Echocardiographic Evaluation of Diastolic Function in Special Populations.

Left ventricular (LV) diastolic dysfunction results from a combination of impaired relaxation, reduced restoring forces, and increased chamber stiffness. Noninvasive assessment of diastology uses a multiparametric approach involving surrogate markers of increased filling pressures, which include mitral inflow, septal and lateral annular velocities, tricuspid regurgitation velocity, and left atrial volume index. However, these parameters must be used cautiously. This is because the traditional algorithms for evaluating diastolic function and estimation of LV filling pressures (LVFPs), as recommended by the American Society of Echocardiography and European Association of Cardiovascular Imaging 2016 guidelines, do not apply to unique patients with underlying cardiomyopathies, significant valvular disease, conduction abnormalities, arrhythmias, LV assist devices, and heart transplants, which alter the relation between the conventional indexes of diastolic function and LVFP. The purpose of this review is to provide solutions for evaluating LVFP through illustrative examples of these special populations, incorporating supplemental Doppler indexes, such as isovolumic relaxation time, mitral deceleration time, and pulmonary venous flow analysis, as needed to formulate a more comprehensive approach.

Depressed right ventricular systolic function in heart failure due to constrictive pericarditis.

AIMS: Heart failure in constrictive pericarditis (CP) is attributed to impaired biventricular diastolic filling. However, diseases that cause CP due to myocardial infiltration and fibrosis can also impair biventricular systolic function (sf) and contribute to heart failure. This study of patients with CP examined biventricular sf and the effect of myocardial infiltration by pericardial diseases and the resulting fibrosis on ventricular sf. METHODS AND RESULTS: Histopathologic examinations of right ventricular (RV) and left ventricular (LV) myocardia and pericardia were performed on three autopsied hearts of patients with pericardial diseases. Additionally, in 40 adults with clinical heart failure and 40 healthy adults (controls), sf of both ventricles was examined by echocardiography, including strain measurements, and biventricular diastolic filling and pulmonary artery pressures were assessed by cardiac catheterization. Cardiac histopathology indicated thickening of the pericardium with fibrosis, disease infiltrating the myocardium, greater infiltration of the RV than the LV, and an association of pericardial thickness with myocardial infiltrations. Functional analysis indicated that RVsf was impaired on all echo indices, including strain measurement, but LVsf was preserved. CONCLUSIONS: Diseases causing CP are not restricted to the pericardium but also infiltrate the biventricular myocardium and affect the thin-walled RV more than the thick-walled LV, resulting in depressed RVsf. The present results help explain clinical heart failure in the presence of restricted diastolic filling in CP. Depression of RVsf due to progression of fibrosis in the RV myocardium may increase the risk of delayed pericardiectomy.