selective coronary arteriography, a percutaneous transfemoral technique. Radiology 1967;89:815.
24. Amplatz K, Formanek G, Stanger P, Wilson W. Mechanics of selective coronary artery catheterization via femoral approach. Radiology 1967;89:1040.
25. Fitzgibbon GM, Kafka HP, Leach AJ, Keon WJ, Hooper DG, Burton JR. Coronary bypass graft fate and patient outcome: angiographic follow-up of 5,065 grafts related to survival and reoperation in 1,388 patients during 25 years. J Am Coll Cardiol 1996;28:616.
26. Eisenhauer TL, Collier E, Cambier PA. Beneficial impact of aorto-coronary graft markers on post-operative angiography. Cathet Cardiovasc Diagn 1997;40:249.
27. Kuntz RE, Baim DS. Internal mammary angiography: A review of technical issues and newer methods. Cathet Cardiovasc Diagn 1990;20:10–16.
28. Ayres RW, et al. Transcatheter embolization of an internal mammary artery bypass graft sidebranch causing coronary steal syndrome. Cathet Cardiovasc Diagn 1994;31:301.
29. Breal JA, et al. Coronary-subclavian steal—an unusual cause of angina pectoris after successful internal mammary artery bypass grafting. Cathet Cardiovac Diagn 1991;24:274.
30. Bilazarian SD, Shemin RJ, Mills RM. Catheterization of coroanry artery bypass graft from the descending aorta. Cathet Cardiovasc Diagn 1990;21:103.
P.220

31. Mills NL, Everson CT. Right gastroepiploic artery: a third arterial conduit for coronary artery bypass. Ann Thorac Surg 1989;47:706.
32. Suma H, et al. The right gastroepiploic artery graft—clinical and angiographic mid-term results in 200 patients. J Thorac Cardiovasc Surg 1993;105:615.
33. Tanimoto Y, et al. Angiography of right gastroepiploic artery for coronary artery bypass graft. Cathet Cardiovasc Diagn 1989;16:35.
34. Sones FM, Shirey EK. Cine coronary arteriography. Mod Concepts Cardiovasc Dis 1962;31:735.
35. Schoonmaker FW, King SB. Coronary arteriography by the single catheter percutaneous femoral technique, experience in 6,800 cases. Circulation 1974;50:735.
36. Ovitt T, et al. Electrocardiographic changes in selective coronary arteriography: the importance of ions. Radiology 1972;102:705.
37. Tragardh B, Bove AA, Lynch PR. Mechanism of production of cardiac conduction abnormalities due to coronary arteriography in dogs. Invest Radiol 1976;11:563.
38. Paulin S, Adams DF. Increased ventricular fibrillation during coronary arteriography with a new contrast medium preparation. Radiology 1971;101:45.
39. Lasser EC, et al. Pretreatment with corticosteroids to alleviate reactions to intravenous contrast material. N Engl J Med 1987;317:845.
40. Parfrey PS, et al. Contrast material-induced renal failure in patients with diabetes mellitus, renal insufficiency, or both. N Engl J Med 1989;329:143.
41. Ritchie JL, et al. Use of nonionic or low osmolar contrast agents in cardiovascular procedures (ACC Position Statement). J Am Coll Cardiol 1993;21:269.
42. Harvey JR, et al. Use of balloon flotation pacing catheters for prophylactic temporary pacing during diagnostic and therapeutic catheterization procedures. Am J Cardiol 1988;62:941.
43. Dodge JT, Nykiel M, Altmann J, Hobkirk Km, Brennan M, Gibson CM. Coronary artery injection technique: a quantitative in vivo investigation using modern catheters. Cathet Cardiovasc Diagn 1998;44:34.
44. Ireland MA, et al. Safety and convenience of a mechanical injector pump for coronary angiography. Cathet Cardiovasc Diagn 1989;16:199.
45. The BARI protocol. Protocol for the Bypass Angioplasty Revascularization Investigation. Circulation 1991;84:V1.
46. Angelini P, Villason S, Chan AV, Diez JG. Normal and amnomalous coronary arteries in humans. In: Angelini P, ed. Coronary artery anomalies—a comprehensive approach. Philadelphia: Lippincott Williams & Wilkins, 1999.
47. Yamanaka O, Hobbs RE. Coronary artery anomalies in 126,595 patients undergoing coronary arteriography. Cathet Cardiovasc Diagn 1990;21:28.
48. Serota H, et al. Rapid identification of the course of anomalous coronary arteries in adults—the “dot and eye” method. Am J Cardiol 1990;65:891.
49. Ishikawa T, Brandt PWT. Anomalous origin of the left main coronary artery from the right aortic sinus—angiographic definition of anomalous course. Am J Cardiol 1985;55:770.
50. Shirani J, Roberts WC. Solitary coronary ostium in the aorta in the absence of other major congenital cardiovascular abnormalities. J Am Coll Cardiol 1993;21:137.
51. Cohen DJ, Kim D, Baim DS. Origin of the left main coronary artery from the “non-coronary” sinus of Valsalva. Cathet Cardiovasc Diagn 1991;22:190.
52. Aldridge HE. A decade or more of cranial and caudal angled projections in coronary arteriography—another look. Cathet Cardiovasc Diagn 1984;10:539.
53. Elliott LP, et al. Advantage of the cranial-right anterior oblique view in diagnosing mid left anterior descending and distal right coronary artery disease. Am J Cardiol 1981;48:754.
54. Grover M, Slutsky R, Higgins C, Atwood JE. Terminology and anatomy of angulated coronary arteriography. Clin Cardiol 1984; 7:37.
55. Taylor CR, Wilde P. An easily constructed model of the coronary arteries. Am J Radiol 1984;142:389.
56. Mintz GS, Popma JJ, Pichard AD, et al. Limitations of angiography in the assessment of plaque distribution in coronary artery disease: a systematic study of target lesion eccentricity in 1446 lesions. Circulation 1996;93:924.
57. Randall PA Mach bands in cine coronary arteriography. Radiology 1978;129:65.
58. Arnett EN, et al. Coronary artery narrowing in coronary heart disease: comparison of cineangiographic and necropsy findings. Ann Intern Med 1979;91:350.
59. Dodge JT, Brown BG, Bolson EL, Dodge HT. Lumen diameter of normal human coronary arteries—influence of age, sex, anatomic variation, and left ventricular hypertrophy or dilation. Circulation 1992;86:232.
60. Gould KL, et al. Physiologic basis for assessing critical coronary stenosis—instantaneous flow response and regional distribution during coronary hyperemia as measures of flow reserve. Am J Cardiol 1974;33:87.
61. Uren NG, et al. Relation between myocardial blood flow and the severity of coronary artery stenosis. N Engl J Med 1994; 330:1782.
62. Gibson CM, Cannon CP, Daley WL, et al. TIMI frame count: a quantitative method of assessing coronary artery flow. Circulation 1996;93:879.
63. Pijls NHJ, de Bruyne B, Peels K, et al. Measurement of fractional flow reserve to assess the functional severity of coronary-artery stenoses. N Engl J Med 1996;334:1703.
64. Gibson CM, Safian RD. Limitations of cineangiography—impact of new technologies for image processing and quantitation. Trends Cardiovasc Med 1992;2:156.
65. Stadius ML, Alderman EL. Coronary artery revascularization—critical need for and consequences of objective angiographic assessment of lesion severity. Circulation 1990;82:2231.
66. Scoblionko DP, et al. A new digital electronic caliper for measurement of coronary arterial stenosis—comparison with visual estimates and computer-assisted measurements. Am J Cardiol 1984; 53:689.
67. Gronenshild E, Jannsen J, Tijdent F. CAAS II—a second generation system for off-line and on-line quantitative coronary angiography. Cathetet Cardiovasc Diagn 1994;33:61.
68. Escaned J, Baptiwsta J, DiMario C, et al. Significance of automated stenosis detection during quantitative angiography: insights gained from intracoronary ultrasound imaging. Circulation 1996; 94:966.
69. Folland ED, Vogel RA, Hartigan P, et al. Relation between coronary artery stenosis assessed by visual, caliper, and computer methods and exercise capacity in patients with single-vessel coronary artery disease. Circulation 1994;89:2005.
70. Danchin N, Foley D, Serruys PW. Visual versus quantitative assessment of the severity of coronary artery stenoses—can the angiographer’s eye be reeducated? Am Heart J 1993;126:594.
71. Ambrose JA, Hjemdahl-Monsen CE. Angiographic anatomy and mechanisms of myocardial ischemia in unstable angina. J Am Coll Cardiol 1987;9:1397.
72. Dangas G, Mehran R, Wallenstein S, et al. Correlation of angiographic morphology and clinical presentation in unstable angina. J Am Coll Cardiol 1997;29:519.
73. Mintz GS, Pichard AD, Popma JJ, et al. Determinants and correlates of lesion calcium in coronary artery disease: a clinical, angiographic and intravascular ultrasound study. J Am Coll Cardiol 1997;29:268.
74. Waxman S, Sassower MA, Mittleman MA, et al. Angioscopic predictors of early adverse outcome after coronary angioplasty in patients with unstable angina and non-Q-wave myocardial infarction. Circulation 1996;93:2106.
75. Fishbein MC, Siegel RJ. How big are coronary atherosclerotic plaques that rupture? Circulation 1996;94:2662.
76. Levin DC. Pathways and functional significance of the coronary collateral circulation. Circulation 1974;50:831.
77. Piek JJ, van Liebergen RAM, Koch KT, Peters TJG, David GK. Clinical, angiographic and hemodynamic predictors of recruitable collateral flow during balloon angioplasty of coronary occlusion. J Am Coll Cardiol 1997;29:275.
78. Seiler C, Fleisch M, Garachemani A, Meier B. Coronary collateral quantitation in patients with coronary artery disease using intravascular flow velocity or pressure measurements. J Am Coll Cardiol 1998;32:1272.
79. Levin DC, Fellows KE, Abrams HL. Hemodynamically significant primary anomalies of the coronary arteries. Angiographic aspects. Circulation 1978;58:25.
P.221

80. Click RL, et al. Anomalous coronary arteries: location, degree of atherosclerosis and effect on survival—a report from the Coronary Artery Surgery Study. J Am Coll Cardiol 1989;13:531.
81. Liberthson RR. Sudden death from cardiac causes in children and young adults. N Engl J Med 1996;334:1039.
82. Doorey AJ, et al. Six-month success of intracoronary stenting for anomalous coronary arteries associated with myocardial ischemia. Am J Cardiol 1000;86:580–582.
83. Newburger JW, et al. Diagnosis, treatment, and long-term management of Kawasaki Disease. Circulation 2004;110: 2747–71.
84. Papadakis MC, et al. Frequency of coronary artery ectasia in patients undergoing surgery for ascending aprtic aneurysms. Am J Cardiol 2004;94:1433–35.
85. Ge J, Erbel R, Rupprecht HJ, et al. Comparison of intravascular ultrasound and angiography in the assesssment of myocardial bridging. Circulation 1994;89:1725.
86. Klues HG, Schwarz ER, vom Dahl J, et al. Disturbed intracoronary hemodynamics in myocardial bridging: early normalization by intracoronary stent placement. Circulation 1997; 96:2905.
87. Dorros G, Thota V, Ramireddy K, Joseph G. Catheter-based techniques for closure of coronary fistulae. Cathet Cardiovasc Diagn 1999;46:143.
88. Sherwood MC, Rockenmacher S, Colan SD, Geva T. Prognostic significance of clinically silent coronary artery fistulas. Am J Cardiol 1999;83:407.
89. Yetman AT, McCrindle BW, MacDonald C, Freedom RM, Gow R. Myocardial bridging in children with hypertrophic cardiomyopathy—a risk factor for sudden death. N Engl J Med 1998; 339:1201.
90. Jennette JC, Falk RJ. Small-vessel vasculitits. N Engl J Med 1997; 337:1512.
91. Weis M, von Scheidt W. Cardiac allograft vasculopathy: a review. Circulation 1997;96:2069.
92. Om A, Ellaham S, Vetrovec GW. Radiation-induced coronary artery disease. Am Heart J 1992;124:1598.
93. Cohen S. Motor disorders of the esophagus. N Engl J Med 1979; 301:183.
94. Maseri A, Chierchia S. Coronary artery spasm: demonstration, definition, diagnosis, and consequences. Prog Cardiovasc Dis 1982;25:169.
95. Mark DB, et al. Clinical characteristics and long-term survival of patients with variant angina. Circulation 1984;69:880.
96. Waters DD, Theroux P, Szlachcic J, Dauwe F. Provocative testing with ergonovine to assess the efficacy of treatment with nifedipine, diltiazem and verapamil in variant angina. Am J Cardiol 1981;48:123.
97. Heupler FA, et al. Ergonovine maleate provocative test for coronary arterial spasm. Am J Cardiol 1978;41:631.
98. Sueda S, Kohno H, Fukuda H, et al. Frequency of provoked coronary spasms in patients undergoing coronary arteriography using a spasm provocation test via intracoronary administration of ergonovine. Angiology 2004;55:403–411.
99. Raizner AE, et al. Provocation of coronary artery spasm by the cold pressor test. Circulation 1980;62:925.
99. Sueda S, Kohno H, Fukuda H, et al. Induction of coronary artery spasm by two pharmacological agents: comparison between intracoronary injection of acetylcholine and ergonovine. Coron Artery Dis 2003;14:451–457.
100. Nakao K, Ohgushi M, Yoshimura M, et al. Hyperventilation as a specific test for diagnosis of coronary artery spasm. Am J Cardiol 1997;80:545.
101. Harding MB, Leithe ME, Mark DB, et al. Ergonovine maleate testing during cardiac catheterization—a 10 year perspective in 3,447 patients without significant coronary artery disease or Prinzmetal’s variant angina. J Am Coll Cardiol 1992;20:107.
102. Cipriano PR, et al. The effects of ergonovine maleate on coronary arterial size. Circulation 1979;59:82.
103. Friedman AC, Spindola-Franco H, Nivatpumin T. Coronary spasm: Prinzmetal’s variant angina vs. catheter-induced spasm; refractory spasm vs. fixed stenosis. Am J Radiol 1979;132:897.
104. Hays JT, Stein B, Raizner AE. The crumpled coronary artery—an enigma of arteriopathic pseudopathology and its potential for misinterpretation. Cathet Cardiovasc Diagn 1994;31:293.
105. Cannon RO III, Watson RM, Rosing DR, Epstein SE. Angina caused by reduced vasodilator reserve of the small coronary arteries. J Am Coll Cardiol 1983;1:1359–1373.
106. Cannon RO III, et al. Left ventricular dysfunction in patients with angina pectoris, normal epicardial coronary arteries, and abnormal vasodilator reserve. Circulation 1985;72:218–226.
107. Kurisu S, Sato H, Kawagoe T, et al. Tako-tsubo-like left ventricular dysfunction with ST-segment elevation: a novel cardiac syndrome mimicking acute myocardial infarction. Am Heart J 2002;143:448–455.
108. Sun H, Mohri M, Shimokawa H, et al. Coronary microvascular spasm causes myocardial ischemia in patients with vasospastic angina. J Am Coll Cardiol 2002;39:847–851.