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11/6/25

 


Noninvasive Cardiac Imaging: Echocardiography, Nuclear Cardiology, and Magnetic Resonance/Computed Tomography Imaging

1841CHAPTER 241

It is important to highlight that most studies included in metaanalyses of the diagnostic accuracy of cardiac imaging modalities for

the diagnosis of CAD were retrospective, small, single-center studies,

comprising predominantly male patients with a high prevalence of

CAD (>50–60%). Multicenter studies assessing the performance of

individual modalities or comparing different modalities have consistently resulted in more modest diagnostic accuracies, tracking more

closely with how these tests perform in clinical practice.

Stress Echocardiography The hallmark of myocardial ischemia

during stress echocardiography is the development of new regional

wall motion abnormalities and reduced systolic wall thickening (Video

241-3). Stress echocardiography can be performed in conjunction

with exercise or dobutamine stress. Stress echocardiography is best at

identifying inducible wall motion abnormalities in previously normally

contracting segments. In a patient with wall motion abnormalities at

rest, the specificity of stress echocardiography is reduced, and worsening regional function of a previously abnormal segment might reflect

worsening contractile function in the setting of increased wall stress

rather than new evidence of inducible ischemia.

The advantages of stress echocardiography over other stress imaging

techniques include its relatively good diagnostic accuracy, widespread

availability, no use of ionizing radiation, and relatively low cost. Limitations of stress echocardiography include (1) the technical challenges

associated with image acquisition at peak exercise because of exertional

hyperpnea and cardiac excursion, (2) the fact that rapid recovery of

wall motion abnormalities can be seen with mild ischemia (especially

with one-vessel disease, which limits sensitivity), (3) difficulty detecting residual ischemia within an infarcted territory because of resting

wall motion abnormality, (4) high operator dependence for acquisition

of echocardiographic data and analysis of images, and (5) the fact

that good-quality complete images viewing all myocardial segments

occur in only 85% of patients. Newer techniques, including second

harmonic imaging and the use of intravenous contrast agents, improve

image quality, but their effect on diagnostic accuracy has not been well

documented.

As with nuclear perfusion imaging, stress echocardiography is often

used for risk stratification in patients with suspected or known CAD. A

negative stress echocardiogram is associated with an excellent prognosis, allowing identification of patients at low risk. Conversely, the risk

of adverse events increases with the extent and severity of wall motion

abnormalities on stress echocardiography.

Stress Radionuclide Imaging SPECT

myocardial perfusion imaging is the most common form of stress imaging tests for CAD evaluation. The presence of a reversible myocardial

perfusion defect is indicative of ischemia (Fig.

241-9, left panel), whereas a fixed perfusion defect

generally reflects prior myocardial infarction

(Fig. 241-9, right panel). As discussed above, PET

has advantages compared to SPECT, but it is not

widely available and is more expensive and, thus,

considered an emerging technology in clinical

practice.

Nuclear perfusion imaging is another robust

approach to diagnose obstructive CAD, quantify

the magnitude of inducible myocardial ischemia,

assess the extent of tissue viability, and guide therapeutic management (i.e., selection of patients for

revascularization). One of the most valuable clinical applications of radionuclide perfusion imaging is for risk stratification. It is well established

that patients with a normal SPECT or PET study

exhibit a low rate of major adverse cardiac events

of <1% annually. Importantly, the risks of death

and myocardial infarction increase linearly with

increasing magnitude of perfusion abnormalities,

reflecting the extent and severity of CAD.

Despite the widespread use and clinical acceptance of radionuclide

imaging in CAD evaluation, a recognized limitation of this approach

is that it often uncovers only coronary territories supplied by the most

severe stenoses. Consequently, it is relatively insensitive to accurately

delineate the extent of obstructive angiographic CAD, especially in

the setting of multivessel disease. The use of quantitative myocardial

blood flow and coronary flow reserve with PET can help mitigate this

limitation. In patients with so-called “balanced” ischemia or diffuse

CAD, measurements of coronary flow reserve uncover areas of myocardium at risk that would generally be missed by performing only

relative assessments of myocardial perfusion (Fig. 241-10). Conversely,

a normal coronary flow reserve is associated with a very high negative

predictive value for excluding high-risk angiographic CAD. These

measurements of coronary flow reserve also contribute to risk stratification across the spectrum of ischemic changes, including patients

with visually normal myocardial perfusion.

HYBRID CT AND NUCLEAR PERFUSION IMAGING Because many of

the newer generation nuclear medicine scanners integrate CT and

a gamma camera in the same acquisition gantry, it is now possible

to acquire and quantify myocardial scar and ischemia and CAC

scoring from a single dual-modality study (SPECT/CT or PET/CT)

(Fig. 241-11). The rationale for this integrated approach is predicated

on the fact that the perfusion imaging approach is designed to uncover

only obstructive atherosclerosis. Conversely, CAC scoring provides a

quantitative measure of the anatomic extent of atherosclerosis. This

provides an opportunity to improve the conventional models for risk

assessment using nuclear imaging alone, especially in patients without

known CAD.

Cardiac CT Voluminous plaques are more prone to calcification,

and stenotic lesions frequently contain large amounts of calcium.

Indeed, there is evidence that high CAC scores are generally predictive

of a higher likelihood of obstructive CAD, and the available data support

the concept of a threshold phenomenon governing this relationship (i.e.,

Agatston score >400). However, given the fact that CAC scores are not

specific markers of obstructive CAD, one should be cautious in using

this information as the basis for referral of patients to coronary angiography, especially in symptomatic patients with low-risk stress tests.

Conversely, CAC scores <400, especially in symptomatic patients with

intermediate-high likelihood of CAD, as in those with typical angina,

may be less effective in excluding CAD, especially in young symptomatic

men and women who may have primarily noncalcified atherosclerosis

(Fig. 241-12).

Stress

Stress

Stress

Rest

Rest

Rest

Reversible perfusion defect Fixed perfusion defect

FIGURE 241-9 Selected technetium-99m sestamibi myocardial perfusion single-photon emission

computed tomography images of two different patients demonstrating a reversible perfusion defect

involving the anterior and septal left ventricular wall, reflecting ischemia in the left anterior descending

coronary territory (arrows in left panel) and a fixed perfusion defect involving the inferior and

inferolateral walls consistent with myocardial scar in the right coronary territory (arrow in right panel).


1842 PART 6 Disorders of the Cardiovascular System

As discussed above, the improved temporal and spatial resolution

of modern multidetector CT scanners offers a unique noninvasive

approach to delineate the extent and severity of coronary atherosclerosis with coronary CTA. The extremely high sensitivity of this

approach offers a very effective means for excluding the presence of

CAD (high negative predictive value) (Table 241-3). In the setting

of high coronary calcium scores (e.g., >400), however, specificity

is reduced because the blooming artifact of calcium does not allow

one to evaluate the vessel lumen accurately. Given the high negative

predictive value of CTA, a normal scan result effectively excludes

Stress

21 22 23 24 25 26 27 28 29 30 31

23 24 25 26 27 28 29 30 31 32 33

35 36 37 38 39 40 41 42 43 44 45

37 38 39 40 41 42 43 44 45 46 47

67 66 65 64 63 62 63 64 65 66

67 66 65 64 63 62 63 64 65 66

Stress

Stress

Stress

LCX

LM

LAD

RCA

Rest

Rest

Ant

Sep Lat

Inf

Rest

Rest

FIGURE 241-10 Coronary angiographic (left panel) and rubidium-82 myocardial perfusion positron emission tomography images (right panel) in an 85-year-old female with

diabetes presenting with chest pain. The coronary angiogram demonstrates significant stenoses of the left main and circumflex coronary arteries. However, the perfusion

images demonstrate only a reversible lateral wall defect. Quantification of stress and rest myocardial blood flow demonstrated a significant, global reduction on coronary

flow reserve (estimated at 1.2, normal value >2.0), reflecting extensive myocardium risk that was underestimated by the semiquantitative estimates of myocardial perfusion.

LAD, left anterior descending artery; LCX, left circumflex artery; LM, left main artery; RCA, right coronary artery.

Stress

ANT

LAT

INF

SEP

STRESS(G)

ANT

LAT

INF

SEP

REST(G)

PA

aAo

dAo

Calcium score: 1330

Stress

Stress

Rest

Rest

Rest

FIGURE 241-11 Stress and rest rubidium-82 myocardial perfusion positron emission tomography (PET) images (left) and noncontrast gated computed tomography

(CT) images (right) delineating the extent and severity of coronary artery calcifications obtained with integrated PET/CT imaging. The images demonstrate extensive

atherosclerosis (Agatston coronary calcium score = 1330) without flow-limiting disease based on the normal perfusion study. aAo, ascending aorta; dAo, descending aorta;

PA, pulmonary artery.


Noninvasive Cardiac Imaging: Echocardiography, Nuclear Cardiology, and Magnetic Resonance/Computed Tomography Imaging

1843CHAPTER 241

Stress

23 24 25 26 27 28 29 30 31 32 33

24 25 26 27 28 29 30 31 32 33 34

64 65 66 67 68

65 66 67 68 69

64 63 62 61 60

64 63 62 61 60

Stress

Rest

LM

LAD

Rest

FIGURE 241-12 Stress and rest rubidium-82 myocardial perfusion positron emission tomography images (top), noncontrast gated computed tomography images (lower

right), and selected coronary angiographic images obtained on a 59-year-old male patient with atypical angina. Despite the absence of significant coronary calcifications

(Agatston calcium score = 0), the perfusion images demonstrated a dense and reversible perfusion defect involving the anterior and anteroseptal walls (arrows), reflecting

significant obstructive disease in the left anterior descending coronary artery (LAD), confirmed on angiography. LM, left main artery.

obstructive CAD and abolishes the need for further investigation.

As discussed below, this may be quite useful in patients with lowintermediate clinical risk presenting to the emergency department

(ED) for chest pain. However, the limited capability of this technique to

determine which coronary plaques are flow limiting can make abnormal scan results more difficult to interpret, especially in terms of the

possible need of revascularization. There are emerging data suggesting

that by adding a stress myocardial perfusion CT evaluation (similar to

stress perfusion CMR) (Fig. 241-13, top panel) or an estimated fractional flow reserve (so-called FFRCT) (Fig. 241-13, lower panel), one

can define the hemodynamic significance of anatomic stenosis. FFRCT

is beginning to enter routine clinical practice. However, CT myocardial

perfusion remains an emerging technology.

As with invasive coronary angiography, assessments of the extent of

CAD by CTA can also provide useful prognostic information. A low

1-year cardiac event rate has been reported for patients without coronary atherosclerosis on CTA. For patients with obstructive CAD, the

risk of adverse cardiac events increases proportionally with the extent

of angiographically obstructive CAD. There is new evidence that even

the presence of nonobstructive atherosclerosis increases the risk of

adverse cardiac events.

Although CTA can be helpful in assessing patency of bypass grafts,

the assessment of stents is somewhat more challenging because the

limited spatial resolution of CT and stent diameter (<3 mm being

associated with the highest number of partial lumen visualization and

nondiagnostic scans) both contribute to limited clinical results.

CMR Imaging CMR evaluates for ischemia from CAD by assessing regional myocardial perfusion or regional wall motion at rest

and during pharmacologic stress with an intravenous infusion of

vasodilator agent or dobutamine. Myocardial perfusion is evaluated

by injecting a GBCA bolus followed by imaging data acquisition as

the contrast passes through the cardiac chambers and into the myocardium. Relative perfusion deficits are recognized as regions of low

signal intensity (black) within the myocardium (Video 241-4). Several

minutes after GBCA injection, LGE imaging allows detection of bright

areas of myocardial scar (white), which permits comparison of regions

of hypoperfusion and infarction to quantify myocardial ischemia

(Fig. 241-14).

With better delineation of the endocardial borders, dobutamine

CMR has better diagnostic accuracy than dobutamine echocardiography for detection of CAD, especially in patients with poor acoustic

window (Table 241-3). High-dose dobutamine carries the risk of serious ventricular arrhythmias (~1%), but most cases can be prevented

with proper monitoring of vital signs and regional cine function. The

advantages of stress perfusion CMR over SPECT include its higher

spatial resolution, which allows detection of subendocardial ischemia

or infarction that may be missed by SPECT. As with other imaging

modalities, stress CMR studies also provide robust risk stratification. In

a recent randomized controlled trial, a stress CMR–guided strategy was

shown to improve the guidance toward the use of invasive investigation

and coronary revascularization.

Selecting a Testing Strategy in Patients without Known

CAD As discussed above, there are many options for the evaluation

of a patient with suspected CAD presenting with chest pain symptoms.

The critical questions to be answered by a testing strategy include the

following: (1) Does the chest pain reflect obstructive CAD? (2) What

are the short- and long-term risks? (3) Does the patient need to be

considered for revascularization? With improved guideline-directed


1844 PART 6 Disorders of the Cardiovascular System

medical therapy (GDMT), large-scale clinical trials have indicated the

benefits of GDMTs in which the majority of the patients with stable

CAD are at low risk of serious cardiac events on the basis of GDMT

alone, with coronary revascularization best reserved for patients with

severe symptoms despite adequate medical therapy. Imaging, however,

will continue to play a significant role in diagnosing the etiology of

chest pain and risk assessment of individual patients.

For symptomatic patients without a prior history of CAD and a normal

or nearly normal resting ECG who are able to exercise, the American

College of Cardiology/American Heart Association guidelines recommend standard exercise treadmill testing (ETT) as the initial testing

strategy. The guidelines further suggest that patients who are categorized as low risk by ETT (e.g., those achieving >10 metabolic equivalents [METS] without chest pain or ECG changes) be treated initially

with medical therapy, and those with high-risk ETT findings (i.e.,

typical angina with >2 mm ST-segment depression in multiple leads,

ST elevation during exercise, drop in blood pressure, or sustained ventricular arrhythmias) be referred for coronary angiography.

The use of exercise testing in women presents difficulties that are

not seen in men, reflecting the differences in the lower prevalence

of obstructive CAD in women and the different accuracy of exercise

testing in men and women. Compared with men, the lower pretest

probability of disease in women means that more test results are false

positive. In some of these patients, a positive ETT may reflect true

myocardial ischemia caused by microvascular coronary artery dysfunction (so-called microvascular disease). In addition, the inability

of many women to exercise to maximum aerobic capacity, the greater

prevalence of mitral valve prolapse and microvascular disease, and

possibly other reasons may contribute to the differences with men as

well. The difficulties of using exercise testing for diagnosing obstructive CAD in women have led to speculation that stress imaging may be

preferred over standard stress testing. However, recent data from the

WOMEN study suggest that in symptomatic, low-risk women who can

exercise, standard ETT is a very effective initial diagnostic strategy as

compared to stress radionuclide imaging. Indeed, the 2-year outcomes

were similar in both diagnostic strategies, and the ETT-first approach

resulted in 48% lower costs compared to exercise radionuclide imaging.

Patients who cannot undergo an ETT or those at intermediate-high

risk after ETT (e.g., low exercise capacity, chest pain, and/or ST-segment

depression without high-risk features) will often require additional

testing, either stress imaging or coronary CTA, to more accurately

characterize clinical risk. Most common stress imaging strategies in

intermediate-risk patients include stress echocardiography and radionuclide imaging. However, CMR and PET in experienced centers have

both been shown to have higher test accuracy than SPECT, and CMR

has been shown to be more cost-effective than SPECT. In patients

FIGURE 241-14 The image shows the late gadolinium enhancement image of a mid

short-axis view. There is no evidence of infarction in the anterior wall, which would

be seen as bright white areas, indicating that the stress perfusion defect primarily

represents myocardial ischemia. This patient had a significant stenosis of the left

anterior descending coronary artery.

FFRCT0.64

LAD

FFRCT

FFR 0.57

0.9

0.8

0.7

FIGURE 241-13 Examples of novel approaches to the assessment of flow-limiting coronary artery disease (CAD) with cardiac computed tomography (CT). In the top

panel, representative views of coronary CT angiogram (CTA; left), coronary angiogram (middle), and stress myocardial perfusion CT (right) images in a patient with CAD and

prior stenting of the left anterior descending coronary artery (LAD) are presented. On the CTA, the stent (arrows) is totally occluded as evidenced by the loss of contrast

enhancement distal to the stent. The coronary angiogram demonstrates a concordant total occlusion of the LAD. On the perfusion CT images, there is a black rim (arrows)

involving the anterior and anterolateral walls, indicating the lack of contrast opacification during stress consistent with myocardial ischemia. (Images courtesy of CORE 320

investigators.) The lower panel illustrates an example of fractional flow reserve (FFR) estimates with coronary CTA (left) compared to the reference standard of invasive FFR.

The FFR reflects the pressure differential between a coronary segment distal to a stenosis and the aorta. In normal coronary arteries, there is no gradient, and FFR is 1. An

FFR <0.80 is consistent with a hemodynamically significant stenosis. (Images courtesy of Dr. James Min, Cornell University, New York.)


Noninvasive Cardiac Imaging: Echocardiography, Nuclear Cardiology, and Magnetic Resonance/Computed Tomography Imaging

1845CHAPTER 241

with intermediate clinical risk, stress imaging with either SPECT or

echocardiography has been shown to accurately reclassify patients who

are initially classified as intermediate risk by ETT as low or high risk

(Fig. 241-15). Following this staged strategy of applying the low-cost

ETT first and reserving more expensive imaging to refine risk stratification to patients initially classified as intermediate risk by ETT is

more cost-effective than applying stress or anatomic imaging as the

initial test routinely.

An imaging strategy is the recommended first step for patients who

are unable to exercise to an adequate workload and/or those with abnormal resting ECGs (e.g., left ventricular hypertrophy with strain, left

bundle branch block). Importantly, the most recent documents regarding appropriate use of imaging also considered that an imaging strategy

may be an appropriate first step in patients with intermediate-high

likelihood of CAD (e.g., diabetics, renal impairment) due to increased

overall sensitivity for diagnosis of CAD and improved risk stratification.

In considering an imaging strategy, the evidence supporting the role of

ischemia assessment versus anatomy must be considered. From the discussion above, for patients with atypical chest pain and a low pretest risk

of CAD, a normal coronary CTA is helpful because it effectively excludes

the presence of obstructive CAD and the need for further testing, defines

a low clinical risk, and makes management decisions regarding referral

to coronary angiography straightforward. However, in patients with

an intermediate or higher pretest risk, coronary CTA is less effective

in excluding obstructive CAD owing to its limited accuracy to define

stenosis severity and predict ischemia; however, abnormal CTA results

are more problematic to interpret and to use as the basis for defining the

potential need of invasive coronary angiography and revascularization.

In such patients, a follow-up stress test is usually required to determine

the possible need of revascularization (Fig. 241-16).

The justification of stress imaging in testing strategies

has hinged on the identification of which patients may

benefit from a revascularization strategy by means of noninvasive estimates of jeopardized myocardium rather than

angiography-derived anatomic stenoses. However, recent

evidence from the ISCHEMIA trial suggests that optimal

medical therapy provides comparable prognostic benefit to

coronary revascularization in patients with moderate myocardial ischemia. Coronary revascularization is reserved

for patients with very extensive evidence of ischemia by

stress imaging and/or inadequate symptom control by

optimal medical therapy. While the available data suggest

similar diagnostic accuracy for SPECT and echocardiography but higher for PET and CMR, the choice of strategy

depends on availability and local expertise.

Selecting a Testing Strategy in Patients with

Known CAD Use and selection of testing strategies

in symptomatic patients with established CAD (i.e.,

prior angiography, prior myocardial infarction, prior

revascularization) differ from those in patients without

prior CAD. Although standard ETT may help distinguish cardiac from noncardiac chest pain, exercise ECG

has several limitations following myocardial infarction

and revascularization (especially coronary artery bypass

grafting). These patients frequently have rest ECG abnormalities. In addition, there is a clinical need to document

both the magnitude and localization of ischemia to be

able to direct therapy, especially the potential need for

targeted revascularization. Consequently, imaging tests

are preferred for evaluating patients with known CAD.

There are also important differences in the effectiveness of imaging tests in these patients. As discussed

above, coronary CTA is limited in patients with prior

revascularization. While CTA provides excellent visualization of the bypass grafts, the native circulation tends

to get heavily calcified and is generally not a good target

for imaging with CTA. Likewise, blooming artifacts from

metallic stents also limit the application of coronary

Duke treadmill score

Low

Event rate (%/year)

0

2

4

6

8

10

12

Intermediate High

10

9.1

3.6

8.9

6.4

0.4

7.8

1.8

0.3

Exercise SPECT

Normal

Mild

Severe

Duke treadmill score

Low Intermediate High

11

5.7

2.7

6.7

3.6

1.7

2.9

1.5 0.7

Exercise Echo

Normal

Single VD

Multi VD

FIGURE 241-15 Incremental risk stratification of stress imaging over Duke treadmill score in patients with suspected coronary artery disease. Stress imaging is most

valuable in the intermediate-risk group. SPECT, single-photon emission computed tomography; VD, vessel disease. (Reproduced with permission from R Hachamovitch

et al: Exercise myocardial perfusion SPECT in patients without known coronary artery disease. Circulation 93:905, 1996; https://www.ahajournals.org/doi/full/10.1161/01.

CIR.93.5.905.)

Stress

Stress

Stress

Rest

Rest

Rest

FIGURE 241-16 Selected views from coronary computed tomography angiographic (CTA) images

(top panel) and stress and rest rubidium-82 myocardial perfusion positron emission tomography

images (lower panel) obtained on a 64-year-old male patient with atypical angina. The CTA

images demonstrate dense focal calcifications in the left main (LM) and left anterior descending

(LAD) coronary arteries and a significant noncalcified plaque in the mid right coronary artery (RCA;

arrow). The myocardial perfusion images demonstrated no evidence of flow-limiting stenosis. LCx,

left circumflex artery; OM, obtuse marginal branch.


1846 PART 6 Disorders of the Cardiovascular System

CTA in patients with prior percutaneous coronary intervention. If an

anatomic strategy is indicated, direct referral to invasive angiography

is preferred.

Stress imaging approaches are especially useful and preferred in

symptomatic patients with established CAD. As in patients without

prior CAD, normal imaging studies in symptomatic patients with

established CAD also identify a low-risk cohort. In those with abnormal stress imaging studies, the degree of abnormality relates to posttest

risk. In addition, stress imaging approaches can localize and quantify

the magnitude of ischemia, thereby assisting in planning targeted

revascularization procedures. As in patients without prior CAD, the

choice of stress imaging strategy depends on availability and local

expertise.

Testing Strategy Considerations in Patients Presenting with

Chest Pain to the ED Although acute chest pain is a frequent reason for patient visits to the ED, only a small minority of those presentations represent an acute coronary syndrome (ACS). Strategies used in

the evaluation of these patients include novel cardiac biomarkers (e.g.,

serum troponins), conventional stress testing (ETT), and noninvasive

cardiac imaging. It is generally accepted that the primary goal of this

evaluation is exclusion of ACS and other serious conditions rather than

detection of CAD.

The routine evaluation of acute chest pain in most centers in the

United States includes admission to a chest pain unit to rule out

ACS with the use of serial ECGs and cardiac biomarkers. In selected

patients, stress testing with or without imaging may be used for further

risk stratification. Stress echocardiography and radionuclide imaging

are among the most frequently used imaging approaches in these

patients. Multiparametric CMR imaging has also been used successfully in patients with acute chest pain (Video 241-5). Due to its ability

to probe multiple aspects of myocardial physiology, cardiac anatomy,

and tissue characterization with LGE imaging, CMR is useful in diagnosing conditions that mimic ACS (e.g., acute myocarditis, takotsubo

cardiomyopathy, pericarditis) (Fig. 241-17).

As discussed above, coronary CTA is a rapid and accurate imaging

technique to exclude the presence of CAD and is well suited for the

evaluation of patients with acute chest pain (Fig. 241-18). Four randomized clinical trials have demonstrated the feasibility, safety, and

accuracy of coronary CTA in the ED as compared to usual care (which

typically includes stress imaging). Patients in these trials had a very low

clinical risk. Overall, there were no deaths and very few myocardial

infarctions without differences between the groups. Likewise, there

were no differences in postdischarge ED visits or rehospitalizations.

These studies showed decreased length of stay with coronary CTA, and

most but not all reported cost savings. An observation from a recent

meta-analysis was that, compared to usual care, more patients assigned

to coronary CTA underwent cardiac catheterization (6.3% vs 8.4%,

respectively) and revascularization (2.6% vs 4.6%, respectively). The

relative increased frequency in the referral to cardiac catheterization

and revascularization after coronary CTA compared to stress imaging

testing strategies has also been observed in patients with stable chest

pain syndromes.

Taken together, the available data clearly suggest that not all patients

presenting with acute chest pain require specialized imaging testing.

Patients with very low clinical risk and negative biomarkers (especially

high-sensitivity troponin assays) can be safely triaged. The use of

imaging tests in patients with low-intermediate risk should be carefully

considered, especially given the trade-offs discussed above.

■ VALVULAR HEART DISEASE

Abnormalities of any of the four valvular structures in the heart can

lead to significant cardiac dysfunction, heart failure, or even death.

Echocardiography, CMR, and cardiac CT can be used for the evaluation of valvular heart disease, although echocardiography is generally

considered the first imaging test for the assessment of valvular heart

disease. In addition, echocardiography is the most cost-effective

screening method for valvular heart disease. In some cases, CMR

can complement echocardiography when echocardiographic acoustic

window is inadequate, to quantify blood flow data more precisely, or

to provide complimentary assessment of adjacent vascular structures

relevant to the valvular condition.

Echocardiography can be used to assess both regurgitant and

stenotic lesions of any of the cardiac valves. Typical indications for

echocardiography to assess valvular heart disease include cardiac murmurs identified on physical examination, symptoms of breathlessness

that may represent valvular heart disease, syncope or presyncope, and

preoperative exams in patients undergoing bypass surgery. A standard

echocardiographic examination should include qualitative and quantitative assessment of all valves regardless of indication and should serve

as an adequate screening test for significant valvular disease.

Assessment of Aortic Stenosis Aortic stenosis, one of the most

common forms of valvular heart disease, most often occurs because

of gradual progression of valvular calcification in both normal and

congenitally abnormal valves. Assessment of aortic stenosis is most

commonly performed with echocardiography, although techniques for

quantitative assessment of aortic stenosis with CMR have been developed and increasingly used over the past decade. Echocardiographic

assessment generally begins with visual inspection of the valve. This

allows for assessment of valvular morphology, whether it is tricuspid,

bicuspid, or some variant; degree of leaflet calcification; and leaflet

excursion.

The normal aortic valve consists of three leaflets or cusps: the right

coronary, the left coronary, and the noncoronary cusps. Abnormalities

of cusp development are some of the most common congenital heart

anomalies, the most common of which is bicuspid aortic valve, with

two opening leaflets rather than three (Fig. 241-19). The aortic valve

can be visualized on echocardiography, although sometimes it can be

difficult to distinguish true bicuspid aortic valve from variants, including the presence of a vestigial commissure (raphe). Bicuspid aortic

valve, one of the most common congenital anomalies, predisposes to

both aortic stenosis and aortic insufficiency.

FIGURE 241-17 A four-chamber long-axis late gadolinium enhancement (LGE)

image of a patient with acute myocarditis. Note that the LGE primarily involved the

epicardial aspect of the myocardium (arrows), sparing the endocardium, which is a

feature that distinguishes myocarditis from myocardial infarction, which affects the

endocardium. Also note the multiple foci of LGE in this case affecting the lateral wall

of the left ventricle. Viral myocarditis often presents with this pattern.


Noninvasive Cardiac Imaging: Echocardiography, Nuclear Cardiology, and Magnetic Resonance/Computed Tomography Imaging

1847CHAPTER 241

The degree of aortic stenosis is assessed by estimating both the

pressure gradient across the valve and the valve area. Patients with

moderate aortic stenosis or higher generally have peak instantaneous

velocities of 3.0 m/s and higher, and often higher than 4.0 m/s, corresponding to pressure gradients of 36 and 64 mmHg, respectively.

Because pressure gradients across the aortic valve can be underestimated in patients with severe left ventricular dysfunction, estimation of

valve area by the continuity principle is the most accurate technique for

assessing the severity of the stenosis. However, evaluation of the patient

with so-called low-flow or low-gradient aortic stenosis can be challenging and sometimes requires provocative testing such as dobutamine

echocardiography. In these cases, it is important to distinguish whether

the valve is indeed capable of opening further or simply behaving like a

stenotic valve because of the low-pressure gradient.

Aortic valve areas <1.0 cm2

 are generally considered severe, and

valve areas <0.6 cm2

 are considered critical. Because patients with good

left ventricular function can often tolerate severe aortic stenosis for a

considerable period of time, valve areas or gradients alone should not

be used to determine whether an individual patient should undergo

aortic valve surgery as this remains a clinical decision.

Some patients with apparent aortic stenosis have subvalvular or even

supravalvular obstruction. Hypertrophic cardiomyopathy represents

the classic form of subvalvular aortic stenosis, but this is usually easily

distinguished from aortic stenosis on echocardiography as the valve

leaflets can be seen opening during systole. Subaortic membranes can

behave very similarly to leaflet aortic stenosis, and the membranes

themselves can be very thin and difficult to visualize, although the

presence of a murmur, a gradient across the valve with aortic leaflets

that appear to open normally, is highly suggestive of a membrane.

Supravalvular aortic stenosis, although exceedingly rare, also occurs.

The emergence of transcatheter aortic valve intervention as a therapeutic option for patients with severe aortic stenosis who are not

optimal candidates for surgical replacement has resulted in a very

important clinical role for multimodality imaging. Imaging plays a critical role in preprocedural planning, intraprocedural implantation optimization, and follow-up of these patients. CT plays an important role

in defining the eligibility of the proposed access site (CTA of the aorta

and iliac arteries) and in defining the anatomic relationships between

the aortic valve and aortic root, left ventricle, and coronary ostia. Cardiac CT and transesophageal echocardiography are also used to define

the device size. Transesophageal echocardiography is used during the

device implantation to ensure the best prosthesis–patient match, to

assess prosthesis position and function after deployment, and to identify immediate complications (e.g., aortic insufficiency, paravalvular

leak resulting from patient–prosthesis mismatch). Echocardiography is

the imaging modality of choice for long-term surveillance.

Assessment of Aortic Regurgitation Assessment of aortic

regurgitation requires qualitative assessment of the aortic valve structure. Aortic regurgitation is common with congenital abnormalities of

the aortic valve, the most common of which is bicuspid aortic valve.

Aortic regurgitation often coexists with aortic stenosis, and it is not

uncommon for patients to have both severe aortic stenosis and regurgitation. Congenital abnormalities of the aortic leaflets, such as bicuspid

aortic valve, are common causes of aortic insufficiency. Dilatation

of the aortic root, as occurs in patients with hypertension and other

disorders in which aortic dilatation can occur, can also lead to aortic

regurgitation even when the valve leaflets are intrinsically normal due

to malcoaptation of the leaflets. Aortic root dilatation is common in

patients with aortic regurgitation, both as a cause or coexisting lesion,

and the aortic root and ascending aorta should be measured and followed in these patients (Fig. 241-20).

Because aortic regurgitation can result in dilatation of the left ventricle over time with ultimate reduction in ventricular function, caring

for the patient with aortic regurgitation requires serial assessment of

ventricular size and function. Patients whose ventricles dilate beyond

an end-systolic diameter of 5.5 cm or whose LVEF declines below

normal are at significantly higher risk of death or heart failure, and

these measures are often used to decide the need for valve surgery.

Quantitation of regurgitation itself can be performed using a number

of methods. Semiquantitative visual assessment of aortic regurgitant jet

width and depth by color flow Doppler remains the most used. The jet

diameter as a ratio of the left ventricular outflow tract diameter proximal to the valve represents one of the most reliable indices of severity

A

RCA

B C

FIGURE 241-18 Representative coronary computed tomography angiographic (CTA) images of two patients presenting to the emergency department with chest pain

and negative biomarkers. The patient in A had angiographically normal coronary arteries; the panel shows a representative view of the right coronary artery (RCA). B

and C show a corresponding significant stenosis in the mid portion of the RCA on both the CTA (B) and invasive angiographic view (C). (Images used with permission from

Dr. Quynh Truong, Massachusetts General Hospital, Boston, MA.)

A B C

FIGURE 241-19 Normal aortic valve in the parasternal long-axis view (A) and short-axis view (B), and bicuspid aortic valve showing typical 10 o’clock to 4 o’clock leaflet

orientation (C).


1848 PART 6 Disorders of the Cardiovascular System

A B

FIGURE 241-20 Aortic regurgitation visualized by color flow Doppler in the parasternal long-axis view (A) and

the parasternal short-axis view (B).

–200

–100

0

100

200

300

400

500

600

700

200 400 600 800 1000 1200

Time (ms)

Forward flow volume 123 mL

Flow (ml/s)

Regurgitant volume 67 mL

FIGURE 241-21 The resultant flow curve generated from phase contrast imaging

demonstrates a forward flow of 123 mL and a regurgitant volume of 67 mL, yielding a

regurgitant fraction of 54% indicating severe aortic regurgitation.

and correlates well with angiographic assessment. Similarly, the vena

contracta, which represents the smallest diameter of the regurgitant

flow at the level of the valve, can be used to assess the severity of aortic

regurgitation. Other Doppler-based methods include assessing the

pressure half-time, or rate of decline of the pressure gradient between

the aorta and left ventricle, a measure of acuity of aortic regurgitation, and assessing aortic flow reversal in the descending aorta. The

regurgitant volume can be calculated by comparing the flow across the

aortic and pulmonic valves, assuming the pulmonic valve is competent.

Central or perivalvular aortic regurgitation is common in patients following TAVR and is generally assessed immediately after the procedure

and on follow-up echocardiography.

CMR offers several advantages over echocardiography in the

assessment of aortic regurgitation. CMR is more accurate than

echocardiography for assessing small changes in cardiac size or function longitudinally in patients with aortic insufficiency. In addition,

CMR can accurately quantify aortic regurgitant volume secondary to

aortic insufficiency better than echocardiography. CMR can also capture aortic size in 3D that may be helpful in determining the etiology of

the aortic regurgitation or in monitoring progression of the condition

(Fig. 241-21 and Video 241-6).

Assessment of Mitral Regurgitation The normal mitral valve

consists of an anterior and posterior leaflet in a saddle shape configuration (Fig. 241-22). The leaflets are attached to the papillary muscles

via chordae tendineae that insert on the ventricular side of the leaflets.

Mitral regurgitation can occur due to abnormalities of the leaflets,

the chordal structures, or the ventricle, or any combination of these

(Fig. 241-23).

Mitral valve prolapse, in which one leaflet moves behind the plane of

the other leaflet, can be due to myxomatous degeneration of the valves

and leaflet redundancy, disruption of chordal structures secondary

to degenerative disease, or papillary muscle rupture or dysfunction

following myocardial infarction. Regurgitant jets can be visualized

using color flow Doppler. The velocity of regurgitant jets is driven

by the pressure gradient between the two chambers. This velocity

tends to be quite high for left-sided regurgitant lesions, including mitral regurgitation and

aortic regurgitation, resulting in turbulent jets

on color flow Doppler (Fig. 241-23). Visual

estimation of color flow Doppler is generally

sufficient for qualitative assessment of regurgitant severity but can dramatically under- or

overestimate regurgitation severity, particularly

when regurgitant jets are quite eccentric. For

this reason, quantitative assessment is generally recommended, especially when making

clinical decisions about surgical intervention.

The proximal isovelocity surface area (PISA)

method is generally used for quantitative

assessment of severity of mitral regurgitation. This method relies on

estimation of the velocity of flow acceleration at a specific distance

proximal to the valve with the assumption that the flow accelerates in

concentric hemispheres.

As with aortic insufficiency, assessment of ventricular structure

and function is also integral in the evaluation of mitral regurgitation.

Although some patients have mitral regurgitation due to intrinsic

abnormalities of the valve itself, in others, the valve can be relatively

normal but the mitral regurgitation can be secondary to dilatation and

remodeling of the left ventricle. So-called functional mitral regurgitation is generally secondary to apical displacement of the papillary

muscles in a dilated ventricle, resulting in the leaflets of the mitral valve

being pulled toward the apex of the heart, resulting in poor coaptation

during systole and resultant relatively central mitral regurgitation. This

type of mitral regurgitation can generally be distinguished from intrinsic mitral valve disease, and the surgical or procedural treatment of

these conditions can be different. Knowledge of the etiology of mitral

regurgitation can be important for a surgeon planning mitral valve

surgery. Moreover, new procedural approaches to mitral valve disease

may be different depending on the etiology.

Ventricular dilatation is an important predictor of outcome in

patients with mitral regurgitation of any cause. It is important to realize

that in a patient with significant mitral regurgitation, a large portion

of the blood being ejected from the left ventricle with every beat is

regurgitant, thus artificially increasing the ejection fraction. Thus, an

ejection fraction of 55% in a patient with severe mitral regurgitation

may actually represent substantial reduction in myocardial systolic

function.

CMR can be helpful in evaluating mitral regurgitation in a subset of

patients when echocardiographic assessment is inadequate. CMR can

directly quantify regurgitant volume of the mitral regurgitant jet or

indirectly quantify regurgitant volume by measuring the difference of

left ventricular stroke volume and aortic forward flow.

Assessment of Mitral Stenosis Rheumatic mitral disease remains

the most common cause of mitral stenosis, although mitral stenosis can

also result from severe calcification of the mitral leaflets. Rheumatic

mitral stenosis has a distinct appearance characterized by tethering at

the leaflet tips and relative pliability of the leaflets themselves, resulting

in a hockey stick–type deformation particularly of the anterior leaflet

(Fig. 241-24). Narrowing of the mitral orifice impedes flow from the

left atrium to the left ventricle, resulting in increased pressures in the

left atrium, which are then transmitted backward into the pulmonary

vasculature and the right side of the heart. When mitral stenosis is

suspected, echocardiography can be useful for determining etiology

(specifically whether it is rheumatic or not), estimating the valve areas

and gradients across the valve, assessing the left atrium, and assessing

right ventricular size and function. Assessment of left atrial size and

right ventricular size and function is particularly useful in helping

determine the severity of the mitral stenosis.

■ MYOCARDIAL INFARCTION AND HEART FAILURE

Role of Imaging after Myocardial Infarction Imaging can

be useful in the immediate and long-term follow-up of patients

with myocardial infarction. As discussed earlier in the chapter, LGE


Noninvasive Cardiac Imaging: Echocardiography, Nuclear Cardiology, and Magnetic Resonance/Computed Tomography Imaging

1849CHAPTER 241

FIGURE 241-22 Normal mitral valve in two-dimensional views (left) and with three-dimensional imaging (right).

A B C

FIGURE 241-23 A. Mitral valve prolapse with posterior leaflet visualized prolapsing behind the plane of the anterior leaflet (arrow). B. Color flow Doppler showing mitral

regurgitation in a patient with mitral valve prolapse. C. Severe functional mitral regurgitation in a patient with a dilated left ventricle.

A B

FIGURE 241-24 A. Rheumatic mitral stenosis showing pliable leaflets tethered at the tips (arrow). Note the characteristically enlarged left atrium. B. Mitral stenosis

visualized from a three-dimensional echocardiogram.


1850 PART 6 Disorders of the Cardiovascular System

FIGURE 241-25 Example of a patient who presented with inferior ST-segment

elevation myocardial infarction (MI) after several days of intermittent chest pain.

The MRI confirmed an inferior MI by the location of late gadolinium enhancement

(LGE; red arrows). In addition, there is a central area of microvascular obstruction

(dark region surrounded by the bright LGE, white arrow). LV, left ventricle; RV, right

ventricle.

FIGURE 241-26 Acute left anterior descending artery distribution myocardial

infarction at end systole showing akinetic region (arrows).

imaging by CMR is the best technique for imaging for presence or the

extent of infarcted myocardium. In a recent multicenter study, LGE

imaging identified infarct location accurately and detected acute and

chronic infarcts at a sensitivity of 99 and 94%, respectively. In addition,

regions of microvascular obstruction (no-reflow) can be seen as dense

hypoenhanced areas within the core of a bright region of infarction

(Fig. 241-25). Both the presence of LGE and microvascular obstruction are markers of increased clinical risk.

While echocardiography is often used to assess myocardial function immediately after myocardial infarction, myocardial stunning is

common in the early post–myocardial infarction period, especially

in patients who undergo reperfusion therapy. In these patients, either

partial or complete recovery of ventricular function is common within

several days, so that early estimation of ejection fraction may be misleading. In patients with uncomplicated myocardial infarction, imaging can generally be deferred for several days so that a more accurate

assessment of cardiac function, including regional wall motion, can be

assessed (Fig. 241-26).

Echocardiography is the best method for assessment of patients with

suspected mechanical complications after myocardial infarction. These

include mitral regurgitation secondary to either papillary muscle dysfunction or rupture of papillary muscle head, ventricular septal defect,

or even cardiac rupture. A new severe systolic murmur should raise

suspicions for either severe mitral regurgitation or ventricular septal

defect. While cardiac rupture is often catastrophic, contained ruptures,

also known as pseudoaneurysms, can occur, and early diagnosis and

surgical treatment are the best way to maximize survival. The presence

of thrombus within the pericardial space following myocardial infarction should immediately raise suspicion of myocardial rupture and

represents a surgical emergency.

Some patients demonstrate progressive left ventricular dilatation

and dysfunction, known as cardiac remodeling, after myocardial infarction. Assessment of cardiac function and regional wall motion is useful

in the follow-up period, generally between 1 and 6 months following

infarction. The persistence of left ventricular systolic dysfunction following infarction is used to determine the type of therapy (e.g., angiotensin-converting enzyme inhibitors or angiotensin receptor blockers

are typically used in patients with systolic dysfunction following myocardial infarction).

In patients with acute or subacute myocardial infarction, investigation of residual ischemia and/or viability is occasionally an important

clinical question, especially among those with recurrent symptoms after

myocardial infarction (Fig. 241-27). All cardiac imaging techniques

can provide information regarding myocardial viability and ischemia.

The available data suggest that radionuclide imaging, especially PET, is

highly sensitive, with higher negative predictive value than dobutamine

echocardiography. In contrast, dobutamine echocardiography tends to

be associated with higher specificity and positive predictive accuracy

than the radionuclide imaging methods. The experience with CMR

suggests that it offers similar predictive accuracies as those seen with

dobutamine echocardiography.

Role of Imaging in New-Onset Heart Failure Echocardiography

is usually a first-line test in patients presenting with new-onset heart

failure. As discussed above, this test provides a direct assessment of

ventricular function and can help distinguish patients with reduced

from those with preserved ejection fraction. In addition, it provides

additional structural information including an assessment of valves,

myocardium, and pericardium.

Although coronary angiography is commonly performed in patients

with reduced ejection fraction, the determination of heart failure

etiology in an individual patient may be difficult even if angiographically obstructive CAD is present. Indeed, patients with heart failure

and no angiographic CAD may have typical angina or regional wall

motion abnormalities on noninvasive imaging, whereas patients with

angiographically obstructive CAD may have no symptoms of angina

or history of myocardial infarction. Thus, the appropriate classification for any given patient is not always clear, and it often requires the

complementary information of coronary angiography and noninvasive

imaging. As discussed above, stress radionuclide imaging and echocardiography can be helpful in delineating the extent and severity of

inducible myocardial ischemia and viability. Multiparametric CMR

can be quite helpful in the differential diagnosis of heart failure etiologies. Apart from quantifying left and right ventricular volumes and

function, CMR can provide information about myocardial ischemia

and scar. The pattern of LGE helps differentiate infarction (typically

starting in the subendocardium and involving a coronary territory)

from other forms of infiltrative or inflammatory cardiomyopathies

(typically involving the mid- or subepicardial layers without following

a coronary distribution) (Fig. 241-28). In addition, it can assess the

presence of myocardial edema using T1 or T2 tissue mapping methods

to provide information about the chronicity of ACSs or noncoronary

inflammatory conditions (e.g., myocarditis). Other methods such as

T2*

 mapping of myocardial iron deposition assess the extent of iron

infiltration that can lead to cardiac toxicity. Infiltrative cardiomyopathy

such as amyloidosis typically has a restrictive cardiomyopathy pattern

characterized by biventricular increased wall thickness and bilateral


Noninvasive Cardiac Imaging: Echocardiography, Nuclear Cardiology, and Magnetic Resonance/Computed Tomography Imaging

1851CHAPTER 241

Contrast-enhanced MRI

Positron emission tomography

Perfusion

Perfusion

Metabolism

Metabolism

FIGURE 241-27 Examples of myocardial viability patterns obtained with cardiac magnetic resonance imaging (MRI) and positron emission tomography (PET) in three

different patients with coronary artery disease. The top panel demonstrates extensive late gadolinium enhancement (bright white areas) involving the anterior, anteroseptal,

and apical left ventricular walls (arrows), consistent with myocardial scar and nonviable myocardium. The lower left panel demonstrates rubidium-82 myocardial perfusion

and 18F-fluorodeoxyglucose (FDG) images showing a large and severe perfusion defect in the anterior, anterolateral, and apical walls, indicating preserved glucose

metabolism (so-called perfusion-metabolic mismatch) consistent with viable myocardium. The right lower panel shows similar PET images demonstrating concordant

reduction in perfusion and metabolism (so-called perfusion-metabolic match) in the lateral wall, consistent with nonviable myocardium.

atrial enlargement, as assessed by both echocardiography and CMR.

CMR of patients with cardiac amyloidosis often also demonstrates a

characteristic pattern of diffuse endocardial infiltration of the left ventricle and the atria (Fig. 241-28). On strain echocardiography, patients

with cardiac amyloidosis show a reduction in systolic function, which

typically spares the apical left ventricular segments. Bone scintigraphy

complements the use of echocardiography and CMR in cardiac amyloidosis by allowing accurate noninvasive distinction of transthyretin

(ATTR) from light chain (AL) cardiac amyloidosis: ATTR typically

shows intense 99mTc tracer uptake compared to patients with AL amyloidosis (Fig. 241-29). Hypertrophic cardiomyopathy has variable

degree of increased ventricular thickness and often is seen to have

outflow obstruction and intense LGE in regions with marked hypertrophy (Fig. 241-30). CMR also can quantify myocardial iron content in

patients at risk of iron-overload cardiomyopathy (Video 241-7).

PET metabolic imaging has a complementary role in the evaluation

of inflammatory cardiomyopathies, especially sarcoidosis where the

presence of focal and/or diffuse glucose uptake can help identify areas

of active inflammation. In addition, for patients undergoing immunosuppressive therapy, PET is frequently used to monitor therapeutic

response (Fig. 241-31). In patients with ischemic cardiomyopathy,

radionuclide imaging in general and PET in particular are frequently

used to quantify the presence and extent of myocardial ischemia and

viability to assist with clinical decision making related to myocardial

revascularization (Fig. 241-26).

■ ASSESSING CARDIAC FUNCTION IN PATIENTS

UNDERGOING CANCER TREATMENT

Therapies used to treat cancer can adversely affect the cardiovascular

system. As the efficacy of cancer treatment and survival improve, many

patients are presenting with late adverse consequences from chemotherapy and/or radiation therapy on cardiovascular function. Thus,

the morbidity and mortality from late cardiovascular complications

threaten to offset the early gains in cancer survival, especially among

children and young adults. Early recognition and treatment of cardiomyocyte injury are critical for successful application of preventative

therapies but difficult because the adverse effects on cardiac function

are a relatively late manifestation after exposure to anticancer therapy.

The accepted standard for clinical diagnosis of cardiotoxicity is

defined as a >5% reduction in LVEF to <55% with symptoms of heart

failure, or a >10% drop in LVEF to <55% in patients who are asymptomatic. Thus, noninvasive imaging plays a major role in diagnosing

and monitoring for cardiac toxicity in patients undergoing cancer

treatment. Radionuclide angiography has been the technique of choice

for quite some time. However, echocardiography now plays a major

role in this application.

Recently, more novel imaging approaches have been advocated,

including deformation imaging with echocardiography and fibrosis

imaging with CMR. These techniques have shown promising results in

experimental animal models and in humans. In addition, there are also

proof-of-concept studies in animal models using molecular imaging

approaches targeting the mechanisms of cardiac toxicity (e.g., apoptosis and oxidant stress), which can presumably provide the earliest signs

of the off-target effects of these therapies. However, these techniques

are currently considered experimental.

■ PERICARDIAL DISEASE

The fibroelastic pericardial sac surrounding the heart consists of a

visceral, or epicardial, layer and a parietal layer, with a generally small

amount of pericardial fluid in between layers. The pericardium is

generally quite pliable and moves easily with the heart during contraction and relaxation. Abnormalities of the pericardium can affect

cardiac function primarily by impairing the heart’s ability to fill.

Inflammation of the pericardium can lead to an accumulation of fluid

between the two layers, or pericardial effusion, which can be visualized

by echocardiography, CMR, or CT. Other reasons for accumulation


1852 PART 6 Disorders of the Cardiovascular System

A

E F G

Anterior Lateral

B C D

FIGURE 241-29 Multimodality cardiac imaging in a 71-year-old man with history of atrial fibrillation, heart failure with preserved ejection fraction, numbness in his

fingers, a history of bilateral carpal tunnel surgery, and remote history of back surgery with L3 and S1 fusion. A. Two-dimensional echocardiogram demonstrating moderate

increase in left ventricular thickness with a visually estimated left ventricular ejection fraction of 45–50% and small pericardial effusion. B and C. Mitral inflow and tissue

Doppler demonstrating abnormal diastolic function (E/e′ was >20, consistent with elevated left ventricular filling pressure). D. Bull’s-eye strain map demonstrating abnormal

global longitudinal strain at the basal segments (pink and blue colors) with characteristic apical sparing (red color). E. Cardiac MRI study showing normal left ventricular

cavity size, mildly increased left ventricular mass, and mildly enlarged right and left atria. F. The MRI shows a large amount of diffuse late gadolinium enhancement of all

myocardial left ventricular segments, but it is more prominent in a circumferential subendocardial pattern (arrowheads). G. The 99mTc pyrophosphate images demonstrate

increased myocardial uptake of the radiotracer (uptake in the heart is greater than ribs, grade 3). (Images courtesy of Dr. Sarah Cuddy, Brigham and Women’s Hospital.)

FIGURE 241-28 Differentiation of various cardiomyopathies by cardiac magnetic resonance (CMR). The left upper panel shows the short-axis late gadolinium enhancement

(LGE) imaging of a patient who suffered an acute myocardial infarction. Note LGE of the endocardial myocardium in the inferior wall extending from the septum to the

lateral wall associated with myocardial thinning (arrows). The right upper panel shows the long-axis LGE imaging of a patient who has cardiac amyloidosis. Note the diffuse

LGE throughout left ventricular myocardium, the left atrium, and the interatrial septum (arrows). In addition, the blood pool is characteristically dark in signal indicating

sequestration of gadolinium contrast out of the blood pool after injection due to a high burden of amyloidosis in other organs. The left lower panel shows a cine diastolic

long-axis image of a patient with a nonischemic dilated cardiomyopathy. Note that there is extensive sponge-like noncompacted myocardium of the left ventricle (LV) as well

as dilatation of all four cardiac chambers. This patient has a nonischemic dilated cardiomyopathy secondary to LV noncompaction. The right lower panel shows a 22-yearold female patient with a recent episode of acute chest pain and troponin elevation. Note the multiple mid-wall foci of LGE, which suggests acute myocarditis (arrows). LA,

left atrium; RA, right atrium; RV, right ventricle.


Noninvasive Cardiac Imaging: Echocardiography, Nuclear Cardiology, and Magnetic Resonance/Computed Tomography Imaging

1853CHAPTER 241

LV

RV

FIGURE 241-30 This figure demonstrates three pulse sequence techniques by cardiac magnetic resonance that are often used to assess patients with hypertrophic

cardiomyopathy, all displayed in the mid short-axis scan plane. The center panel demonstrates that the left ventricle (LV) was markedly thickened in its wall thickness

especially in the LV septum (red arrows). This finding was matched by marked regions of late gadolinium enhancement (LGE), which was consistent with fibrosis in these

segments (right panel, white arrows). The left panel was cine myocardial tagging in the same slice plane. Myocardial tagging is used to assess the normal intramyocardial

strain by assessing distortion of the myocardial grids during systole. In this case, despite normal-appearing systolic radial wall thickening, the myocardial strain as assessed

by the distortion of grids was markedly reduced (left panel, white arrows). This finding is consistent with substantial myofibril disarray in the anterior and anteroseptal

segments in this patient. RV, right ventricle.

RV

Perfusion

Perfusion

Metabolism

Metabolism

Ant

Inf

Lat

21 22 23 24 25 26 27 28 29 30 31

24 25 26 27 28 29 30 31 32 33 34 35

34 35 36 37 38 39 40 41 42 43 44 45

38 39 40 41 42 43 44 45 46 47 48 49

Sep

LV

RV

LV

FIGURE 241-31 Representative cardiac magnetic resonance (CMR; top panel) and positron emission tomography (PET; lower panel) images from a 45-year-old male

presenting with complete heart block. The CMR images demonstrate extensive late gadolinium enhancement in the subepicardial left ventricular (LV) anterior and

anteroseptal walls and also in the right ventricular (RV) free wall (arrows). The PET images demonstrate extensive fluorodeoxyglucose uptake in the same areas, most

consistent with active inflammation due to sarcoidosis.

of pericardial fluid include infection, malignancy, and bleeding into

the pericardium. The latter can be the result of catastrophic processes

such as trauma, cardiac rupture, perforation in the setting of a cardiac

procedure, cardiac surgery, or dissection of the aorta with extension in

the pericardium.

Echocardiography remains the initial test of choice for assessing

pericardial disease, especially effusions (Fig. 241-32). Moreover,

echocardiography can be useful in evaluating for pericardial constrictive physiology, in which a thick noncompliant pericardium impairs

cardiac filling. The location, size, and physiologic consequences of

accumulated pericardial effusion can generally easily be determined

by echocardiography. Pericardial tamponade occurs when enough

pericardial fluid accumulates so that the intrapericardial pressure

exceeds filling pressures of the heart, generally the right ventricle. The

balance between intrapericardial pressure and ventricular pressure is

more important than the extent of fluid accumulation. Conditions in

which pericardial effusions accumulate over a long period of time, as

can be the case in the setting of malignant effusions, can lead to large

pericardial fluid accumulations without the classic hemodynamic

findings associated with pericardial tamponade. In contrast, rapid

accumulations of pericardial fluid, such as those that occur due to cardiac rupture or perforation, can lead to tamponade physiology without


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