Cardiac Testing

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Chapter 5 Cardiac Testing

Patients presenting for heart surgery have usually undergone a number of cardiac investigations preoperatively. In this chapter, the indications, principles, and interpretations of common preoperative cardiac investigations are discussed. Chest radiography and echocardiography are discussed in Chapters 6 and Chapter 7, respectively.

ANGIOGRAPHY OF THE CORONARY ARTERIES AND LEFT VENTRICLE

Coronary angiography is the standard method of assessing the anatomy of the coronary circulation and the location and extent of coronary artery stenoses. The major indications for coronary angiography are angina symptoms and a positive stress test, an acute coronary syndrome, and patients at risk for coronary artery disease undergoing other cardiac surgery. A left ventriculogram and measurements of left ventricular and aortic pressures are often obtained at the same time as the coronary angiogram.

The complex and overlapping nature of the coronary anatomy necessitates image acquisition from a variety of angles to ensure complete visualization. The relationship between the patient, the x-ray tube, and the image intensifier during coronary angiography is shown in Figure 5-1. Images of normal coronary arteries obtained from some of the standard angiographic projections are shown in Figures 5-2 and 5-3.

Coronary Anatomy

The anatomy of the coronary circulation varies among individuals but most patients have similar distributions of the major epicardial vessels. The left main-stem coronary artery arises from the left coronary sinus and divides after a short distance into the left anterior descending (LAD) and the left circumflex coronary arteries. Occasionally, the circumflex coronary artery arises directly from the right coronary sinus, adjacent to the right coronary artery (RCA). The LAD coronary artery (see Fig. 5-2) runs along the surface of the interventricular septum, passing anteriorly, inferiorly, and to the left in the anterior interventricular groove. It usually terminates a short distance beyond the apex, having turned onto the inferior surface of the heart in the posterior interventricular groove. The LAD coronary artery gives rise to septal branches that pass into the substance of the anterior interventricular septum, supplying the majority of this structure. The LAD coronary artery also gives rise to branches to the anterior (or diagonal) surface of the left ventricle, known as diagonal branches (see Fig. 5-2A, 5-2F). The number, size, and point of origin from the LAD coronary artery of the septal and diagonal branches are highly variable.

The circumflex coronary artery passes to the left and inferiorly in the left atrioventricular groove, usually terminating close to the junction of the lateral and the inferior surfaces of the left ventricle. The circumflex artery gives rise to a series of branches to the lateral surface of the left ventricle known as obtuse marginal (OM) branches (see Fig. 5-2 B, 5-2C, 5-2E). The number, size, and point of origin of the OM vessels vary greatly. A large branch, known as the intermediate coronary artery (see Fig. 5-2 B, 5-2C, 5-2D), may arise directly from the left main bifurcation or from the very proximal course of either the LAD or circumflex arteries to supply a portion of the diagonal (anterior) and OM (lateral) surfaces of the heart. Intermediate arteries can supply a substantial amount of the left ventricle and may be much larger than the circumflex artery.

The RCA (see Fig. 5-3) arises from the right coronary sinus and passes inferiorly and to the right in the right atrioventricular groove before passing around the acute margin onto the inferior surface of the heart to reach the crux, the point at which the atrioventricular and interventricular grooves meet. The major branch to the posterior septum is the posterior descending coronary artery (PDA) (Fig. 5-3 A). The PDA normally arises from the RCA proximal to or at the crux, and passes anteriorly in the posterior interventricular groove, giving off a number of septal branches that enter the posterior portion of the interventricular septum. In some individuals, the RCA is so small it supplies none of the left ventricle, and the PDA arises from the circumflex coronary artery. The origin of the PDA determines the dominance of the coronary circulation. In more than 90% of the population the PDA arises from the RCA (right dominance); in about 6% of the population the PDA arises from the circumflex coronary artery (left dominance); and in less than 2% of individuals the supply to the posterior septum is shared (indeterminate dominance). Distal to the crux, the RCA continues along the posterior atrioventricular groove and gives rise to a number of branches which pass anteriorly on to the inferior surface of the left ventricle. The supply to the sinoatrial node arises from the proximal RCA. The supply to the atrioventricular node is a small artery that arises in the region of the crux, usually from the RCA.

The coronary arteries are epicardial vessels lying on the surface of the heart, but it is possible for segments of a coronary artery to lie within the substance of the myocardium. This situation may be recognized at the time of angiography by the presence of a dynamic coronary stenosis during ventricular systole. Intramyocardial coronary segments are particularly likely in patients with hypertrophic cardiomyopathy and can create difficulties for the surgeon in performing distal coronary anastomoses.

Coronary Stenoses

The severity of a stenosis in a coronary artery is usually expressed as a percentage reduction in diameter. Many stenoses are eccentric, and the apparent degree of stenosis varies with the angle from which the vessel is visualized. In this situation, the most severe apparent reduction in diameter is used. A diameter reduction of 50% represents a reduction in cross-sectional area of 75%, which is the degree of stenosis at which distal coronary flow is reduced on exertion. A diameter reduction of 75% represents an area reduction of 90%, which is the degree of stenosis at which distal flow is reduced at rest. With a diameter loss of 90%, antegrade flow beyond the stenosis is insufficient to fill the vessel. However, the distal vessel may still fill via flow from collaterals arising from other coronary branches.

Stenoses due to chronic atherosclerotic disease cause angina and exercise-induced myocardial ischemia. In contrast, unstable angina or acute coronary syndromes are usually associated with thrombus formation on a ruptured plaque, which prior to thrombus formation may have been causing only minor narrowing. Patients with acute coronary syndrome should have urgent coronary angiography with a view to revascularization. However, if a thrombolytic drug such as streptokinase has been administered, the thrombus may have resolved by the time of angiography.

The presence of significant stenosis (>50%) of the left main stem coronary artery (Fig. 5-4) or of severe disease in the proximal course of both LAD and circumflex coronary arteries (left main equivalent disease) represents a situation of special concern because of the large proportion of the left ventricular myocardium whose vascular supply is in jeopardy. This is particularly the case in patients with left-dominant circulations. Urgent revascularization is indicated. Patients with severe stenoses of the proximal LAD coronary artery (Fig. 5-5) or extensive coronary artery disease (Fig. 5-6) also have a survival benefit from revascularization (Chapter 9).

Left Ventriculography and Pressure Recordings

A left ventriculogram (Fig. 5-7) is commonly performed at the time of coronary angiography. Left ventriculography allows measurement of ventricular volumes and ejection fraction (Table 5-1) and provides some assessment of regional wall motion. The degree of mitral regurgitation, if any, may also be assessed. Care should be taken in the interpretation of measurements made of postectopic beats, as the measured ejection fraction will be greater than that obtained from a normal sinus beat (due to increased end-diastolic and reduced end-systolic volumes). The left ventriculogram is often omitted in patients with diabetes or left main-stem disease in order to reduce the dose of radiographic contrast medium. Radiographic contrast medium is nephrotoxic, especially in diabetics, and also has vasodilator and myocardial depressant effects, which may critically reduce myocardial perfusion in patients with left main-stem disease.

Table 5-1 Normal Values for Left Ventricular Volumes and Ejection Fraction

End-diastolic volume index < 90 ml/m2
End-systolic volume index < 30 ml/m2
Ejection fraction 55% to 75%

A left ventricular pressure trace is recorded prior to performing the ventriculogram. From this pressure recording, end-diastolic pressure (LVEDP) is obtained. An elevated LVEDP (>15 mmHg) in the presence of a high left ventricular end-diastolic volume (LVEDV) usually represents systolic dysfunction, whereas a raised LVEDP in the presence of a normal or low LVEDV represents diastolic dysfunction. An LVEDP greater than 30 mmHg is a sign of imminent left ventricular failure, and many operators desist from performing a left ventriculogram in this situation. The administration of radiographic contrast, either systemically or into the coronary arteries, may result in an acute increase in the end-diastolic pressure; this effect must be borne in mind when interpreting the LVEDP recordings.

A pressure recording is made across the aortic valve as the catheter is withdrawn after the left ventricular study to check for aortic valve stenosis. Comparison of angiographic and echocardiographic transvalvular pressure gradients may reveal surprising discrepancies for a variety of reasons. Aortic valve gradients obtained from echocardiography are instantaneous measurements, whereas those from a cardiac catheter study are peak-to-peak pressure measurements (Fig. 5-8). Underestimation of transvalvular gradients in echocardiography may occur if imaging windows are poor or if the Doppler signal has not been lined up accurately with the jet of stenotic flow. Cardiac output may appear to be different on the angiogram and the echocardiogram. Cardiac catheterization is typically performed under mild benzodiazepine sedation, which may result in reduced gradients.

RIGHT HEART CATHETERIZATION

Right heart catheterization is performed for the evaluation of right ventricular function, pulmonary vascular disease, and intracardiac shunting. Common clinical scenarios in which right heart catheterization is indicated include the assessment of pulmonary vascular resistance prior to heart transplantation (Chapter 14), in patients with suspected Eisenmenger syndrome (Chapter 15), and in the diagnosis of idiopathic (or primary) pulmonary hypertension. Patients with pulmonary hypertension secondary to valvular heart disease are usually assessed with echocardiography but may occasionally undergo right heart catheterization.

The procedure may be performed using a standard balloon-tipped flow-directed pulmonary artery catheter (Chapter 8) or a catheter without a balloon (e.g., a Cournand catheter). It is often carried out in conjunction with left heart catheterization. Measurements that may be made during a right heart catheter study include right atrial pressure, pulmonary arterial pressure, pulmonary artery wedge pressure, cardiac output, and oxygen saturations from the vena cavae, right atrium, and pulmonary artery. In most catheter laboratories, cardiac output is routinely measured by using the thermodilution technique (Chapter 8). If thermodilution is likely to be inaccurate (e.g., due to the presence of severe tricuspid regurgitation) the Fick method may be used (see Equation 1-15). The Fick method necessitates obtaining pulmonary arterial and systemic arterial oxygen saturations and measuring oxygen consumption. From the measured variables (cardiac output, pulmonary artery wedge pressure, mean pulmonary artery pressure), transpulmonary gradient (Chapter 24) and pulmonary vascular resistance are calculated (see Equation 1-6).

Pulmonary vascular resistance is measured in Wood units (mmHg min/l). A normal value is less than 2 Wood units. Alternatively, pulmonary vascular resistance is reported in units of dynes.sec.cm−5, which are obtained by multiplying Wood units by 80. A normal value is less than 160 dynes.sec.cm−5. Resistance measurements are indexed to body-surface area in children. In patients with raised pulmonary vascular resistance, pulmonary reactivity may be assessed with the administration of 100% oxygen, nebulized iloprost, inhaled nitric oxide, or intravenous sodium nitroprusside.

Right heart catheterization provides useful information about the extent of left-to-right shunting in patients with atrial septal defects (ASDs) and ventricular septal defects (VSDs). In a VSD, there will be a step-up in the oxygen saturation between the right atrium (SRAo2) and the pulmonary artery (SPAo2). However, this may not occur if there is significant tricuspid regurgitation due to the regurgitation of left-sided (oxygenated) blood into the right atrium. In an ASD, the SRAo2 and SPAo2 are usually similar (although with streaming and incomplete mixing in the atrium, this may not always be true), but there will be a step-up in oxygen saturation from the vena cavae (superior and inferior) to the pulmonary artery. The amount of shunting is usually expressed as the ratio of pulmonary to systemic blood flow (Qp/Qs) and can be estimated from the shunt equation:

(5-1) image

where Sao2 = systemic arterial oxygen saturation, Svo2 = mixed venous oxygen saturation, and SPVo2 = pulmonary venous oxygen saturation.

In the presence of an intracardiac shunt, the term mixed venous saturation does not equate to pulmonary artery saturation as described elsewhere in the book, but is a measure of the average saturation of the systemic venous return. The saturation of the systemic venous return can be estimated from the weighted average of saturations from the superior (SSVCo2) and inferior vena cavae (SIVCo2):

(5-2) image

For left-to-right shunts, SPVo2 can be assumed to be the same as Sao2. However, for right-to-left shunting with systemic hypoxemia, Sao2 will be much less than SPVo2; therefore, this assumption is not true. For right-to-left shunting, SPVo2 is assumed to be 100%, provided pulmonary function is normal, or it can be measured directly by pulmonary venous sampling.

By way of example: if a patient with an ASD has an SSVCo2 of 60%, an SIVCo2 of 65%, an Sao2 of 98%, and an SPAo2 of 80% then, as a general rule, closure of a defect is indicated if the Qp/Qs is greater than 2 and is not indicated if the Qp/Qs is less than 1.5.

(5-3) image

ISCHEMIA AND VIABILITY TESTING

The identification of inducible ischemia and myocardial viability in patients with known or suspected coronary artery disease has important treatment and prognostic implications (Chapter 9). The presence of inducible ischemia on stress testing is an important criterion for proceeding to coronary angiography and subsequent percutaneous or surgical revascularization. The term viable myocardium refers to dysfunctional cardiac muscle that has the potential for partial or complete recovery of function following revascularization. Viable myocardium is composed of ischemic, stunned, or hibernating myocardium (Chapter 1) and must be distinguished from infarction. In patients with coronary artery disease and impaired ventricular function, the presence of viable, as opposed to infarcted, myocardium is associated with improved outcome following surgical revascularization.1 Therefore, viability testing is an important part of the preoperative evaluation of these patients (Chapter 9).

The first-line investigation to establish the presence of coronary artery disease and inducible myocardial ischemia remains the exercise electrocardiogram (ECG). However, in certain situations, alternatives such as stress echocardiography, nuclear imaging, and magnetic resonance (MR) imaging are indicated. Tests of myocardial viability include stress echocardiography, nuclear imaging, MR imaging, and positron emission tomography (PET). Each method has its advantages and disadvantages, but the choice of technique is largely dependent on institutional practice.

Protocols

A number of exercise modalities and protocols are in use, but the most common remains treadmill exercise using the original or a modified version of the Bruce protocol (Table 5-2). The original Bruce protocol consists of 3-minute stages of increasing speed and elevation.3 The Naughton and Cornell protocols are modifications of the Bruce protocol designed for elderly or deconditioned patients, in which each standard stage is divided into 2-minute half-stages.4 The exercise target is to achieve 85% or more than a patient’s maximum predicted heart rate and a double product greater than 25,000. Maximal predicted heart rate is calculated by subtracting the patient’s age from 220; double product is the peak heart rate multiplied by peak systolic blood pressure. The exercise protocol should be individualized to allow a test duration of at least 8 to 12 minutes.5,6 A 12-lead ECG is recorded at baseline and each minute during exercise, at peak exercise, and every minute during the recovery period. Blood pressure and heart rate are recorded serially, and symptoms are assessed continuously throughout the study.

Risks and Contraindications

Although the risks involved in exercise testing in appropriately selected patients are extremely low, there is a risk for death and major morbid events of 0.5 of 10,000 and 6 to 8 of 10,000, respectively.7 Thus, emergency resuscitation equipment must be always be available. Absolute contraindications to exercise testing include myocardial infarction within the previous 2 days, unstable angina, uncontrolled cardiac arrhythmias, severe symptomatic aortic stenosis, symptomatic heart failure, and severe hypertension. Exercise testing may be performed with caution in patients with severe aortic stenosis but must be supervised by an experienced clinician.

The test should be terminated if a patient develops progressive angina, signs of poor perfusion, non-sustained ventricular tachycardia, ST-segment elevation greater than or equal to 1 mm in leads without diagnostic Q-waves (other than V1 or aVR), or a fall in blood pressure of more than 10 mmHg compared to baseline in association with other signs of ischemia (more than 2 mm ST depression, arrhythmias or heart block) or severe hypertension.

Interpretation

A number of variables are assessed as part of an exercise test: heart rate and blood pressure responses, exercise duration and workload, symptoms, and ECG changes (ST-segment abnormalities and arrhythmias). The most widely used definition of a positive test is a greater than or equal to 1 mm of horizontal or downsloping STsegment depression (or elevation in leads without Q waves) 60 to 80 ms following the J point (see Fig. 8-4). Upsloping ST depression is considered borderline or negative.8 The pooled sensitivity and specificity of ST-segment depression for the identification of significant coronary artery disease, confirmed with coronary angiography, is 68% and 77%, respectively, although there is a wide variability among reported studies.9 The likelihood that ST segment depression represents important coronary artery disease is greatest when the magnitude of the depression is more than 2 mm, the ST depression occurs early in the test (stages 1 through 3), and the ST segment depression is associated with hypotension. ST-segment elevation in leads with Q waves is of uncertain clinical significance. However, ST elevation in leads without Q waves usually represents transmural ischemia and, in contrast to ST-segment depression, localizes the ischemia.

Stress Echocardiography

Stress echocardiography is indicated for myocardial viability testing and as an alternative to the exercise ECG for the diagnosis of inducible ischemia. The technique involves the assessment of systolic wall motion at rest and with progressive stress.

Protocols

Stress may be induced with exercise, using a treadmill or bicycle, or pharmacologically. For treadmill exercise, a standard or modified Bruce protocol is commonly used. For patients who cannot exercise, pharmacologic stress, usually with dobutamine, is indicated. Other pharmacologic stressors include dipyridamole and adenosine.

Dobutamine stress protocols vary, depending on the institution and on the purpose of the investigation. A low-dose dobutamine protocol may be used to assess viability, or a full stress protocol may be utilized to assess both viability and inducible ischemia. For a typical full-stress protocol, dobutamine is commenced at 5 μg/kg/min and increased every 3 minutes to 10, 20, 30, 40, and 50 μg/kg/min. If the goal heart rate is not achieved, atropine may also be administered. The stress targets are similar to those for the exercise ECG, including achieving a heart rate of greater than or equal to 85% of the predicted maximum for the patient’s age.

At each dobutamine dose, standard parasternal and apical echocardiographic images (see Fig. 7-4) and a 12-lead ECG are obtained. Wall motion is graded from normal to dyskinetic based on the degree of systolic thickening and wall movement. Using a standard model of the left ventricle (see Fig. 7-6), segmental wall motion abnormalities (SWMAs) are localized to specific myocardial segments. Images are recorded in digital cine loop format with side-by-side display to enable assessment of wall motion at various heart rates. Assessment of SWMAs is typically qualitative (i.e., a visual assessment of wall motion) but quantitative techniques, including measurement of myocardial tissue velocity, are being progressively refined.11

Interpretation

The normal cardiac response to stress is a reduction in left ventricular size and an increase in systolic wall motion. Abnormal responses are summarized in Table 5-3. In patients with inducible ischemia, wall motion is typically normal at rest, augments with low-dose dobutamine, and develops an SWMA at higher doses of dobutamine. Analysis of inducible ischemia can be difficult in patients with resting SWMAs and left ventricular dysfunction. Features on stress echocardiography that are predictive of adverse ischemic events include multiple resting SWMAs, reduced poststress ejection fraction, and extensive poststress SWMAs.12,13

A resting SWMA may be due to infarcted or viable myocardium (see earlier material and Chapter 1). Wall thinning and dyskinesis are suggestive of infarcted rather than viable myocardium. An SWMA due to myocardial stunning typically augments with low-dose dobutamine, but at high doses the response is variable. The typical response of hibernating myocardium is an improvement in the SWMA with low-dose dobutamine and deterioration at higher doses (biphasic response), but other responses also occur. A progressive deterioration of wall motion with increasing stress is consistent with ischemic, stunned, or hibernating myocardium.

The biphasic response is the most predictive of contractile recovery following revascularization.14,15 However, patients with viable myocardium, but greatly increased ventricular volumes, have a lower likelihood of recovery compared to patients with smaller ventricular volumes.16 A lack of augmentation in wall motion with dobutamine in the first few days following myocardial infarction implies the presence of infarcted rather than stunned myocardium and identifies patients at increased risk for ventricular remodeling (Chapter 1).17

For myocardial viability testing, dobutamine stress echocardiography has a slightly lower sensitivity and negative predictive value and a slightly higher specificity and positive predictive value compared with nuclear cardiac imaging.18 Based on postrevascularization improvement in function, pooled sensitivities and specificities for the identification of viability with dobutamine stress echocardiography are 74% and 80%, respectively.18

Nuclear Cardiac Imaging

Nuclear cardiac imaging provides information on myocardial perfusion and wall motion from which evidence for inducible ischemia and myocardial viability can be inferred.20,21 The indications are similar to those for stress echocardiography.

Nuclear cardiac imaging involves the use of a gamma-wave-emitting radioactive isotope, which is usually bound to a carrier molecule. The carrier molecule determines the distribution of the isotope in the body. Imaging is performed by a camera, which contains scintillation crystals that fluoresce when a gamma wave is absorbed by the crystal. Image acquisition is performed over several minutes, providing an averaged signal over a large number of heartbeats. For this reason, nuclear techniques are the preferred methods of perfusion and viability imaging in patients with atrial fibrillation. Scans are typically performed at rest and during stress.

Types of Perfusion Imaging

The original perfusion agent used was thallium 201 (201Tl). 201Tl acts as a potassium analog. It is rapidly taken up into actively metabolizing cardiac myocytes and therefore does not require a carrier molecule. Following injection, 201Tl is rapidly redistributed, so imaging must take place immediately after isotope injection. The initial imaging sequence is usually performed as part of a stress study, with resting images taken 2 to 4 hours later. Disadvantages of 201Tl include difficulties in camera scheduling, relatively high radiation doses, the long radioactive half-life of 201Tl, and gamma-wave emission energies that are relatively poor for imaging.

Because of the limitations of thallium scanning, most nuclear medicine departments now use technetium 99 (99Tc) for cardiac imaging. 99Tc must be bound to a carrier molecule, either tetrofosmin or, more commonly, sestamibi. Sestamibi binds irreversibly to myocyte mitochondria. Therefore, unlike 201Tl, isotope distribution on imaging performed some hours after isotope administration is determined by myocardial perfusion at the time of injection, not at the time of imaging. Stress and resting studies must therefore be performed 24 hours apart (four half-lives of the 99Tc isotope). Typically, the stress test is performed first, and the resting study is carried out only if the stress results are abnormal. A time delay of less than 24 hours between tests may be used if the rest dose of isotope is much larger than the stress dose.

Advantages of 99Tc over 201Tl include the lower dose of isotope required, a much shorter radioactive half-time, and a gamma energy emission profile ideal for imaging. The increased gamma-count of 99Tc allows for ECG-gated acquisition and the construction of ECG-gated single photon emission computed tomogram (SPECT) images. Each tomographic slice can be imaged at various points in the cardiac cycle, allowing for assessment of focal wall motion and ventricular function, in addition to standard perfusion imaging.

Interpretation

Normal myocardium demonstrates good isotope uptake on both stress and resting images. The patterns of tracer uptake with ischemic, viable, and infarcted myocardium are shown in Table 5-4. Ischemic myocardium has normal perfusion at rest but reduced perfusion during stress. A globally ischemic left ventricle may not demonstrate a focal perfusion defect during stress if perfusion to all myocardial segments is equally reduced. Ejection fraction will be reduced, and left ventricular diastolic volume will be increased. Mismatched perfusion defects that are present on stress imaging but not rest imaging represent areas of either inducible ischemia or hibernation. The two conditions can be difficult to distinguish on the basis of perfusion imaging alone, but they may be differentiated on the basis of differences in resting wall motion (Table 5-4).

Positron Emission Tomography

PET scanning, using fluorine 18 (18 Fl)-labeled fluorodeoxyglucose, can be used to assess cellular glucose utilization, which may then be compared with perfusion. Normal myocardium has normal perfusion and normal glucose uptake, whereas both are reduced in infarcted myocardium. Hibernating myocardium has reduced perfusion on stress, but normal glucose uptake. PET scanning is not widely available, and standardized metabolic conditions have to be present to achieve reproducible results; this can be difficult to achieve, especially in diabetics (see Table 5-4).

Cardiac Magnetic Resonance Imaging

Until recently the application of MR imaging to the heart has been used predominantly for congenital cardiac disease. MR imaging is now the definitive method of assessing left ventricular function,22 although in clinical practice, echocardiography and ventriculography are more commonly used. The advantages of MR imaging of ventricular function are the excellent signal contrast between myocardium and blood and the lack of restrictive imaging windows, allowing imaging of the entire epicardial and endocardial surfaces throughout the cardiac cycle. A three-dimensional reconstruction of the ventricle can be performed and assessed over time, allowing SWMAs to be measured objectively.

An emerging indication for MR imaging is in the assessment of myocardial perfusion and viability.23 Myocardial perfusion can be assessed with the use of gadolinium contrast media.24 There is avid first-pass uptake of gadolinium, which provides a measure of relative myocardial perfusion, either at rest or during the administration of a pharmacologic stressor, such as adenosine or dobutamine. Ischemia appears as subendocardial defects in myocardial enhancement (Fig. 5-9). The comparability of MR perfusion imaging and nuclear techniques is unclear at present unless the patient is in atrial fibrillation, when the averaged acquisition of nuclear techniques is a significant advantage.

Myocardial viability is assessed by looking for delayed enhancement.25 The amount of contrast taken up by a soft tissue depends on the relative proportion of extracellular space, which is increased in myocardial scar compared with viable myocardium. Within viable myocardium, rapid wash-in and wash-out of contrast occurs, but within infarcted myocardium, enhancement develops more slowly and is washed out more slowly. The use of an inversion-recovery sequence (which nulls the signal from normal myocardium) 10 to 30 minutes after contrast administration allows for imaging of regions of infarction (Figs. 5-10 and 5-11), which are brightly enhanced and are characteristically subendocardial. The superior spatial resolution ofs MR imaging allows for differentiation between viable and nonviable myocardium with a high degree of accuracy. In particular, small regions of subendocardial infarction can be identified by MR imaging with a higher sensitivity and specificity than by nuclear imaging techniques.26 The relative thickness of infarction of a myocardial segment can be used to predict the likelihood of useful functional activity’s being restored by revascularization.27

image

Figure 5.11 Cardiac MR imaging viability scan. An imaging technique similar to that shown in Figure 5-10 has been used. A long-axis view of the left ventricle is shown. Extensive infarction involving the distal anterior, apical, and inferior regions of the left ventricle (arrows) can be seen.

MR imaging also allows for accurate noninvasive measurement of blood flow, so MR imaging is useful for the quantitative assessment of regurgitant volume in patients with valvular disease. However, imaging of valve structure is best performed using echocardiography. Flow measurements can also be used to quantify cardiac shunts noninvasively.

Cardiac Computed Tomogram Scanning

Recent developments in the technology of computed tomogram (CT) scanners have made feasible the use of this modality to evaluate coronary artery disease (Fig. 5-12). In a CT scanner, an x-ray source is rotated around the patient while a stationary row of detectors collects radiation that is then converted into a digital signal, which in turn is processed by using a complex mathematical algorithm (a Fourier transform) to generate an image. The speed of rotation of x-ray tubes has increased such that one rotation can now be performed in 0.375 seconds rather than the 1-second minimum that prevailed for some years. In addition, in the past few years the number of rows of detectors, and thus potential simultaneous imaging slices, has increased from 4 to 64, resulting in a reduction in the length of breathholding required to image the entire heart from 45 to 5 seconds. Improvements in the reconstruction algorithms have allowed for higher spatial resolution. Image acquisitions are gated to the cardiac cycle, resulting in reduced radiation exposure.

In order to perform a multidetector CT (MDCT) coronary angiogram, the patient must be in sinus rhythm and, ideally, have a slow heart rate. Radiographic contrast is administered as an intravenous bolus and images are acquired as contrast passes through the coronary circulation, with the patient holding his or her breath for the few seconds required. Subsequent image processing is performed on the basis of data acquired at a particular point in the cardiac cycle. Reconstruction of images of a particular coronary artery is performed at the point in the cardiac cycle at which the motion of that vessel is minimized, which may be different for various vessels, necessitating multiple reconstructions. An MDCT coronary angiogram allows for imaging not only of the artery lumen but also of the vessel wall. Thus, some assessment of the nature of an atherosclerotic plaque can be made noninvasively.28

There are problems with the technique. Variation in heart rate during the acquisition can result in considerable artifact, potentially rendering the study useless. Despite the advances in technology, the spatial resolution of MDCT angiography remains lower than it is in conventional angiography. Structures of very high radiographic density appear larger than they really are. Thus, coronary stenoses caused by calcified plaque appear to be more significant than they appear to be in conventional angiography. Imaging of the lumen inside a coronary stent is complicated by artifact from the metal in the stent.29 It is often very difficult to visualize tortuous coronary side-branches; the OM vessels are usually the most problematic. The recent increase in the number of detectors, with concomitant improvement in spatial resolution, partly resolves some of these issues.30,31 Coronary grafts are especially suited to MDCT imaging because they are of relatively large caliber, run in relatively straight lines, and move little with cardiac motion.32 However, the run-off vessels to which the grafts are anastomosed tend to be small and heavily calcified, and MDCT may be inadequate for their assessment.

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