Table 2-1 lists generally agreed on indications for cardiac catheterization. With respect to CAD, approximately 15% of the adult population studied will have normal coronary arteries. Coronary angiography is, for the moment, still consideredthe gold standard for defining CAD. With advances in magnetic resonance imaging and multislice computed tomography, the next decade may well see a further evolution of the catheterization laboratory to an interventional suite with fewer diagnostic responsibilities.

Table 2-1 Indications for Diagnostic Catheterization in the Adult Patient

Coronary Artery Disease

Symptoms

Unstable angina

Postinfarction angina

Angina refractory to medications

Typical chest pain with negative diagnostic testing

History of sudden death

Diagnostic Testing

Strongly positive exercise tolerance test

Early positive, ischemia in > 5 leads, hypotension, ischemia present for > 6 minutes of recovery

Positive exercise testing following after myocardial infarction

Strongly positive nuclear myocardial perfusion test

Increased lung uptake or ventricular dilation after stress

Large single or multiple areas of ischemic myocardium

Strongly positive stress echocardiographic study

Decrease in overall ejection fraction or ventricular dilation with stress

Large single area or multiple or large areas of new wall motion abnormalities

Valvular Disease

Symptoms

Aortic stenosis with syncope, chest pain, or congestive heart failure

Aortic insufficiency with progressive heart failure

Mitral insufficiency or stenosis with progressive congestive heart failure symptoms

Acute orthopnea/pulmonary edema after infarction with suspected acute mitral insufficiency

Diagnostic Testing

Progressive resting LV dysfunction with regurgitant lesion

Decreased LV function and/or chamber dilation with exercise

Adult Congenital Heart Disease

Atrial Septal Defect

Age > 50 with evidence of coronary artery diseaseSeptum primum or sinus venosus defects

Ventricular Septal Defect

Catheterization for definition of coronary anatomy

Coarctation of the Aorta

Detection of collateral vessels

Coronary arteriography if increased age and/or risk factors are present

Other

Acute myocardial infarction therapy—consider primary PCI

Mechanical complication after infarction

Malignant cardiac arrhythmias

Cardiac transplantation

Pretransplant donor evaluation

Post-transplant annual coronary artery graft rejection evaluation

Unexplained congestive heart failure

Research studies with institutional review board review and patient consent

LV = left ventricular.

Patient Evaluation before Cardiac Catheterization

Diagnostic cardiac catheterization in the 21st century is universally considered an outpatient procedure except for the patient at high risk. Therefore, the precatheterization evaluation is essential for quality patient care. Evaluation before cardiac catheterization includes diagnostic tests that are necessary to identify the high-risk patient. An ECG must be performed on all patients shortly before catheterization. Necessary laboratory studies before catheterization include a coagulation profile (prothrombin time [PT], partial thromboplastin time [PTT], and platelet count), hemoglobin, and hematocrit. Electrolytes are obtained along with a baseline determination of blood urea nitrogen (BUN) and creatinine to assess renal function. Urinalysis and chest radiograph may provide useful information but are no longer routinely obtained by all operators. Prior catheterization reports should be available. If the patient had prior PCI or coronary artery bypass surgery, this information must also be available.

Patient medications must be addressed. On the morning of the catheterization, antianginal and antihypertensive medications are routinely continued while diuretic therapy is held. Diabetic patients are scheduled early, if possible. Because breakfast is held, no short-acting insulin is given. Patients on oral anticoagulation should stop warfarin sodium (Coumadin) therapy 48 to 72 hours before catheterization (INR ≤ 1.8). In patients who are anticoagulated for mechanical prosthetic valves, the patient may best be managed with intravenous heparin before and after the procedure, when the warfarin effect is not therapeutic. Low-molecular-weight heparins (LMWHs) are used in this setting, but this is controversial. LMWHs vary in their duration of action, and their effect cannot be monitored by routine tests. This effect needs to be considered, particularly with regard to hemostasis at the vascular access site. Intravenous heparin is routinely discontinued 2 to 4 hours before catheterization, except in the unstable angina patient. Aspirin therapy for angina patients or in patients with prior CABG is often continued, particularly in patients with unstable angina.

CARDIAC CATHETERIZATION PROCEDURE

Whether the procedure is elective or emergent, diagnostic or interventional, coronary or peripheral, certain basic components are relatively constant in all circumstances.

Patient Preparation

Patients with previous allergic reactions to iodinated contrast agents require adequate prophylaxis. Greenberger and colleagues studied 857 patients with a prior history of an allergic reaction to contrast media. In this study, 50 mg of prednisone was administered 13, 7, and 1 hour before the procedure. Diphenhydramine, 50 mg, was also administered intramuscularly 1 hour before the procedure. Although no severe anaphylactic reactions occurred, the overall incidence of urticarial reactions in known high-risk patients was 10%. The use of nonionic contrast agents may further decrease reactions in patients with known contrast allergies. The administrationof histamine-2 blockers (cimetidine, 300 mg) is less well studied. For patients undergoing emergent cardiac catheterization with known contrast allergies, 200 mg of hydrocortisone is administered intravenously immediately and repeated every 4 hours until the procedure is completed. Diphenhydramine, 50 mg, given intravenously, is recommended 1 hour before the procedure.

Patient Monitoring and Sedation

Standard limb leads with one chest lead are used for ECG monitoring during cardiac catheterization. One inferior and one anterior ECG lead are monitored during diagnostic catheterization. During an interventional procedure, two ECG leads are monitored in the same coronary artery distribution as the vessel undergoing PTCA. Radiolucent ECG leads improve monitoring without interfering with angiographic data.

Cardiac catheterization laboratories routinely monitor arterial oxygen saturation by pulse oximetry (SpO₂) on all patients. Utilizing pulse oximetry, Dodson and associates demonstrated that 38% of 26 patients undergoing catheterization had episodes of hypoxemia (SpO₂ < 90%) with a mean duration of 53 seconds. Variable amounts of premedication were administered to the patients.

Sedation in the catheterization laboratory, either from preprocedure administration or subsequent intravenous administration during the procedure, may lead to hypoventilation and hypoxemia. The intravenous administration of midazolam, 1 to 5 mg, with fentanyl, 25 to 100 μg, is common practice. Institutional guidelines for conscious sedation typically govern these practices. Light to moderate sedation is beneficial to the patient, particularly for angiographic imaging and interventional procedures. Deep sedation, in addition to its widely recognized potential to cause respiratory problems, poses distinct problems in the catheterization laboratory. Deep sedation often requires supplemental oxygen, and this complicates the interpretation of oximetry data and may alter hemodynamics. Furthermore, deep sedation may exacerbate respiratory variation, altering hemodynamic measurements.

Sparse data exist regarding the effect of sedation on hemodynamic variables and respiratory parameters in the cardiac catheterization laboratory. One study examined the cardiorespiratory effects of diazepam sedation and flumazenil reversal of sedation in patients in the cardiac catheterization laboratory. A sleep-inducing dose of diazepam was administered intravenously in the catheterization laboratory; this produced only slight decreases in mean arterial pressure (MAP), pulmonary capillary wedge pressure, and left ventricular (LV) end-diastolic pressure (LVEDP), with no significant changes in intermittently sampled arterial blood gases. Flumazenil awakened the patient without significant alterations in either hemodynamic or respiratory variables.

More complex interventions have resulted in longer procedures. Although hospitals require conscious sedation policies, individual variation in the type and degree of sedation is common. Although general anesthesia is rarely required for adult patients, it is needed more frequently for pediatric procedures. In the future, more complex adult interventions may well require the presence of an anesthesiologist in the catheterization laboratory, similar to the early days of adult coronary intervention.

Left-Sided Heart Catheterization

Left-sided heart catheterization has traditionally been performed by either the brachial or femoral artery approach. In the 1950s, the brachial approach was first introduced utilizing a cutdown with brachial arteriotomy. The brachial arteriotomy is often time consuming, can seldom be performed more than three times in the same patient, and has higher complication rates. This led operators to adopt the femoral approach. Introduced more than 15 years ago, the percutaneous radial artery approach is an alternative that is increasingly used. The percutaneous radial approach is also more time consuming than the femoral approach but may have fewer complications. This approach may be preferred in patients with significant peripheral vascular disease or recent (<6 months) femoral/abdominal aortic surgeries and those with significant hypertension, on oral anticoagulants with a PT greater than 1.8, or who are morbidly obese. With increasing utilization of the radial artery as a conduit for CABG, care must be taken if this vessel has been used for radial access during catheterization.

Right-Sided Heart Catheterization

Clinical applications of right-sided heart hemodynamic monitoring changed greatly in 1970 with the flow-directed, balloon-tipped, pulmonary artery (PA) catheter developed by Swan and Ganz. This balloon flotation catheter allowed the clinician to measure PA pressure (PAP) and pulmonary capillary wedge pressure (PCWP) without fluoroscopic guidance. It also incorporated a thermistor, making the repeated measurement of cardiac output feasible. With this development, the PA catheter left the cardiac catheterization laboratory and entered both the operating room and intensive care unit.

Diagnostic Catheterization Complications

Complications are related to multiple factors, but severity of disease is important. Mortality rates are shown in Table 2-2. Complications are specific for both right- and left-heart catheterization (Table 2-3). Although advances in technology continue, these complication rates are still present today, most likely due to the higher risk patient undergoing catheterization.

Table 2-2 Cardiac Catheterization Mortality Data

Rights were not granted to include this table in electronic media. Please refer to the printed book.

From Pepine CJ, Allen HD, Bashore TM, et al: ACC/AHA guidelines for cardiac catheterization and cardiac catheterization laboratories. Circulation Nov, 84(5): 2213–2247

Table 2-3 Complications of Diagnostic Catheterization

Definition of Pressure Waveforms—Cardiac Cycle

Right-Sided Heart Pressures

The right-sided heart pressures, as measured in the cardiac catheterization laboratory, consist of the central venous pressure (CVP) or right atrial (RA) pressure (RAP), right ventricular (RV) pressure (RVP), PAP, and PCWP. The CVP consists of three waves and two descents (Fig. 2-1, Box 2-3). The A wave occurs synchronously with the Q wave of the ECG and accompanies atrial contraction. Next, a smaller C wave appears, which results from tricuspid valve closure and bulging of the valve into the right atrium as the right ventricle begins to contract. After this, with the tricuspid valve in the closed position, the atrium relaxes, resulting in the X descent. This is followed by the V wave, which corresponds to RA filling that occurs during RV systole with a closed tricuspid valve. As the RV relaxes, the RVP then becomes less than the RAP, the tricuspid valve opens, and the atrial blood rapidly empties into the ventricle. This is signified by the Y descent.

Figure 2-1 The cardiac cycle, demonstrating simultaneous left ventricular, aortic, and left atrial pressures (top); right ventricular, pulmonary arterial, and right atrial pressures (middle); and electrocardiogram (ECG) and aortic and pulmonary flows (bottom). Also displayed are the temporal relationships of mitral valve opening (MO) and closure (MC), aortic valve opening (AO) and closure (AC), tricuspid opening (TO) and closure (TC), and pulmonic valve opening (PO) and closure (PC).

(From Milnor WR: Hemodynamics, 2nd ed. Baltimore, Williams & Wilkins, 1989, p 145.)

Beginning in early diastole, the RV waveform reaches its minimum pressure shortly before or as the tricuspid valve opens. During the rapid filling phase of diastole, the ventricular pressure rises slowly and usually an A wave, which signifies atrial contraction, is seen just before the onset of ventricular systole. As ventricular contraction occurs, peak systolic pressure is rapidly reached. Just before the onset of contraction, and after the A wave, the RV end-diastolic pressure (RVEDP) can be determined.

The PAP is usually greater than the RVP during the time the pulmonic valve is closed, during ventricular relaxation and filling. During systole, RVP crosses over PAP by a small margin, causing the pulmonic valve to open, and the ventricle ejects blood into the PA. It is not uncommon for a 5-mm gradient to exist between the RV and PA during peak systolic contraction. The minimal PA diastolic pressure can also be measured just before the onset of contraction, as an estimate of the PCWP; however, the presence of increased pulmonary vascular resistance will invalidate this correlation. With an inflated balloon, the tip of the PA catheter is protected from pulsatile pressures and “looks forward” to the pressure in the pulmonary venous system and the left atrium. This “wedge” pressure shows many of the characteristics of the left atrial (LA) pressure (LAP). The differences between these two waves are considered in the discussion of LAP below.

Left-Sided Heart Pressures

The LA, LV, aortic, and peripheral pressures are commonly measured in the cardiac catheterization laboratory. The LAP can be measured directly if a transseptal catheter is placed. Because this is not commonly done, the PCWP is used to estimate LAP. The LAP has a very similar appearance (A, C, V waves; X, Y descent) to that in the RA, although the pressures seen are about 5 mm Hg higher. The A wave in the RA tracing is normally larger than the V wave whereas the opposite is true in the LA (or PCWP). The PCWP provides reasonable estimations of the LAP, although the waveform is often damped and also delayed in time compared with the LAP (Fig. 2-2).

Figure 2-2 Simultaneous left atrial (LAP) and pulmonary capillary wedge (PCW) pressures, demonstrating the accuracy of the PCW in replicating the A, C, and V waves seen in the LAP (corresponding to a, c, and v waves in the PCW). Also shown is the time delay seen in the PCW trace, which results from the pressure wave traveling back through the compliant pulmonary venous system to the pulmonary artery catheter.

(Modified from Grossman W, Barry WH: Cardiac catheterization. In Braunwald E [ed]: Heart Disease: A Textbook of Cardiovascular Medicine, 3rd ed. Philadelphia, WB Saunders, 1988, p 252.)

LV pressure also has many similar characteristics to the RVP, although because this is a thick-walled chamber, the generated pressures are higher than those reached in the RV. The central aortic pressure displays a higher diastolic pressure than that seen in the ventricle due to the properties of resistance in the arterial tree and the presence of a competent aortic valve. The dicrotic notch, which signifies the aortic valve closure, is a prominent feature of the aortic pressure wave in the central aorta. As the site of pressure measurement moves more distally in the arterial tree, there is a progressive distortion of the arterial waveform, usually demonstrated as an increase in systolic pressure. This is thought to be due to the addition of the pressure wave of reflected waves from the elastic arterial wall. Summation of reflected pressure waves has been postulated as a contributing factor in aneurysm formation. Additionally, the rapid propagation of reflected waves along stiff arteries has been advanced as an explanation of the systolic hypertension seen in the elderly. Table 2-4 displays the range of normal pressures on the right and left side of the heart.

Table 2-4 Normal Values on Right and Left Side of the Heart

Cardiac Output Measurements

The techniques of measuring an average CO remain important means to a complete assessment of the patient in the cardiac catheterization laboratory. The measurement of CO along with other information allows the physician to estimate whether the metabolic needs of the patient are being met, that is, whether the oxygen supply or oxygen delivery is matching the oxygen demand. In addition, quantitating the CO also allows the calculation of shunt flows, regurgitant fractions, systemic vascular resistance (SVR), and pulmonary vascular resistance (PVR).

Valvular Pathology

Each type of valvular pathology has its own particular hemodynamic “fingerprint,” the character of which depends on the severity of the pathology, as well as its duration.

Stenotic Lesions

To assess the severity of stenotic lesions, the transvalvular gradient as well as the transvalvular flow must be quantified. For a given amount of stenosis, hydraulic principles state that as flow increases, so also will the pressure drop across the orifice. Both the CO and the HR determine flow; it is during the systolic ejection period that flow occurs through the semilunar valves and during the diastolic filling period for the atrioventricular (AV) valves.

Gorlin and Gorlin derived a formula from fluid physics to relate valve area with blood flow and blood velocity:

In general, as a valve orifice becomes increasingly stenotic, the velocity of flow must progressively increase if total flow across the valve is to be maintained. To estimate valve area, flow velocity can be measured by the Doppler principle; however, in the catheterization laboratory, this is not as practical as measuring blood pressures on either side of the valve.

As described by Gorlin, the velocity of blood flow is related to the square root of the pressure drop across the valve:

Stated another way, for any given orifice size, the transvalvular pressure gradient is a function of the square of the transvalvular flow rate. For example, with mitral stenosis, as the valve area progressively decreases, a modest increase in the rate of flow across the valve causes progressively larger increases in the pressure gradient across the valve (Fig. 2-3).

Figure 2-3 Rate of flow in diastole versus mean pressure gradient for several degrees of mitral stenosis. The pressure gradient is directly proportional to the square of the flow rate, such that as the degree of stenosis progresses, modest increases in flow (as with light exercise) will require large increases in the pressure gradient. As an example, a cardiac output (CO) of 5.2 L/min, heart rate (HR) of 60 beats per minute, and diastolic filling time of 0.5 second results in a 200 mL/s flow during diastole (see text for details). For mild mitral stenosis (valve area = 2.0 cm²), the required pressure gradient remains small (<10 mm Hg). In the case of severe stenosis (valve area < 1.0 cm²), the resultant gradient is high enough to place the patient past the threshold for pulmonary edema.

(From Wallace AG: Pathophysiology of cardiovascular disease. In Smith LH Jr, Thier SO [eds]: The International Textbook of Medicine, Vol 1, Pathophysiology: The Biological Principles of Disease. Philadelphia, WB Saunders, 1981, p 1192.)

ANGIOGRAPHY

Ventriculography

Determination of Ejection Fraction

Ventriculography is routinely performed in the single-plane 30-degree right anterior oblique (RAO) or biplane 60-degree left anterior oblique (LAO) and 30-degree RAO projections using 20 to 45 mL of contrast agent with injection rates of 10 to 15 mL/s (Box 2-4). Complete opacification of the ventricle without inducing ventricular extrasystole is necessary for accurate assessment during ventriculography. These premature contractions not only alter the interpretation of mitral regurgitation (MR) but also result in a false increase in the global ejection fraction (EF).

The EF is a global assessment of ventricular function and is calculated as follows:

where EF is ejection fraction, EDV is end-diastolic volume, ESV is end-systolic volume, and SV is stroke volume.

Abnormalities in Regional Wall Motion

Segmental wall motion abnormalities (SWMAs) are defined in both the RAO and LAO projections. A 0 to 5 grading scale may be used with hypokinesis (decreased motion), akinesis (no motion), and dyskinesis (paradoxical or aneurysmal motion):

0 = normal

1 = mild hypokinesis

2 = moderate hypokinesis

3 = severe hypokinesis

4 = akinesis

5 = dyskinesis (aneurysmal)

Each wall segment is identified as outlined in Figure 2-4 for both the LAO and RAO projections. These segments correspond roughly to vascular territories.

Figure 2-4 A, Terminology for left ventricular segments 1 through 5 analyzed from a right anterior oblique ventriculogram. B, Terminology for left ventricular segments 6 through 10 analyzed from left anterior oblique ventriculogram. LV = left ventricle; LA = left atrium.

Rights were not granted to include this figure in electronic media. Please refer to the printed book.

(From Principal Investigators of CASS and their Associates: National Heart, Lung, and Blood Institute Coronary Artery Surgery Study. Circulation 63[suppl II]:1, 1981.)

Assessment of Mitral Regurgitation

The qualitative assessment of the degree of MR can be made with LV angiography. It is dependent on proper catheter placement outside the mitral apparatus in the setting of no ventricular ectopy. The assessment is, by convention, done on a scale of 1+ to 4+, with 1+ being mild and 4+ being severe MR. As defined by ventriculography, 1+ regurgitation is that in which the contrast agent clears from the LA with each beat, never causing complete opacification of the LA. Moderate or 2+ MR is present when the opacification does not clear with one beat, leading to complete opacification of the LA after several beats. In 3+ MR (moderately severe), the LA becomes completely opacified, becoming equal in opacification to the LV after several beats. In 4+ or severe regurgitation, the LA densely opacifies with one beat and the contrast agent refluxes into the pulmonary veins.

By combining data from left ventriculography and right-sided heart catheterization, a more quantitative assessment of MR can be made by calculating the regurgitantfraction. This can be effectively calculated by measuring the following: LVEDV, LVESV, and the difference between these two, or the total LV stroke volume (TSV). The TSV (stroke volume calculated from angiography) may be quite high, but it must be remembered that a significant portion of this volume will be ejected backward into the LA. The forward stroke volume (FSV) must be calculated from a measurement of forward CO by the Fick or thermodilution method. The regurgitant stroke volume (RSV) can then be calculated by subtracting the FSV from the TSV (TSV − FSV). The regurgitant fraction (RF) is then calculated as the RSV divided by the TSV:

A regurgitant fraction less than 20% is considered mild, 20% to 40% is considered moderate, 40% to 60% is considered moderately severe, and greater than 60% is considered severe MR.

Coronary Arteriography

Description of Coronary Anatomy

The left main coronary artery is 1 to 2.5 cm in length (Fig. 2-5). It bifurcates into the circumflex (CX) and left anterior descending (LAD) arteries. Occasionally, the CX and LAD arteries may arise from separate ostia or the left main artery may trifurcate, giving rise to a middle branch, the ramus intermedius, which supplies the high lateralventricular wall. Both septal perforators and diagonal branch vessels arise from the LAD artery, which is described as proximal, mid, and distal based on the location of these branch vessels. The proximal LAD artery is before the first septal and first diagonal branch; the mid LAD artery is between the first and second septal and diagonal branches; and the distal LAD artery is beyond the major septal and large diagonal vessels. The distal LAD artery provides the apical blood supply in two thirds of patients, with the distal right coronary artery (RCA) supplying the apex in the remaining one third.

Figure 2-5 Representation of coronary anatomy relative to the interventricular and atrioventricular valve planes. RAO = right anterior oblique; LAO = left anterior oblique. 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; RV = right ventricle; AcM = acute marginal; PD = posterior descending; PL = posterolateral left ventricular.

Rights were not granted to include this figure in electronic media. Please refer to the printed book.

(From Baim DS, Grossman W: Coronary angiography. In Grossman W, Baim DS [eds]: Cardiac Catheterization, Angiography, and Intervention, 4th ed. Philadelphia, Lea & Febiger, 1991, p 200.)

The CX artery is located in the AV groove and is angiographically identified by its location next to the coronary sinus. The latter is seen as a large structure that opacifies during delayed venous filling after left coronary injections. Marginal branches arise from the CX artery and are the vessels in this coronary artery system that are usually bypassed. The CX artery in the AV groove is often not surgically approachable.

The dominance of a coronary system is defined by the origin of the posterior descending artery (PDA), which through septal perforators supplies the inferior one third of the ventricular septum. The origin of the AV nodal artery is often near the origin of the PDA. In 85% to 90% of patients, the PDA originates from the RCA. In the remaining 10% to 15% of patients, the CX artery gives rise to the PDA. Codominance, or a contribution from both the CX artery and RCA, can occur and is defined when septal perforators from both vessels arise and supply the posteroinferior aspect of the left ventricle. Surgical bypass of this region may be difficult when this anatomy exists.

Assessing the Degree of Stenosis

By convention, the severity of a coronary stenosis is quantified as percent diameter reduction. Multiple views of each vessel are recorded, and the worst narrowing is recorded and used to make clinical decisions. This diameter reduction correspondsto cross-sectional area reduction; a 50% and 75% diameter reduction results in a 75% and 90% cross-sectional area reduction, respectively. Using the reduction in diameter as a measure of lesion severity is difficult when diffuse CAD creates difficulty in defining “normal” coronary diameter. This is particularly true in insulin-dependent diabetic patients as well as in individuals with severe lipid disorders.

Coronary Collaterals

Common angiographically defined coronary collaterals are described in Table 2-5. Although present at birth, these vessels become functional and enlarge only if an area of myocardium becomes hypoperfused by the primary coronary supply. Angiographic identification of collateral circulation requires both the knowledge of potential collateral source as well as prolonged imaging to allow for coronary collateral opacification.

Table 2-5 Collateral Vessels

Left Anterior Descending Coronary Artery (LAD)

Right-to-Left

Conus to proximal LAD

Right ventricular branch to mid LAD

Posterior descending septal branches at mid vessel and apex

Left-to-Left

Septal to septal within LAD

Circumflex-OM to mid-distal LAD

Circumflex Artery (Cx)

Right-to-Left

Posterior descending artery to septal perforator

Posterior lateral branch to OM

Left-to-Left

Cx to Cx in AV groove (left atrial circumflex)

OM to OM

LAD to OM via septal perforators

Right Coronary (RCA)

Right-to-Right

Kugels—proximal RCA to AV nodal artery

RV branch to RV branch

RV branch to posterior descending

Conus to posterior lateral

Left-to-Right

Proximal mid and distal septal perforators from distal LAD OM to posterior lateral

OM to AV nodal

AV groove Cx to posterior lateral

AV = atrioventricular; OM = obtuse marginal; RV = right ventricular.

The increased flow from the collateral vessels may be sufficient to prevent ongoing ischemia. To recruit collateral vessels for an ischemic area, a stenosis in a main coronary or branch vessel must reduce the luminal diameter by 80% to 90%. Clinical studies suggest that collateral flow can double within 24 hours during an episode of acute ischemia. However, well-developed collateral vessels require time to develop and only these respond to nitroglycerin (NTG). The RCA is a better collateralized vessel than the left coronary artery. Areas that are supplied by good collateral vessels are less likely to be dyskinetic or akinetic.

INTERPRETING THE CATHETERIZATION REPORT

Information obtained in the cardiac catheterization laboratory is representative of the patient’s pathophysiologic process at only one point in time. Therefore, these data are static and not dynamic. In addition, alterations in fluid and medication management before catheterization can influence the results obtained. The hemodynamic information is usually obtained after the patient has fasted for 8 hours. Particularly in patients with dilated, poorly contractile hearts, the diminished filling pressures seen in the fasted state may lower the CO. In other circumstances fluid status will be altered in the opposite direction. Patients with known renal insufficiency are hydrated overnight before administration of a contrast agent. In these instances, the right- and left-sided heart hemodynamics may not reflect the patient’s usual status. Additionally, medications may be held before catheterization, particularly diuretics. Acute β-adrenergic blocker withdrawal can produce a rebound tachycardia, altering hemodynamics and potentially inducing ischemia. These should be noted in interpreting the catheterization data.

Sedation may falsely alter blood gas and hemodynamic measurements if hypoxia occurs. Patients with chronic lung disease may be particularly sensitive to sedatives, and respiratory depression may result in hypercapnia and hypoxia. Careful notations in the catheterization report must be made of medications administered as well as the patient’s symptoms. Ischemic events during catheterization may dramatically affect hemodynamic data. Additionally, therapy for ischemia (e.g., NTG) may affect both angiographic and hemodynamic results.

Technical factors may influence coronary arteriography and ventriculography. The table in the catheterization laboratory may not hold very heavy patients. Patient size may limit x-ray tissue penetration and adequate visualization and may prevent proper angulations. Stenosis at vessel bifurcations may not be identified in the hypertensive patient with tortuous vessels. Catheter-induced coronary spasm, most commonly seen proximally in the RCA, must be recognized, treated with NTG, and not reported as a fixed stenosis. Myocardial bridging results in a dynamic stenosis seen most commonly in the mid-LAD artery during systole. This is seldom of clinical significance and should not be confused with a fixed stenosis present throughout the cardiac cycle. With ventriculography, frequent ventricular ectopy or catheter placement in the mitral apparatus may result in nonpathologic (artificial) MR. This must be recognized to avoid inappropriate therapy.

Finally, catheterization reports are often unique to institutions and are often purely computer generated, including valve area calculations. Familiarity with the catheterization report at each institution and discussions with cardiologists are essential to allow for a thorough understanding of the information and its location in the report and the potential limitations inherent in any reporting process.

INTERVENTIONAL CARDIOLOGY: PERCUTANEOUS CORONARY INTERVENTION

This section is designed to present the current practice of interventional cardiology (Box 2-5). Although begun by Andreas Gruentzig in September 1977 as percutaneous transluminal coronary angioplasty (PTCA), catheter-based interventions have dramatically expanded beyond the balloon to include a variety of percutaneous coronary interventions (PCIs). Worldwide, this field has expanded to include approximately 900,000 PCI procedures annually.

BOX 2-5 Interventional Cardiology–Timeline

1977	Percutaneous transluminal coronary angioplasty
1991	Directional atherectomy
1993	Rotational atherectomy
1994	Stents with extensive antithrombotic regimen
1995	Abciximab approved
1996	Simplified antiplatelet regimen after stenting
2001	Distal protection
2003	Drug-eluting stents

The interventional cardiology section is divided in two subsections. The first subsection consists of a general discussion of issues that relate to all catheter-basedinterventions. This includes a general discussion of indications, operator experience, equipment and procedures, restenosis, and complications. Anticoagulation and controversial issues in interventional cardiology are also reviewed. The second subsection is devoted to a discussion of the various catheter-based systems for PCI. Beginning with the first, PTCA, most devices are presented, including current technology and devices in development. With this review, the cardiac anesthesiologist may better understand the current practice and future direction of interventional cardiology.

General Topics for All Interventional Devices

Indications

Box 2-6 provides a summary of current clinical indications for PCI. Although initially reserved only for patients who were also suitable candidates for CABG, PCI is routinely performed in patients who are not candidates for CABG. In considering both the indications as well as the appropriateness of PCI, the physician must review the patient’s historical presentation, including functional class, treadmill results with or without perfusion data, and wall motion assessment.

BOX 2-6 Clinical Indications for Percutaneous Coronary Interventional Procedures

Cardiac Symptoms

• Unstable angina pectoris/non−ST-segment myocardial infarction

• Angina refractory to antianginal medications

• Post−myocardial infarction angina

• Sudden cardiac death

Diagnostic Testing

• Early positive exercise tolerance testing

• Positive exercise tolerance test despite maximal antianginal therapy

• Large areas of ischemic myocardium on perfusion or wall motion studies

• Positive preoperative dipyridamole or adenosine perfusion study

• Electrophysiologic studies suggestive of arrhythmia related to ischemia

Equipment and Procedure

Significant advances have been and will continue to be made with all aspects of PCI. Although the femoral artery is still the most commonly utilized access site, the radial artery is utilized more frequently for coronary interventions. Despite numerous advances, all percutaneous coronary interventions still involve sequential placement of the following: guide catheter in the ostium of the vessel, guidewire across the lesion and in the distal vessel, and device(s) of choice at the lesion site.

Guide catheters are available in multiple shapes and sizes for coronary and graft access, device support, and radial artery entry. Guidewires offer more flexible tips for placement in tortuous vessels as well as stiffer shafts to allow for the support of the newer devices during passage within the vessel. Separate guidewire placement within branch vessels may be required for coronary lesions at vessel bifurcations (Fig. 2-6). In selecting the appropriate device for the lesion, quantitative angiography and/or intravascular ultrasound (IVUS) may be used to determine the size of the vessel and composition of the lesion.

Figure 2-6 Complex coronary angioplasty. A, Lesion in the left anterior descending (LAD) artery at its bifurcation as well as a severe ostial diagonal stenosis. B, “Kissing balloon” inflation performed simultaneously within both the deployed LAD and diagonal stents. C, After dilation with patent LAD artery and diagonal branch.

Restenosis

Once PTCA/PCI became an established therapeutic option for treating patients with CAD, it was soon realized that there were two major limitations: acute closure and restenosis. Stents and antiplatelet therapy significantly decreased the incidence ofacute closure. Before stents were available, restenosis occurred in 30% to 40% of PTCA procedures. With stent use, this figure decreased to about 20%. Thus, restenosis remained the Achilles heel of intracoronary intervention until the current drug-eluting stent era.

Restenosis usually occurs within the first 6 months after an intervention and has three major mechanisms: vessel recoil, negative remodeling, and neointimal hyperplasia. Vessel recoil is caused by the elastic tissue in the vessel and occurs early after balloon dilation. It is no longer a significant contributor to restenosis because metal stents are nearly 100% effective in preventing any recoil. Negative remodeling refers to late narrowing of the external elastic lamina and adjacent tissue. This accounted for up to 75% of lumen loss in the past. This process is also prevented by metal stents and no longer contributes to restenosis. Neointimal hyperplasia is the major component of in-stent restenosis. Neointimal hyperplasia is exuberant in the diabetic patient, and this serves to explain the increased incidence of restenosis in this population.

The major gains in combating restenosis have been in the area of stenting. Intracoronary stents maximize the increase in lumen area during the PCI procedure and decrease late lumen loss by preventing recoil and negative remodeling. However, neointimal hyperplasia is enhanced owing to a “foreign body–like reaction” to the stents. Different stent designs as well as varying strut thickness lead to different restenosis rates. Systemic administration of antiproliferate drugs decreases restenosis but causes significant systemic side effects. Drug-eluting stents, with a polymer utilized to attach the antiproliferative drug to the stent, have shown the best results to date for decreasing restenosis.²

Anticoagulation

Thrombosis is a major component in acute coronary syndromes as well as acute complications during PCI; its management is in constant evolution (Box 2-7). During interventional procedures, the guide catheter, guidewire, and device in the coronary artery serve as nidi for thrombus. Additionally, most catheter interventions disrupt the vessel wall, exposing thrombogenic substances to blood. Table 2-6 summarizes the current anticoagulation agents utilized in the setting of PCI.

Table 2-6 Anticoagulation in Interventional Cardiology

Outcomes: Success and Complications

In the 20 years of catheter-based interventional procedures, the marked improvement in success rates with simultaneous decreases in adverse events clearly reflects both the significant technologic advancement as well as increased operator experience. PCI was once considered successful with the luminal narrowing reduced to less than 50% residual stenosis. In current practice with stent placement, seldom is a residual stenosis greater than 20% accepted, and excellent stent expansion without edge dissection is required before termination of the procedure. The initial National Heart, Lung, and Blood Institute (NHLBI) PTCA registry from 1979 to 1983 reported a success rate of 61% and a major coronary event rate of 13.6%. The 1985 to 1986 NHLBI registry reported a success rate of 78%, with the incidence of acute myocardial infarction as 4.3% and the emergency CABG rate as 3.4%. In the stent era, success rates are over 90% and emergent surgery rates less than 1% in laboratories performing more than 400 PCIs.³

Operating Room Backup

When PTCA was introduced, all patients were considered candidates for CABG. The physicians’ learning curve in the early 1980s was considered 25 to 50 cases; increased complications were seen during these initial cases. All PCI procedures had immediate operating room availability, with the anesthesiologist often in the catheterization laboratory. In the 1990s, operating room backup was needed less often. Perfusioncatheter technology developed to allow for longer inflation times with less ischemia. The role for perfusion balloons and operating room backup has diminished with the use of stents. With the current low incidence of emergent CABG, few institutions maintain a cardiac room on standby for routine coronary interventions.

Infrequently, high-risk interventional cases may still require a cardiac room on immediate standby. Preoperative anesthetic evaluation, which allows for preoperative assessment of the overall medical condition, past anesthetic history, current drug therapy, allergic history, and a physical examination concentrating on airway management considerations, is reserved for these high-risk cases.

As a less stringent policy for operating room backup is required, PCI procedures are now performed in hospitals with no in-house cardiac surgery, although this is not standard practice and remains controversial. Regardless of the location of the interventional procedure, when an emergency CABG is required, it is important to provide enough “lead” time to adequately prepare an operating room. Additionally, because this happens infrequently, cooperation among the interventionalist, surgeon, and anesthesiologist is essential for optimal patient care in this critically ill population.

General Management for Failed Percutaneous Coronary Intervention

Several possible scenarios may result from a failed PCI (Box 2-8). First, the interventional procedure may not successfully open the vessel but no coronary injury has occurred; the patient often remains in the hospital until a CABG can be scheduled. The second type of patient has a patent vessel with an unstable lesion. This most often occurs when a dissection cannot be contained by stents but the vessel remains open. The third patient type has an occluded coronary vessel after a failed PCI with stenting either not an option or unsuccessful. In this instance, myocardial ischemia/infarction ensues dependent on the degree of collateralization. This patient most commonly requires emergent surgical intervention.

In preparation for the operating room, a perfusion catheter, intra-aortic balloon pump, pacemaker, and/or PA catheter may be inserted dependent on patient stability, operating room availability, and patient assessment by the cardiologist, cardiothoracic surgeon, and anesthesiologist. Although designed to better stabilize the patient, these procedures are at the expense of ischemic time. Once in the operating room, decisions on the placement of catheters for monitoring should take several details into consideration. If perfusion has been reestablished, and the degree of coronary insufficiency is mild (no ECG changes, absence of angina), time can be taken to place an arterial catheter and a PA catheter. It must be remembered, however, that these patients have usually received significant anticoagulation with heparin and often glycoprotein IIb/IIIa platelet receptor inhibitors; attempts at catheter placement should not be undertaken when direct pressure cannot be applied to a vessel. The most experienced individual should perform these procedures.

The worst scenario is the patient who arrives in the operating room in either profound circulatory shock or full cardiopulmonary arrest. In these patients, cardiopulmonary bypass (CPB) should be established as quickly as possible. No attempt should be made to establish access for monitoring that would delay the start of surgery. The only real requirement to start a case such as this is to have good intravenous access, a five-lead ECG, airway control, a functioning blood pressure cuff, and arterial access from the PCI procedure.

In many cases of emergency surgery, the cardiologist has placed femoral artery sheaths for access during the PCI. These should not be removed, again because of heparin, and possibly glycoprotein IIb/IIIa inhibitor therapy during the PCI. A femoral artery sheath will provide extremely accurate pressures, which closely reflect central aortic pressure. Also, a PA catheter may have been placed in the catheterization laboratory, and this can be adapted for use in the operating room.

Several surgical series have looked for associations with mortality in patients who present for emergency CABG after failed PCI. The presence of complete occlusion, urgent PCI, and multivessel disease has been associated with an increased mortality.

In addition, long delays due to not having a rapid surgical alternative will lead to increases in morbidity and mortality. The paradigm shift in cardiovascular medicine toward PCIs and away from surgery will be slowed if significant numbers of serious complications occur due to prolonged delays in moving the patient to surgery.^4,⁵

Controversies in Interventional Cardiology

Therapy for Acute Myocardial Infarction: Primary Percutaneous Coronary Intervention Versus Thrombolysis

Thrombolytic therapywas introduced for patients with acute myocardial infarction in the 1970s (Box 2-9). The decades of the 1980s and 1990s have seen extensive multicenter trials comparing the benefits of (1) thrombolytic therapy versus no thrombolytic therapy, (2) one thrombolytic agent compared with another, (3) different adjunctive medications given with thrombolytic therapy (platelet glycoprotein inhibitors, LMWHs, direct thrombin inhibitors), and (4) thrombolytic therapy versus primary PCI (bringing the patient directly to the catheterization laboratory). Table 2-7 lists the currently available drugs used for thrombolytic therapy in patients with acute myocardial infarction.

Table 2-7 Current Thrombolytic Therapy

The recently published guidelines by the ACC/AHA on management of patients with ST-segment elevation myocardial infarction emphasize early reperfusion and discuss the choice between thrombolytic therapy and primary PCI.⁶ If a patient presents within 3 hours of symptom onset, the guidelines express no preference for either strategy with the following caveats: Primary PCI is preferred if (1) door-to-balloon time is less than 90 minutes and is performed by skilled personnel (operator annual volume > 75 cases with 11 primary PCI, and laboratory volume > 200 cases with 36 primary PCI); (2) thrombolytic therapy is contraindicated; and (3) the patient is in cardiogenic shock. Thrombolytic therapy should be considered if symptom onset is less than 3 hours and door to balloon time is more than 90 minutes. Patients older than age 75 years should be individually assessed, because they have a higher mortality from the myocardial infarction but a higher risk of complications, particularly intracranial bleeding, with thrombolytic therapy.

Therapy for acute myocardial infarction is evolving. With encouraging results from PCI in experienced hands when a facility is immediately available, more centers are considering acute primary PCI as standard of care, some in catheterization laboratories without operating room backup.⁷ Many patients present late or undergo thrombolytic therapy. If such patients are hemodynamically or electrically unstable, or if they have recurrent symptoms, a consensus would favor catheterization and revascularization. If such patients are stable, their management is controversial, although many cardiologists in the United States would recommend catheterization and revascularization.

PCI VERSUS CABG

The choice of therapy for multivessel CAD must be made by comparing PCI with CABG. In the mid 1980s, when PCI consisted only of balloon PTCA, the first comparisons of catheter intervention to CABG were begun. By the early to mid 1990s, nine randomized clinical trials had been published comparing PTCA with CABG in patients with significant CAD. Only the Bypass Angioplasty RevascularizationInvestigation (BARI) trial was statistically appropriate for assessing mortality. These results are summarized in Figure 2-7. The conclusions of these studies included similarities between the two approaches with respect to relief of angina and 5-year mortality. Costs were initially lower in the PCI group, but by 5 years they had converged because of repeat PCI procedures precipitated by restenosis, which occurred in 20% to 40% of the PCI group.⁸

Figure 2-7 Randomized trials of coronary artery bypass graft surgery (CABG) versus percutaneous transluminal coronary angioplasty (PTCA) in patients with multivessel coronary disease showing risk difference for all-cause mortality for years 1, 3, 5, and 8 after initial revascularization. A, All trials. B, Multivessel trials.

(Redrawn from Hoffman SN, TenBrook JA, Wolf MP, et al: A meta-analysis of randomized controlled trials comparing coronary artery bypass graft with percutaneous transluminal coronary angioplasty: One- to eight-year outcomes. J Am Coll Cardiol 41:1293, 2003. Copyright 2003, with permission from The American College of Cardiology Foundation.)

The only clear difference between PCI and CABG for patients with multivessel disease was identified in the diabetic patient subset of the BARI trial. A difference in mortality was seen in a subgroup analysis of the BARI trial in which both insulin-dependent and non−insulin-dependent diabetic patients with multivessel disease had a lower 5-year mortality with CABG (19.4%) than with PCI (34.5%).

Regretfully, these trials were outdated by the time of their publication. For the patient undergoing PCI, stents had become the norm with a significant decrease in emergent CABG, due to reduced acute closure, as well as a decrease in repeat procedures, due to less restenosis. For the patient undergoing CABG, off-pump bypass (OPCAB) became more common during this time period with its potential to decrease complications. Additionally, the importance of arterial grafting with its favorable impact on long-term graft patency was recognized.

To address the changes in PCI and CABG therapy, four more randomized trials were undertaken, and these are included in Figure 2-7. The results of these newer studies were similar to the results of the earlier ones. In the arterial revascularization therapy study (ARTS) trial, diabetic patients had poorer outcomes with PCI. Repeat procedures, although higher in the PCI group at 20%, were significantly lower than with the earlier trials. CABG patients also had improved outcomes; for instance, cognitive impairment occurred in fewer patients in the recent studies. A meta-analysis of all 13 randomized trials identified a 1.9% absolute survival advantage at 5 years in the CABG patients, but no significant difference at 1, 3, or 8 years.⁹ As with the first generation of PCI versus CABG trials, the second-generation trials were outdated before publication due to the advent of the drug-eluting stents. The ARTS II and BARI II trials are now in progress and will address this issue.

Other contentious issues exist in the management of CAD. The roles of staged PCI procedures in patients with multivessel disease, ad hoc PCI, and combination procedures [left internal mammary artery (LIMA) to LAD and PCI of other vessels] have generated debate within the interventional and surgical communities.

In conclusion, the physician must weigh the data and explain the advantages and disadvantages of both techniques to each patient. CABG offers a more complete revascularization with survival advantages in selective groups and a decreased need for repeat procedures. The disadvantages of a CABG are the higher early risk, longer hospitalization and recovery, initial expense, increased difficulty of second procedures, morbidity associated with leg incisions, and limited durability of venous grafts. The current high cost of drug-eluting stents will negate the initial cost advantage of PCI if multiple stents are used. From the perspective of a hospital administrator in the United States, current reimbursement policies favor CABG over the placement of multiple drug-eluting stents.¹⁰

SPECIFIC INTERVENTIONAL DEVICES

Interventional Diagnostic Devices

Three intravascular diagnostic tools for the interventionalist are currently available. Angioscopy, the least applied of the three, offers the most accurate assessment of intravascular thrombus. Cineangiography and IVUS are often inadequate for visualization of thrombus. Although useful as an investigative technique, angioscopy has not entered into routine interventional practice.

IVUS is the only method by which the vessel wall of the coronary artery can be visualized in vivo. A miniature transducer mounted on the tip of a 3-Fr catheter is advanced over the standard guidewire into the coronary artery. The IVUS transducer is about 1 mm in diameter with frequencies of about 30 MHz. These high frequencies allow for excellent resolution of the vessel wall. By comparison, contrast angiography images only the lumen, with the status of the vessel wall inferred from the image of the lumen.¹¹ IVUS is useful in evaluating equivocal left main lesions, ostial stenoses, and vessels overlapping angiographically (Fig. 2-8). IVUS is superior to angiography in the early detection of the diffuse, immune-mediated arteriopathy of cardiac transplant allografts.

Figure 2-8 A, Diagnostic angiography reveals a borderline occlusive lesion of 50% stenosis (by diameter) in the distal left main artery. B, Intravascular ultrasound reveals an eccentric plaque to the left of the ultrasonographic catheter (central lucency) that is nonocclusive by both diameter and cross-sectional area.

Atherectomy Devices: Directional and Rotational

Atherectomy devices are designed to remove some amount of plaque or other material from an atherosclerotic vessel. Of these devices, directional coronary atherectomy (DCA; Guidant Corporation, Indianapolis, IN) became the first nonballoontechnology to gain U.S. Food and Drug Administration (FDA) approval, in 1991. DCA removes tissue from the coronary artery, thus “debulking” the area of stenosis utilizing a low-pressure balloon located on one side of the metal housing, which, when inflated, forces tissue into an elliptical opening on the opposite side of the housing. A cylindrical cutting blade shaves the tissue and stores it in the distal nose cone of the device. Although tissue removal is an attractive concept, application of DCA was limited by the need for large (9.5 to 11 Fr) guiding catheters with early devices. Trials comparing DCA with PTCA did not show improved angiographic restenosis rates, and higher rates of acute complications were seen with DCA. Newer iterations of the device can be used with smaller (7 to 8 Fr) guide catheters. DCA is used infrequently in most institutions because its clinical benefit is inconclusive.¹²

The FDA approved rotational coronary atherectomy in 1993. The Rotablator catheter (Boston Scientific Corp, Natick, MA) is designed to differentially remove nonelastic tissue, utilizing a diamond-studded bur rotating at 140,000 to 170,000 rpm. Designed to alter lesion compliance, particularly in heavily calcified vessels, rotational atherectomy is often used before balloon dilation to permit full expansion of the vessel. The ablated material is emulsified into 5-μm particles, which pass through the distal capillary bed. Heavily calcified lesions are commonly chosen for rotational atherectomy.

Intracoronary Laser

Excimer laser coronary angioplasty (ELCA) (Spectranetics, Colorado Springs, CO) uses xenon chloride (XeCl) and operates in the ultraviolet range (308 nm) to photochemically ablate tissue. Currently, ELCA is indicated for use in lesions that are long (>2 mm in length), ostial, in saphenous vein bypass grafts, and unresponsive to PTCA. With the development of the eccentric directional laser, treatment of eccentric or bifurcation lesions can be approached with increased success. Also, in-stent restenosis can be effectively treated with the excimer laser.¹³ The Prima FX laser wire (Spectranetics, Colorado Springs, CO) is a 0.018-inch wire with the ability to deliver excimer laser energy to areas of chronic, total occlusion. With conventional equipment, failure to cross such lesions with a guidewire is frequent. The Prima FX has CE mark approval in Europe but is investigational in the United States. The optimal wavelength for the treatment of coronary atheroma has yet to be determined.

Intracoronary Stent

The term stent was used first in reference to a dental mold developed by an English dentist, Charles Thomas Stent, in the mid-19th century. The word evolved to describe various supportive devices used in medicine. To date, the introduction of intracoronary stents has had a larger impact on the practice of interventional cardiology than any other development.

The use of intracoronary stents exploded during the mid 1990s (Box 2-10). Receiving FDA approval in April 1993, the Gianturco-Roubin (Cook Flex stent), a coiled balloon-expandable stent was approved for the treatment of acute closure after PCI. Use of the Gianturco-Roubin stent was limited by difficulties with its delivery and high rates of restenosis. The first stent to receive widespread clinical application was the Palmaz-Schatz (Johnson and Johnson, New Brunswick, NJ) tubular slotted stent approved for the treatment of de novo coronary stenosis in 1994. Throughout the 1990s, multiple stents were introduced with improved support and flexibility and thinner struts, resulting in improved delivery and decreased restenosis rates.