Evaluation of the Patient with Diastolic Dysfunction

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3 Evaluation of the Patient with Diastolic Dysfunction

Restrictive Cardiomyopathy

Storage Endomyocardium

TABLE 3-2 OVERALL ECHOCARDIOGRAPHIC APPROACH FOR ASSESSING DIASTOLIC DYSFUNCTION

Modality View/Technique Findings
2D Apical, parasternal, subcostal
Pulsed wave Doppler 4-chamber: Ultrasound beam aimed at an angle of 20 degrees laterally to apex, and the sample volume between the tips of the mitral valve leaflets
Suprasternal short-axis
Subcostal
Tissue Doppler imaging 4-Chamber: 2-mm sample volume at the medial mitral annulus with the Doppler beam parallel to the longitudinal movement. Gain settings and wall filters should be low and velocity scale expanded. Varying E, E/E patterns (see text for details)

TABLE 3-3 Approaches and Findings in RCM

Modality General Findings Specific Findings
Chest radiograph Normal-sized heart.
Dilated atria.
Signs of pulmonary congestion or interstitial edema.
Pleural effusion may occur.
Mediastinal lymphadenopathy; pulmonary parenchymal disease in sarcoidosis.
Electrocardiogram Nonspecific ST- and T-wave abnormalities.
Conduction abnormalities.
Same chamber and wall dimensions and functions as in echocardiography.
Low voltage in precordial leads is seen in ~50% of patients with amyloidosis with cardiac involvement.
Pseudo-infarct pattern (QS wave in consecutive leads) is seen in ~50% of patients with cardiac amyloidosis.
Fibrosis caused by cardiac sarcoidosis can be detected with late gadolinium enhancement.
Trilaminar appearance (normal myocardium, thickened fibrotic endocardium, and overlying thrombus) may be detectable in endomyocardial diseases.
Global reduction in T2* cardiac tissue is commonly seen in hemochromatosis.
CT Same chamber and wall dimensions and functions as in echocardiography.  
Biposy In most cases nonspecific. Apple-green birefringence, electron microscopy findings in amyloidosis.
Radionuclide imaging Mainly nonspecific findings in RCM. With increased cardiac involvement in amyloidosis, Tc-99m labeled tracers are detectable.
Cardiac catheterization Nonspecific findings of diastolic dysfunction (increased diastolic pressures, right-sided square root sign, and often LVEDP ≥5 mm Hg greater than RVEDP).  

LVEDP, LV end-diastolic pressure; RVEDP, RV end-diastolic pressure; Tc-99m, 99-mtechnetium.

Specific Diagnoses

Hypertrophic Cardioymopathy

Overview of Echocardiographic Approach

Acquisition

Analysis/Pitfalls

A number of echocardiographic parameters (2D, M-mode, TDI, and strain) have been demonstrated to have diagnostic value in HCM.6

Differential Diagnosis

Alternative Approaches

Cardiac magnetic resonance imaging (MRI) has emerged as a useful tool for diagnosing HCM by the magnitude and distribution of hypertrophy7 and in prognosis (extent of delayed gadolinium enhancement, a radiographic surrogate for myocardial fibrosis, may predict sudden cardiac death).8

RCM versus Constrictive Pericarditis

Monitoring Effects of Treatment

Control of Blood Pressure (BP)

References

1 Nagueh SF, Lakkis NM, Middleton KJ, Spencer WH3rd, Zoghbi WA, Quiñones MA. Doppler estimation of left ventricular filling pressures in patients with hypertrophic cardiomyopathy. Circulation. 1999;99:254-261.

The first paper to identify Doppler parameters that accurately estimate filling pressures in HCM patients.

2 Nishimura RA, Appleton CP, Redfield MM, Ilstrup DM, Holmes DRJr, Tajik AJ. Noninvasive Doppler echocardiographic evaluation of left ventricular filling pressures in patients with cardiomyopathies: A simultaneous Doppler echocardiographic and cardiac catheterization study. J Am Coll Cardiol. 1996;28:1226-1233.

A definitive hemodynamic-echocardiographic correlation study demonstrating that E/A and DT are useful in predicting filling pressures in patients with systolic dysfunction, but not in patients with HCM.

3 Ho CY, Sweitzer NK, McDonough B, et al. Assessment of diastolic function with Doppler tissue imaging to predict genotype in preclinical hypertrophic cardiomyopathy. Circulation. 2002;105:2992-2997.

A small study demonstrating the feasibility of detecting abnormal diastolic function in gene-positive but phenotypically normal subjects with a α-myosin heavy chain mutation.

4 Ho CY, Carlsen C, Thune JJ, et al. Echocardiographic strain imaging to assess early and late consequences of sarcomere mutations in hypertrophic cardiomyopathy. Circ Cardiovasc Genet. 2009;2:314-321.

A comprehensive echocardiographic analysis of a large cohort of genotyped individuals with HCM. The authors validate that E, but not systolic strain or strain rate, is reduced in preclinical HCM, whereas individuals with overt hypertrophy have abnormal systolic mechanics as well as diastolic abnormalities, despite a normal EF.

5 Nagueh SF, Lakkis NM, Middleton KJ, et al. Changes in left ventricular diastolic function 6 months after nonsurgical septal reduction therapy for hypertrophic obstructive cardiomyopathy. Circulation. 1999;99:344-347.

This paper documents marked improvements in diastolic function following septal reduction in a small cohort of patients with hypertrophic obstructive cardiomyopathy.

6 Afonso LC, Bernal J, Bax JJ, Abraham TP. Echocardiography in hypertrophic cardiomyopathy: The role of conventional and emerging technologies. JACC Cardiovasc Imaging. 2008;1:787-800.

A concise overview of echocardiographic findings in HCM with an emphasis on novel modalities such as strain imaging.

7 Rickers C, Wilke NM, Jerosch-Herold M, et al. Utility of cardiac magnetic resonance imaging in the diagnosis of hypertrophic cardiomyopathy. Circulation. 2005;112:855-861.

In a small minority of patients, cardiac MRI was able to detect regions of LV hypertrophy not readily detected by echocardiography. Echocardiography tends to underestimate the magnitude of hypertrophy, especially in the anterolateral free wall.

8 O’Hanlon R, Grasso A, Roughton M, et al. Prognostic significance of myocardial fibrosis in hypertrophic cardiomyopathy. J Am Coll Cardiol. 2010;56:867-874.

One of several single-center studies showing that myocardial fibrosis measured by late gadolinium enhancement is an independent predictor of adverse cardiac outcomes. The study is limited by a small number of clinical events and relatively short follow-up.

9 Lang RM, Bierig M, Devereux RB, et al. Recommendations for chamber quantification: A report from the American Society of Echocardiography’s Guidelines and Standards Committe and the Chamber Quantification Writing Group, developed in conjunction with the European Association of Echocardiography, a branch of the Europena Society of Cardiology. J Am Soc Echocardiogr. 2005;18:1440-1463.

Extensive recommendations for echocardiographic measurement of heart chambers and aorta, with reference values.

10 Borlaug BA, Melenovsky V, Redfield MM, et al. Impact of arterial load and loading sequence on left ventricular tissue velocities in humans. J Am Coll Cardiol. 2007;50:1570-1577.

This detailed and well-conducted study in human subjects convincingly demonstrates that late systolic loading and arterial compliance influence both systolic and diastolic tissue velocities.

11 Tapp RJ, Sharp A, Stanton AV, et al. Differential effects of antihypertensive treatment on left ventricular diastolic function: an ASCOT (Anglo-Scandinavian Cardiac Outcomes Trial) substudy. J Am Coll Cardiol. 2010;55:1875-1881.

This interesting ASCOT substudy shows a statistically significant improvement in E, E/E, and brain natriuretic peptide (BNP) with amlodipine versus atenolol, despite similar BP reductions. The clinical implications of these findings merit further investigation.