1. Answer: B. Contractility is a term that is often misused to describe systolic function. In fact, this parameter describes systolic function independent of loading. Changes in cardiac function can be attributed to alterations in contractility if heart rate, conduction velocity, preload, and afterload are held constant. Strain rate corresponds to the contractility marker, dp/dt. In contrast, ejection fraction, strain, and the Tei index are load-dependent. Although LV dp/dt can be measured from the MR jet, this is restricted to when an MR signal is available and may be compromised in severe MR, as the calculation assumes that LA pressure is zero.

2. Answer: E. The diagnosis of RV infarction should be suspected with hemodynamic changes in a patient after inferior MI, and echocardiography is confirmatory in a qualitative sense. The problem relates to quantitation—the RV is a nongeometric chamber and 2D volumes are often underestimated because images are frequently off-axis. Depending on whether end-systolic and end-diastolic volumes are underestimated to the same degree (they may not be), 2D-EF may even vary according to view. TAPSE, RV S′, and strain reflect longitudinal displacement. Although they offer a means of overcoming the geometric limitations of EF calculation in global RV dysfunction, they are regional measures that may be influenced by the site of MI. Potentially, they might be averaged over multiple segments (this necessitates an RV view orthogonal to the standard 4-chamber view). The Tei index is also a reasonable choice, as it is independent of RV geometry but is not purely a measure of systolic function.

RV systolic function is notoriously difficult to quantify! There is evidence that the use of 3D echocardiography (3DE) can overcome the complexities that derive from its crescentic and irregular shape, and very likely RV evaluation will become an important indication for 3DE.

3. Answer: A. Wall stress appears to be a determinant of local remodeling and the development of cell therapies will eventually mandate an approach to the measurement of this entity. Wall stress is proportionate to transmural pressure and chamber size and inversely related to wall thickness. However, accurate quantification of wall stress using the law of Laplace without cognizance of material properties is now looked upon as an oversimplification. Moreover, although global equations for stress are described, regional stress varies in accordance with regional curvature. The measurement of wall stress is one of the Holy Grails of hemodynamic assessment and should be matched to systolic strain—although there are sufficient ranges of error with the measurement of both as to make this correlation difficult with current technologies.

4. Answer: E. Visual EF should not be considered the “standard of care”; current guidelines propose the biplane Simpson method as the methodology of choice for volume and EF measurement and support the use of 3D echocardiography when possible. Accuracy and reproducibility are especially important when echo measurements of EF may be a component of major decisions, such as suitability for implantable defibrillator or cardiac resynchronization devices. However, although quantitation is accepted as the preferred method, this may not be achievable under all circumstances. As in other qualitative assessments in echocardiography, an expert eye has been shown to be analogous to the trackball for EF measurements, and it is dependent on image quality. Extremes of heart rate can make the assessment challenging and the tomographic approach to the postinfarct ventricle is important.

Although quantitation is accepted as the preferred method, potential problems with respect to spatial and temporal resolution need to be considered. Concerns about spatial resolution can be addressed by appropriate depth and zoom; LV opacification should be considered if two or more myocardial segments are inadequately visualized. Temporal resolution is an issue to the extent that the time course of contraction is neglected by assessment of only end-diastolic and end-systolic images, and global strain or similar parameters may help address this.

5. Answer: C. Wall motion abnormalities are usually identified with thickening of <50% or excursion <5 mm. They are not necessarily a marker of abnormal myocardium (normal inferior and posterior walls in particular may be hypokinetic) and do not necessarily indicate ischemia (they may be pre-existing). Wall thickening (rather than motion or timing) is interpretable with a LBBB. The extent and severity of wall motion abnormality have similar prognostic values to ejection fraction.

6. Answer: C. The benefit of AV optimization is supported by its performance in the landmark CRT studies and smaller trials. The most feasible is the iterative technique for AV optimization. This involves pulsed Doppler mitral inflow estimation, with shortening and lengthening of AV delay, and observation of the morphology of the transmitral filling wave. If AV delay is too short, ventricular activation will occur before completion of the mitral A-wave. If AV delay is too long, ventricular systole will encroach on diastolic filling time. At the optimal setting of paced AV delay, the time-velocity integral of transmitral flow will be optimized, with no truncation of the mitral A-wave (see Fig. 12-19).

Patient selection for CRT is based on clinical, ECG and ejection fraction criteria. Despite the best efforts for appropriate selection, 30% of implanted subjects fail to demonstrate a symptomatic or physiologic response to CRT. Enthusiasm for using measures of mechanical synchrony has abated since the report of the PROSPECT trial. Indeed, consideration of the variability of both synchrony and response markers (e.g., LV volumes) suggests that the expected levels of accuracy of LV synchrony markers are unattainable.

The site of previous infarction and position of the LV lead are pertinent to response but less so to optimization. The adverse effects of extensive scarring and lead malposition on CRT response have been shown by studies showing response to be predicted by concordance between pacing site and strain magnitude and/or time to maximal delay.

7. Answer: D. The assessment of LV volumes carries incremental prognostic information to ejection fraction alone. Angiographic data have shown that in patients with mild LV dysfunction, end-systolic volume (ESV) <95 mL is associated with a 5-year mortality of 10%, but more dilated ventricles are associated with a much worse outcome (30%), and similar findings have been described with echocardiography. Because of avoidance of geometric assumptions, 3D echocardiography may be especially useful for assessment of volumes (see Fig. 12-20). The evidence of incremental information on the basis of LV volumes is an argument for more accurate LV volume calculations (e.g., with 3D echocardiography). Importantly, these studies have assessed systolic volume rather than diastolic volume, which may be increased in the setting of mitral regurgitation.

8. Answer: D. Repeat 2D echocardiography—although often performed for the reassessment of LV function—is not a sensitive or reliable tool for this purpose. The 95% confidence intervals for EF are ±11% and those for LV mass are ±60 g. Both are large changes in biologic terms, meaning that minor changes (such as may occur from year to year in the progression of heart failure—may be 5%, or in response to antihypertensive therapy over a year or two—may be 20 g) are well under the limits of variability of the measurement. The resulting changes are more meaningful in populations than they are in individuals.

Sources of variability include not only intra- and interobserver variation, acquisition issues (equipment and sonographers), regression to mean, and biologic variation. As some of this variation arises from differences in imaging axis between studies, it is potentially reducible using 3D imaging techniques, and there is some evidence to support this.

9. Answer: B. Strain can be considered as an analog of regional ejection, as it reflects shortening from the beginning to the end of systole. Reduced preload—which is associated with reduced LV cavity size—will reduce strain, reflecting the lower position of the ventricle on the Frank-Starling curve as well as the lower deformation of an already empty LV cavity. Conversely, reduction of afterload is associated with increased strain, reflecting the lower impedance to LV ejection. Higher heart rate is associated with a reduction of LV filling and reduced strain. These observations are important in understanding the strain and strain rate response to dobutamine stress. Strain rate (which is time dependent) shows a linear increment with dobutamine, whereas strain increases initially but decreases toward peak dose, as the stroke volume falls at higher heart rates.

10. Answer: D. The use of M-mode LV dimensions as the serial marker of LV size in regurgitant valve lesions risks potentially misleading data from off-axis imaging. The underestimation of LV volumes using 2D imaging is reduced by LV opacification, probably because the sonographer becomes more able to identify the true apex and avoid foreshortening. Probably for similar reasons, 3D echocardiography also avoids the underestimation of LV volumes. The combination of 3D imaging and LV opacification offers LV volumes that are closest to those provided by cardiac magnetic resonance.

11. Answer: A. The ability to derive strain from 2D images (rather than tissue Doppler, which is directional) has enabled strain assessment in not only the longitudinal but also radial and circumferential planes. Subendocardial dysfunction causes a reduction of longitudinal function (as subendocardial fibers have a longitudinal orientation). Infarctions of relatively limited extent may cause a reduction in longitudinal strain, and the susceptibility of this to worsening strain in proportion to the infarct extent is not completely clear. However, the degree of reduction of circumferential and transverse strain is related to the transmural extent of subendocardial dysfunction (see Fig. 12-21).

Real-time perfusion imaging has been used to delineate the extent of subendocardial scar, as flow and function can be appreciated in the same sequence (triggered imaging provides perfusion data alone). Calibrated integrated backscatter offers a means of defining the reflectivity of myocardium relative to an external frame of reference (e.g., pericardium). Although this technique has been used to define scar and viable tissue, anisotropy makes this difficult to interpret in other than the parasternal long-axis views.

12. Answer: C. There has been a prolific expansion of new technologies, and it has been difficult to keep track of which modality can help with which clinical question. Generally, tissue velocity has been useful for timing (e.g., synchrony) and measurement of global phenomena (e.g., e′ velocity), but it is subject to tethering by adjacent segments, so it is not a good marker of segmental function. Accurate volumetric measurements are possible with 3D, but at a low temporal resolution—although there are no data to confirm this, it seems unlikely this modality will be useful for the assessment of diastolic function, where the time for volume changes is critical. Deformation analysis with speckle strain can provide information on the transmural distribution of scar, and the response to low-dose dobutamine has been quantified with both tissue velocity and speckle strain (see Table 12-1).

13. Answer: E. The ongoing adverse outcomes associated with heart failure have spurred an increasing interest in recognition of the earlier stages of heart failure and attempts to prevent progression. The main contribution of tissue velocity has been for the assessment of tissue e′, which is a sensitive marker of myocardial impairment that may be reduced even in the presence of risk factors, and in the estimation of LV filling pressure, which may support the diagnosis of later-stage heart failure. Myocardial strain may be a sign of preclinical dysfunction in early-stage disease, although its ability to quantify scar may also make it helpful in later disease. The main contributions of LV volume calculation are of most value in late-stage disease, where the LV cavity is dilated and EF reduced (see Table 12-2).

14. Answer: C.

Relative wall thickness (RWT) = 2 × PWd/LVd = 2 × 13/52 = 0.5.

LV mass = 1.04([LVd + IVS + PW]³ – LVd³) – 13.6 = 1.04(7.7³ – 5.2³) – 13.6 = 315 g (or 175 g/m² for BSA – 1.8 m²)

Both LV mass and LV geometry are important determinants of outcome. In this patient, both LV mass and relative wall thickness are increased, indicating concentric LVH. Concentric remodeling (wall thickening without increased mass) is also associated with adverse outcome (Fig. 12-22).

15. Answer: E. All of the above. Generally, an EF of ˜35% corresponds to a strain of ˜12%, so this case exemplifies a situation in which the degree of GLS impairment exceeds what might be expected from a relatively minor regional wall motion abnormality. GLS may be impaired by a variety of causes of subclinical LV dysfunction (impairment in asymptomatic individuals with normal ejection fraction), which may have preceded the ACS. Importantly, strain is an independent determinant of outcome, especially in the normal or near-normal LV.

16. Answer: B. The development of a systolic murmur postinfarction may be due to mitral regurgitation or a VSD. In contrast to congenital VSDs, postinfarct VSDs are identified within areas of wall motion abnormality and are often irregularly shaped. Cardiac magnetic resonance is an alternative diagnostic approach, but the defects are normally readily visualized by transthoracic echocardiography. The use of 3D echocardiography may minimize the possibility of missing multiple defects, which may be important in planning device closure.

17. Answer: C. The pattern of apical thickening is typical of apical HCM. Like other localized abnormalities, these may be more readily recognized with contrast (or magnetic resonance imaging). This condition is most commonly an incidental ECG finding, based on giant negative T waves (1-4 mV). These findings usually evolve over several years, although they can be abrupt. Apical HCM is generally benign, although heart failure may occur because of atrial fibrillation and LV aneurysm.

The alternative responses (apical fibroma or muscular band) would be expected to be more localized. Apical foreshortening is a potential consideration, but the ventricular length seems normal. Noncompaction cardiomyopathy is associated with apical thickening but does not encroach on the cavity and is characterized by deep apical trabeculations.