The Time Constant of Left Ventricular Relaxation

Abstract

Left ventricular (LV) diastolic dysfunction induces the increase of LV diastolic pressure and subsequently of left atrial and pulmonary capillary pressures independent of systolic function, resulting in the onset of heart failure. In the early 1990s, several clinical studies demonstrated that diastolic dysfunction is an independent prognostic factor in patients with heart failure with reduced ejection fraction (EF).1,2 In the past decade, many clinical studies have clarified that heart failure with preserved EF (HFPEF) accounts for ≈40% of heart failure and that its prognosis is as poor as heart failure with reduced EF.3 With the growing interest in HFPEF, the important role of diastolic dysfunction in the pathogenesis of heart failure has been realized again, because it is plausible that LV diastolic dysfunction is one of the principal causes for this phenotype of heart failure.4 Article see p 268 Major determinants of LV diastolic function are relaxation and stiffness.5 Despite the clinical requisite for their evaluation in understanding the pathophysiology of each patient with heart failure, there are no established indices for the noninvasive assessment of these factors. An invasive measure of LV pressure is required for the evaluation of LV relaxation, and the simultaneous recording of LV pressure and geometry is necessary for the assessment of LV stiffness. LV relaxation abnormality is likely to precede LV stiffening or systolic dysfunction during the development of chronic heart failure and has been assigned as a sensitive sign of LV dysfunction. Peak negative value of the first derivative of LV pressure (peak−dP/dt) has been used as a quantitative index for LV relaxation, but it depends on many other hemodynamic and functional factors. Weiss et al6 showed that the time course of isovolumic pressure decrease subsequent to peak−dP/dt is exponential and proposed the time …