Non-selective angiography of the coronary arteries was accomplished first in the 1920s and 1930s using an aortic injection of radiographic contrast media and cut film imaging [16]. Coronary imaging was limited by the toxicity and limited opacity of the di-iodinated contrast media, the restricted rate of contrast injection through the needle or small lumen catheters used for intravascular access, and poor radiographic imaging resolution. A variety of methods were used subsequently to enhance coronary filling, including acetylcholine-induced cardiac arrest and occlusion of the distal aorta to limit peripheral arterial runoff [17]. Although normal proximal coronary anatomy could be discerned by these methods, the structure of distal vessels and diseased arteries was poorly defined.

Semi-selective coronary angiography was performed later using a circular catheter with numerous sideholes [18]. When placed in the aorta, some of the side holes opposed the coronary ostia and contrast injection opacified these arteries. Selective injection of contrast media into the coronary arteries was limited by fear that the available radiographic contrast agents would cause ventricular fibrillation. This was quite justified because in an era before direct current cardioversion, fibrillation was a lethal complication.

The advent of selective coronary opacification was introduced by Mason Sones, who inadvertently selectively injected a right coronary artery during an attempted left ventricular angiogram. The patient did not develop ventricular fibrillation and Sones went on to develop a selective coronary catheter that could be deflected off the aortic valve into either coronary ostium, whereupon contrast could be injected [19]. Changes in contrast media and improvements in radiographic imaging have lead to better resolution of the coronary tree with less toxicity and radiation exposure. Improvements in radiographic positioning equipment enabled steep angulated views of the coronary circulation that are needed to image effectively the proximal left coronary vessels.

With the prior introduction of the Seldinger method of peripheral vascular cannulation, Judkins, Amplatz, Abrams, Schoonmaker and others invented preformed catheters that could be passed with great ease from the femoral artery to the coronary ostium [19, 19b, 19c, 19d, 20–24]. Since then an explosion of catheter material and shapes has made possible nearly effortless cannulation of most coronary arteries and bypass grafts. As Melvin Judkins is quoted as saying, “The catheter will find the coronary ostium unless impeded by the operator.” The technique of coronary cannulation and opacification is important, however, because both the safety and quality of coronary arteriography can be improved by rigorous attention to certain principles.

The evaluation of patients about to undergo coronary angiography should emphasize a detailed history concerning factors that affect the approach and risks of angiography, a physical examination concentrating on the cardiovascular system, and a frank discussion of the procedure and its anticipated risks and benefits.

The history should include questions about prior experience with angiography, and prior or current vascular diseases (e.g. stroke, transient ischemic attack, claudication) and previous vascular procedures (particularly aortic or iliofemoral revascularization). Additionally, the presence of factors increasing sensitivity to drugs used during catheterization should be noted so that appropriate precautions can be taken. This includes radiographic contrast materials (e.g. diabetes, pre-existing nephropathy, prior reaction to contrast), protamine sulfate (e.g. alpha₁ antitrypsin deficiency), narcotics, benzodiazepines, and heparin or other anticoagulants (e.g. gastrointestinal disease, antiphospholipid antibody).

The physical examination should concentrate on the vascular system and elements that might change the approach for the procedure. The quality of the pulses in both upper (brachial, radial, and ulnar) and lower extremities (femoral, dorsalis pedis, popliteal, and posterior tibia) should be recorded because problems in obtaining vascular access may necessitate a change in cannulation site and embolic complications can occur in any vascular territory. In patients where radial access is anticipated, an Allens test should be performed to insure patency of the ulnar artery. This test is now often performed with a finger oximeter, which adds greatly to accurate assessment of the patency of the palmar vascular arch. Particular attention also should be paid to the quality of carotid artery upstroke and the presence of carotid, abdominal (renal), or femoral bruits. Although not always possible, it is better to obtain arterial access in arteries without diminished pulse or bruit. The presence of an abdominal aneurysm should be assessed because aneurysms frequently contain thrombus or other friable material that can be embolized during vascular cannulation.

The physical examination should also concentrate on the cardiovascular illness necessitating angiography. The jugular venous pressure and wave form should be noted to assess right heart filling pressure and possible tricuspid regurgitation. The presence of left heart failure should be assessed and the ability of the patient to lie flat for prolonged periods should be ascertained (usually by observing the patient supine for 15–30 min). If possible, patients with severe left heart failure should undergo diuresis prior to angiography.

After interviewing and examining the patient, the anticipated procedure should be explained in sufficient detail to give the patient an understanding of what will be done, when it will be done, what will occur after the procedure, and what the likely expected findings might be. The main goal of this discussion is to insure informed consent and to allay anxiety on the day of the procedure. The procedural description can be supplemented with written or video format materials. It also can be quite useful to discuss the implications of certain findings in order to lay the groundwork for future recommendations for treatment. We find it quite useful to involve a responsible family member in the pre-angiography preparation.

After a discussion of the procedure itself, a frank discussion of the potential risks should occur and informed consent should be obtained. A description of potential complications should be tailored to the patient’s risk factors to provide an estimate that is as accurate as possible (see below). It is to no one’s advantage to minimize or exaggerate the risks of angiography.

Before angiography, an electrocardiogram should be obtained. The serum potassium and creatinine concentrations and hemoglobin concentration should be measured to assure that special precautions need not be taken. Generally, measurement of blood clotting time (prothrombin time or partial thromboplastin time) is not required unless there is a clinical suspicion that they might be abnormal (e.g. anticoagulant use, liver disease, severe right heart failure, bleeding history) [25]. If the patient has had prior coronary bypass or other heart surgery, the operative report should be read and the position of bypass grafts noted. The patient’s report of the operation or the brief notes of other physicians frequently can be incomplete or inaccurate.

The day of the procedure, the patient should be instructed to withhold oral intake for 6 h before the procedure. Medications should generally be continued, except for hypoglycemic agents. Oral hypoglycemic agents should be held the day of the procedure. Doses of long-acting insulin (such as NPH insulin) should be halved and regular insulin should be held. Ultra-long acting insulin (such as Lantus) should be administered in the usual dose. If insulin is given, a 5 % glucose solution should be infused until catheterization and supplemental oral glucose can be given as needed. Metformin, an oral hypoglycemic agent, should be held before and after angiography in patients with increased risk of renal failure. The drug can lead to lactic acidosis in the presence of renal failure [26].

In all patients, a reliable intravenous access line should be established prior to angiography. The infusion port should be large enough to permit a rapid infusion of fluid, should the patient develop reduced intravascular pressure (e.g. as a result of increased vagal tone or nitrate induced veno-relaxation). Patients with renal dysfunction, particularly those with diabetes, should be adequately hydrated before angiography. Dehydration increases the risk of contrast induced renal failure [26]. Many patients present for angiography dehydrated because they are instructed not to drink anything for 6–12 h before the procedure.

The best deterrent to contrast induced nephropathy is hydration, both before and immediately after the procedure [26a]. In addition, minimization of radiographic contrast media dose is important. A diagnostic angiogram can be obtained using less than 30 mL of contrast and biplane angiography. There is little evidence to support the use of mannitol, Lasix, N-acetylcysteine, or alkalizied saline prior to angiography to reduce renal dysfunction. In patients with pre-existing renal dysfunction (creatinine clearance less than 50 ml/min) measures should be taken to reduce the incidence of contrast induced nephropathy.

Proper sedation is also an important preparation of the patient. Patients awaiting angiography are anxious. Treatment with anxiolytic drugs can improve their perception of the procedure, although elderly patients may have paradoxical excitation with benzodiazepines and other sedatives. Before coming to the catheterization laboratory, the patient should void urine and take a non-soporific sedative (e.g. benzodiazepine). Careful monitoring of respiration is important during conscious sedation. If a long procedure is anticipated, insertion of a urinary catheter may be useful in men with prostatism or other patients who have trouble voiding.

Access to the arterial vasculature can be accomplished by cutdown and direct catheter insertion, or by the percutaneous Seldinger technique [28]. For many years, the brachial artery was exposed directly and incised with a blade to insert Sones catheters into the central circulation. After arteriography, the catheter was withdrawn and the artery was sutured closed. The advantages of cutdown cannulation are control of the artery and minimal bleeding after the completion of the repair. The disadvantage is a higher risk of arterial thrombosis or injury (see below), infection, a scar on the arm, and limited reuse of the same access site.

Introduction of a direct percutaneous needle puncture method for angiography made possible the development of femoral approach angiography, the method used overwhelmingly at present [28]. The skin and subcutaneous tissues about the artery are infiltrated with a local anesthetic, (e.g. lidocaine or the longer acting bupivacaine). The common femoral artery is punctured with a thin walled needle. The site of entry is important because an inferior puncture may enter the smaller superficial femoral artery and a superior puncture may pass into the pelvis and increase the risk of retroperitoneal bleeding. The common femoral artery can be located by finding the superior, anterior iliac crest and the symphysis pubis (landmarks of the inguinale ligament). The puncture site should be approximately 5 cm inferior to the line at the site of the pulse. Particularly in obese patients, the puncture site may be above the groin crease. Where landmarks are difficult to ascertain, fluoroscopy can be used. In 97 % of patients, a portion of the common femoral artery overlies the medial femoral head [29]. Alternatively, ultrasound imaging can be used to identify the common femoral artery, with the advantage that stenotic lesions precluding cannulation can be prospectively identified.

Once the artery is punctured, a 0.035–0.038 in. (.88–.95 mm) flexible guidewire with a “J” tip is passed through the needle into the arterial lumen [30]. Heparin coating on the wire reduces platelet adhesion [31]. Once the guidewire is in place, a dilator is employed to enlarge the tract into the artery, after which a catheter (with a tip tapered down to the wire) or hemostatic sheath (a short tube with a one-way valve) is advanced into the vessel. The angiographic catheters are advanced through hemostatic valve in the sheath and up to the ascending aorta with the aid of the “J” tip guidewire. If a hemostatic sheath is used, the outer diameter of arteriotomy will be about 0.3 mm larger than the inner diameter of the sheath, enlarging the puncture site by one French size.

Although not preferred to a native femoral artery, vascular access can be obtained through prosthetic femoral artery grafts (e.g. Dacron), provided that the grafts have been in-place long enough to develop extraluminal fibrosis (i.e. 2–4 months). Fears of uncontrollable bleeding, infection, and disruption of the pseudointima within the graft, in general, have not been realized [32, 33, 34a] and catheter insertion into grafts is usually safe. In our experience, however, it may take slightly longer to achieve hemostasis after catheter withdrawal and dislodgment of the pseudointima within the graft can occur very infrequently. It has been suggested that catheters in vascular grafts be removed after straightening with a guidewire.

More recently, radial artery access has been used, particularly in patients with severe femoral or aorto-iliac disease [34b, 34c]. After performing an Allen test to insure that the ulnar artery is patent, a small needle and guidewire is passed into the radial artery. An intravascular sheath with a hydrophilic coating is then passed into the artery. Vasospasm is common; administration of intra-arterial nitroglycerine, calcium channel antagonist (e.g. nicardipne 200 mcg) and heparin is critical.

The advantage of radial access is that hemostasis after the procedure can be obtained with simple wrist pressure (several devices to apply pressure have been developed). This allows the patient to ambulate quickly and avoids some of the bleeding complications of femoral access, such as retroperitoneal hematoma. The disadvantage is that about 2 % of radial arteries are permanently occluded after the procedure and catheters are usually limited to 4–6 Fr size [34c].

After angiography, the extremity with the arteriotomy site should be extended and held straight. The catheters should be withdrawn from the artery, aspirating during withdrawal to help avoid extrusion of thrombus. Immediately after decannulation, the arterial puncture site should be compressed by hand or, in the case of femoral puncture, with the use of a device (i.e. a Femostop) to apply local pressure. Some authors suggest that compression devices lead to a higher complication rate, there is little evidence to support this view. An unwatched Femostop or other hemostatic device, however, can be dangerous because changes in patient position or muscle tone alter the pressure applied to the artery and may lead to bleeding, total vessel occlusion, venous thrombosis or pressure injury of the femoral nerve or soft tissue. The Femostop is meant to save the hands, not time.

For patients with radial artery access, a wrist band with a balloon centered over the radial puncture site can be very useful. Importantly, the pressure applied by the band should be rapidly diminished to avoid radial artery occlusion due to thrombosis. Occlusion of the radial artery rarely can lead to ischemia of the hand.

Several vascular closure devices have been developed recently. They are divided into percutaneous suture devices (e.g. Perclose), devices that apply a hemostatic material (collagen or thrombin) to the puncture site (e.g. Angioseal), and clips that seal the artery (e.g. Starclose). These devices allow patients to ambutate quickly, usually within an hour or less. They do not, however, reduce the bleeding complications of arteriotomy. The incidences of bleeding, femoral pseudoanuerysm, retroperitoneal hematoma and surgical repair are similar in patients treated with manual compression and those in whom a closure device is used [34c, 34d].

Regardless of method used for hemostasis, the distal pulse should be monitored frequently until pressure is withdrawn and for at least several hours thereafter (e.g. every 15 min for 1 h after hemostasis, then every 30–60 min) [34]. The patient should avoid actions that increase arterial pressure (e.g. coughing, straining to urinate, sitting up) for 1–6 h, depending on the type of closure used. The precise duration of bedrest needed after arterial puncture is not clear but probably decreases with the size of the catheter used [27].

The essential features of a coronary angiographic catheter are an adequate lumen area, shape retention, torque control, radiographic opacity, and safety. Catheters used to cannulate the coronary arteries were initially constructed of a woven Dacron or hydrocarbon polymers. Polymers, predominantly polyurethanes and polyethylenes, are advantageous because they can be extruded and easily shaped. Their drawbacks are that they also can soften when inserted into the body and frequently do not transmit torque to the catheter tip. To improve shape retention and torque transmission, most manufacturers use wire braiding within the catheter wall. Improved polymers have allowed a reduction in the thickness of the catheter wall, preserving the caliber of the inner lumen, without a significant loss in handling characteristics.

After Sones developed catheters for brachial approach angiography, Judkins and Amplatz designed a series of coronary catheters for cannulation from the femoral approach [19, 19b, 19c, 19d, 20–24]. Each design has a primary and secondary curve, and tapers at the tip to hug the guidewire (Figs. 5.3 and 5.4) [19, 19b, 19c, 19d, 20–24].

Catheter caliber is measured in French size (French size = circumference in mm). In the 1990s, catheter construction improved remarkably, allowing the manufacture of 4–6 French sizes. The smaller arteriotomy required by 4–6 French size catheters has reduced the time needed for hemostasis and bedrest after catheter withdrawal, and may prevent peripheral vascular complications [27, 34]. However, smaller catheters (particularly less than 5 French size) can have insufficient lumen area to inject contrast adequately into the coronary artery (leading to contrast streaming), poor torquing characteristics and instability within the coronary lumen [35, 36]. Rapid injection through a small catheter endhole orifice can lead to damage of the coronary wall [73]. The likelihood of coronary injury is related directly to the energy content of the contrast jet. A single report also describes an increase in catheter-induced coronary artery dissections associated with 6 French size catheter use by less experienced operators [38]. Newer small catheters have a remarkably large lumen area and may be safer than earlier versions. In general, however, newer catheters 4–6 French in size produce acceptable angiography, particularly when used with a mechanical injector.

Cannulation of the coronary ostium is the most important step in angiography. Catheters should be advanced to the ascending aortic root with the use of a guidewire. Inserting catheters without a guidewire can lead to retrograde peripheral arterial dissection. After aspirating the catheter to insure that any debris or air has been removed, the catheter should be filled with contrast and connected to the pressure transducer. Left Amplatz and Judkins catheters can be advanced to the coronary ostium directly and usually require little manipulation (Figs. 5.3 and 5.4) [20, 22]. Right coronary Amplatz and Judkins catheters should be advanced to the aortic valve, withdrawn 1–1½ cm and rotated clockwise until the ostium is engaged (Fig. 5.4). The William 3D right coronary catheter cannuates the anatomically normal right coronary without manipulation. Radial artery approach has been facilitated by a number of new catheter curves.

When cannulating a coronary ostium, fluoroscopy in the 40–45° LAO projection can be useful because the coronary ostia are nearly perpendicular to the view. Alternatively, when the coronary origin is rotated posteriorly (e.g. with left ventricular hypertrophy) or anteriorly (e.g. with lung disease), a RAO 45° projection can help significantly. If the coronary cannot be cannulated, a different catheter shape should be used, keeping in mind the shape of the aorta, the angle of the coronary origin and the rotation of the heart. If a coronary ostium cannot be found, the possibility of an aberrant origin should be considered (see below).

After cannulation, the pressure at the catheter tip should be observed. Pressure damping implies that the catheter has burrowed into the wall of the artery, that there is catheter-induced vasospasm, or that there is an organic ostial stenosis. If present, injection of contrast should be avoided because it could cause a coronary dissection [37]. The catheter should be withdrawn slowly. If the pressure normalizes with the catheter in the orifice, a test injection should be done. Free flowing contrast without staining of the arterial wall should be observed before angiography. Since contrast emerges from the catheter as a jet, it is important that the catheter tip is coaxial with the proximal artery to avoid contrast-jet induced injury to the ostial wall.

Pressure damping from an improper catheter position (e.g. cannulation of the small conus branch or vasospasm is common in the right coronary artery, but in the left coronary it should alert the angiographer to the possibility of stenosis in the left main coronary, a particularly dangerous problem. A test injection below the artery or use of a “cusp” catheter can define the coronary ostium and permit selection of the best catheter shape. Administration of nitroglycerin can reduce the tendency for catheter-induced ostial vasospasm, although it is not always effective.

Catheterization itself is associated with platelet activation and a rise in thromboxane A₂ metabolite excretion [72]. The presence of catheters within the vascular lumen causes endothelial denudation and combined with the foreign body of the catheter is a stimulus for intravascular thrombosis. Several, but not all, studies suggest that systemic anticoagulation with heparin reduces the incidence of thrombotic complications of angiography (primarily thrombosis at the site of catheter insertion) [73–75], although heparin has also been reported to cause additional activation of platelets [76]. Anticoagulation is not necessary for patients undergoing routine diagnostic angiography from the femoral approach. There is uniform agreement, however, that heparin (e.g. 2,000 u into the artery and 3,000 u intravenously) should be given to all patients in whom the brachial or radial approach is used, because of the higher incidence of thrombosis at the catheter insertion site. In patients undergoing femoral approach angiography, the risk of thrombotic complications probably increases with the duration of the procedure, a smaller femoral artery or larger catheter, and the presence of peripheral vascular disease. Patients at higher risk of thrombosis should be anticoagulated (3,000–5,000 u intravenously) unless a contraindication exists.

The optimal dose of heparin may vary between patients because plasma antithrombin III and platelet factor four (which binds heparin) concentrations affect heparin efficacy and availability respectively [77]. Heparin pharmacokinetics are not affected by the type of contrast media selected [78]. Aspirin decreases platelet activation caused by angiography, but its efficacy in reducing complications has not been evaluated [72].

At the end of the procedure, the anticoagulant effects of heparin can be reversed by administering protamine [79]. Protamine is a polycationic compound derived from fish sperm (primarily from salmon and herring) that binds to heparin. One mg of protamine binds approximately 100 u (1 mg) of heparin [9]. Since heparin is essentially eliminated by first order kinetics, the amount of protamine needed is a function of the initial heparin dose and the time since administration. For a 5,000 unit heparin dose, the initial protamine dose should be 50 mg if less than 20 min have passed and progressively less thereafter (e.g. 30 mg if 60 min has elapsed) [8]. If insufficient protamine is given, a phenomenon known as “heparin rebound” can occur [10]. After initial normalization of clotting times from the first protamine dose, protamine degradation by proteinases leads release of free heparin and a rebound increase in clotting time [80, 81].

Protamine should be administered cautiously to patients with a prior exposure to the drug (such as NPH insulin, or protamine sulfate or chloride), patients with a “fish allergy,” and should not be given to patients with alpha₁ antitrypsin deficiency (see below) [82, 83]. Very large protamine doses (>4.0:1 protamine:heparin concentration) can have an anticoagulant effect, although it is rarely observed in a clinical setting [9].

The lumen caliber of epicardial coronary arteries measured at angiography reflects a variable degree of tone. Both atherosclerotic and normal coronary arteries dilate after nitroglycerin but proximal vessels exhibit less dilation than distal epicardial vessels (9 % vs. 34 % diameter increase) [84]. Stenotic lesions also relax after nitroglycerine, although severely narrowed segments usually dilate little [85]. Removal of tone by nitroglycerin permits an assessment of maximal coronary caliber, effectively eliminates vasospastic coronary lesions, and facilitates assessments of stenosis severity.

Nitroglycerin primarily affects the large diameter epicardial portion of the coronary artery and dilation in these vessels lasts for 10–20 min. When administered by the intracoronary route, only small doses of nitroglycerin (100 μg in the right coronary, 150 μg in the left coronary artery) are needed to effect maximal epicardial coronary dilation and these doses have a minimal impact on systemic hemodynamics [84]. A 400 μg sublingual dose of nitroglycerin also causes maximal dilation of the conduit coronary arteries. Nitroglycerin administered into the coronary ostium also has very brief effects on the microcirculation (usually causing a 1.5–2.5 fold increase in coronary blood flow lasting less than 2 min), but causes negligible changes in blood flow when given by intravenous infusion or by mouth [86, 87].

It should be remembered that the nitrate response in the large coronary arteries is not complete for 2 min after intracoronary administration and 4 min after a sublingual dose. Additionally, patients undergoing angiography are often intravascular volume depleted because oral intake has been withheld for some time. This can lead to an increased sensitivity to nitrate-induced venodilation and transient hypotension. Since coronary caliber is dependent on distending pressure, the reproducibility of coronary angiographically defined measurements of coronary diameter overtime is dependent on maintenance of arterial pressure [88]. In patients without heart failure, saline is often given prior to nitroglycerin administration to blunt the fall in arterial pressure.

In some patients and particularly in radial artery bypass graft conduit, nitroglycerine may not entirely reduce arterial tone. Intra coronary or graft calcium channel blocking agents (e.g. nicardipine 100–400 mcg) may be effective.

Although once performed exclusively as an in-patient procedure, the majority of angiography is now be performed in the out-patient setting [94–98]. Outpatient angiography generally has a 25 % lower hospital cost, but it places some strains on pre-angiography patient preparation [94, 98]. For example, intravenous hydration of patients with renal failure is important and more difficult to achieve immediately prior to an outpatient procedure. It also imposes more responsibility on the patient for pre-catheterization medication and site preparation, and post-angiography catheter insertion site observation.

Patients with acute ischemic syndromes (unstable angina, infarction) should not go home immediately after angiography because of the risk of recurrent ischemic episodes [97]. Patients with left main or severe three vessel coronary disease, severe heart failure, bleeding diathesis, and severe aortic valve stenosis generally should be observed longer after contrast angiography [97]. Many patients undergoing outpatient angiography are admitted to the hospital after the procedure, 1–2 % for observation after a complication and the remainder for a surgical procedure (e.g. angioplasty or bypass surgery) [94, 95, 98].

Coronary angiography has been performed in mobile truck trailers stationed at smaller hospitals [99, 100]. With the exclusion of higher risk patients through proper patient selection, the complications of “mobile angiography” appear not to be increased and patient satisfaction may be improved [100]. Several logistical problems remain. Since a significant fraction of patients undergo a revascularization procedure based on the information gained from the angiogram, many (if not the majority) patients will need to travel to a larger hospital anyway, obviating the advantages of mobile angiography. Additionally, patients who subsequently have angioplasty may need to have two procedures (at two hospitals) instead of proceeding with angioplasty in the same procedure as the angiogram. More information will be needed to know if catheterization in mobile structures is cost effective.

Arrhythmias during angiography can occur from abrasion of the conduction system by catheters, contrast media-induced changes in repolarization, reflex-mediated changes in neural traffic to the heart, and transient myocardial ischemia from hemodynamic deterioration. The left bundle branch of the conduction system courses near the surface of the left ventricular septum and can be injured transiently during cannulation of the left ventricle [159, 160]. The right bundle branch is located near the tricuspid annulus and can be rendered dysfunctional by a right heart catheter (particularly if the catheter is rubbed against the superior annulus repeatedly). In a patient with a pre-existing contralateral bundle branch block, complete heart block can occur [159, 160]. In these patients, the immediate availability of cardiac pacing (external or by catheter) should be ascertained prior to catheterization.

Contrast media can induce sinus bradycardia, sinus node block, and atrioventricular node block by two mechanisms. The hyperosmolar and chemical properties of contrast cause activation of ventricular afferent chemoreceptors which reflexively trigger a parasympathetic surge, reducing sinus and AV node repolarization [52, 53, 63]. The reflex is blocked partially by muscarinic receptor blockade with atropine. Iso-osmolar contrast media significantly reduce or eliminate vagally mediated bradycardia.

Neurally-mediated syncope can also complicate angiography, particularly when the patient is dehydrated and experiences pain. Contrast material may also directly depress conduction tissue repolarization and transiently slow heart rate. Vigorous coughing can maintain blood pressure but does not hasten clearance of contrast material from the coronary circulation [161].

Prolongation of the ventricular refractory period by contrast media can initiate ventricular fibrillation. Fibrillation occurs more commonly after right compared to left coronary injection. The incidence is less with “non-ionic” or iso-osmolar contrast material and with “ionic” contrast which with a physiological calcium ion content [41–44, 49]. The probability of ventricular fibrillation also is higher if an excessive volume of contrast material is injected in a single dose.

Although catheterization of the coronary arteries does not by itself change ventricular function, injection of contrast media causes a reduction in diastolic ventricular compliance and a brief reduction in systolic function. These effects appear to be mediated by the osmolarity of the contrast agent because iso osmolar contrast has only minimal effects of ventricular function [161a].

In patients with normal or near normal ventricular function, the ventricular effects of contrast are not important clinically. Patients with markedly reduced systolic function (ejection fraction <35 %) or elevated ventricular filling pressure (regardless of systolic function), however, must be approached with caution, for these are the patients who develop pulmonary edema after contrast injection [61, 46, 48]. We often ascertain the left ventricular end diastolic or pulmonary artery wedge pressure prior to angiography in patients with a prior history of congestive left heart failure, pulmonary edema or severe left ventricular dysfunction, particularly if they are decompensated. If the pulmonary wedge pressure is more than 20 mmHg, it should be reduced prior to contrast injection and the pulmonary wedge or mean pressure should be monitored during the angiogram. Iso-osmolar contrast should be used. If the pressure rises significantly, contrast injections should be withheld. Intravenous nitroglycerin or nitroprusside infusion during angiography can be used to rapidly reduce filling pressures and facilitate angiography. It is important to remember that contrast can affect ventricular diastolic function for up to 20 min.

The importance of obtaining adequate angiographic views of the coronary arteries cannot be overemphasized. Since the orientation between the planes of the major cardiac grooves and septum are different from the standard anterior-posterior (AP) and lateral projections utilized for chest roentgenology, oblique views must be used to obtain optimal angiographic visualization of the coronary arteries. An understanding of the orientation of these structures and the coronary vessels in the oblique positions can be difficult for the novice, but several teaching models have been developed to facilitate understanding [183–185].

We have utilized the following schematic diagram. In Fig. 5.9 the eyes represent the line of sight of the viewer. In the left anterior oblique (LAO) projection the viewer is sighting down the interventricular and interatrial septum. All left sided cardiac chambers appear to the viewer’s right. In the left anterior oblique (LAO) projection, the anterior and posterior descending coronary arteries are seen coursing vertically in the middle of the cardiac silhouette, following the path of the interventricular septum. In the right anterior oblique (RAO) projection, the viewer’s line of sight is the atrio-ventricular groove plane. In this projection the two atria and the two ventricles are superimposed. The proximal circumflex and proximal right coronary arteries are well visualized as they follow their course in the atrio-ventricular groove.

The angiographer must evaluate the entire vessel in several different views to avoid the effects of vessel foreshortening that can hide a stenotic lesion and because of coronary lesions are frequently eccentric. Although the severity of a coronary stenosis is often reported as the most severe appearance measured in any of the views, physiological studies show that an integration of lumen stenosis from many views more accurately predicts the degree of blood flow impairment imparted by the lesion [186]. In truth, if the lesion can be well visualized, all views are contributory toward assessing stenosis severity. Additionally, when quantitative angiographic methods are employed, coronary lesions are best evaluated in at least two orthogonal projections (e.g. LAO 60° and RAO 30°) in which the lesion can be seen well in both projections without foreshortening or overlap [187].

In 1981 Paulin [188] proposed that radiographic projections be named by following the course of the x-ray beam as it passes through the heart. The x-ray gantry can be angled in the horizontal and coronal planes. The position of the imaging device defines the projection. In the left anterior oblique (LAO) projection, the x-ray beam is angled in the horizontal plane such that it is projected from under and to the right of the patient (right posterior) to the image intensifier which is anterior and to the patients left. Similarly, the x-ray beam of the right anterior oblique (RAO) view originates left posterior aspect and passes to the image tube which is anterior and rotated to the patient’s right. In caudo-cranial views the x-ray beam is angled in the coronal (frontal) plane. In the “cranial” view, the x-ray beam originates caudally and passes through the heart to the image intensifier which is angled cranially. Conversely in a caudal projection the x-ray tube is angled cranially and projects the x-ray beam caudally to the image tube. The use of multiple oblique views in the antero-lateral projection in conjunction with angulation in the caudo-cranial plane has greatly facilitated optimal visualization of coronary lesions and minimized the problem of foreshortening of the coronary arteries.

The use of a “standard set of optimal projections” for coronary angiography is at best only a guide, since variations in normal coronary anatomy are the rule rather than the exception. The following suggestions may be of some help. The left main coronary artery, which under most circumstances should be visualized first and with great care, can be seen best in the PA (Fig. 5.10) or in a very shallow oblique projection (either RAO or LAO) so that the left main coronary is just off the spine. The circumflex artery and its marginal branches can be defined n the RAO projection (20° or 30° angulation) with 20–30° of caudal angulation (Fig. 5.10). A second less steep RAO or PA view coupled with marked cranial angulation (30°) (Fig. 5.10) may be helpful in delineating the course of the anterior descending artery, avoiding overlap by other branches. A steep LAO view (40°) with severe cranial angulation (40°) (Fig. 5.10) is essential in viewing the left anterior descending and diagonal branch bifurcation. An additional LAO caudal view (LAO 40°, caudal 30°, the so-called ‘spider’ view) (Fig. 5.10) may be of use in visualizing the bifurcation of the left main, the proximal circumflex and left anterior descending and at times the distal left anterior descending. The proximal and mid right coronary artery are usually seen well in a 30–45° LAO projection. A moderate LAO view with cranial angulation (LAO 20°, cranial 20°) (Fig. 5.11a) may be ideal for viewing the bifurcation of the distal right coronary into the posterior descending and posterior lateral branches. One view of the right coronary in the RAO view is necessary. At times visualization of the distal right coronary is helped by adding cranial angulation (sometimes up to 60°) to the RAO view (Fig. 5.11b).

A common series of initial projections are as follows:

Atherosclerosis is a disease of the arterial wall which can encroach on the vessel lumen and limit blood supply to the myocardium. In interpreting coronary angiograms, it is important to understand the nature of the atherosclerotic process as it relates to coronary dimensions and the angiographic appearance of atherosclerosis.