Left ventricular chamber stiffness at rest as a determinant of exercise capacity in heart failure subjects with decreased ejection fraction

Abstract

. Left ventricular chamber stiffness at rest as a determinant of exercise capacity in heart failure subjects with decreased ejection fraction. J Appl Physiol 97: 1667-1672. First published June 18, 2004 doi:10.1152/japplphysiol.00078.2004.-Impaired exercise tolerance, determined by peak oxygen consumption (V O2 peak), is predictive of mortality and the necessity for cardiac transplantation in patients with chronic heart failure (HF). However, the role of left ventricular (LV) diastolic function at rest, reflected by chamber stiffness assessed echocardiographically, as a determinant of exercise tolerance is unknown. Increased LV chamber stiffness and limitation of V O2 peak are known correlates of HF. Yet, the relationship between chamber stiffness and V O2 peak in subjects with HF has not been fully determined. Forty-one patients with HF New York Heart Association [(NYHA) class 2.4 Ϯ 0.8, mean Ϯ SD] had echocardiographic studies and V O2 peak measurements. Transmitral Doppler E waves were analyzed using a previously validated method to determine k, the LV chamber stiffness parameter. Multiple linear regression analysis of V O2 peak variance indicated that LV chamber stiffness k (r 2 ϭ 0.55) and NYHA classification (r 2 ϭ 0.43) were its best independent predictors and when taken together account for 59% of the variability in V O2 peak. We conclude that diastolic function at rest, as manifested by chamber stiffness, is a major determinant of maximal exercise capacity in HF. diastole; echocardiography; oxygen consumption CHRONIC HEART FAILURE (HF) is a major health problem that carries a high mortality rate despite continued significant advances in medical therapy. With ϳ400,000 new cases of HF diagnosed each year, 4.7 million Americans suffer from this debilitating disease (1). It has been established that patients with HF have impaired exercise tolerance that is predictive of mortality and the need for cardiac transplantation (10). Characteristically, the failing heart demonstrates an inability to maintain an adequate cardiac output, first during effort and later also at rest. Cardiac decompensation ultimately leads to impaired exercise capacity, fatigue, and exertional dyspnea. Patients with HF thus may have a decreased left ventricular (LV) ejection fraction (LVEF), large end-diastolic volume, and impaired contractile reserve (33, 34). Ventricular dysfunction as quantitated by a decreased LVEF is the main manifestation of HF that ultimately results in circulatory failure. Advanced LV dysfunction is associated with a variety of neurohumoral, peripheral circulatory, skeletal muscle, and respiratory adaptations that determine the syndrome's overall clinical presentation and prognosis (33, 34). The known mechanisms that lead to HF are highly complex, involving chamber enlargement and remodeling and decreased LV contractile reserve (10). The factor common to all types of HF regardless of etiology is increased LV end-diastolic pressure (LVEDP), which compromises LV filling, diminishes stroke volume and cardiac outpu...

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Diastolic ventricular-vascular stiffness and relaxation relation: elucidation of coupling via pressure phase plane-derived indexes

“…Data from 13 patients were selected from an existing Cardiovascular Biophysics Laboratory database of simultaneous high-fidelity micromanometric pressure and Doppler echocardiography recordings (3,9,34,38,39,49). Subjects were chosen specifically because of good-quality (low noise) data; demographics are listed in Table 1.…”

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