Left ventricular hypertrophy in aortic valve stenosis: preventive or promotive of systolic dysfunction and heart failure?

Abstract

In isolated AS, increased LV mass predicts the presence of systolic dysfunction and HF independent of the severity of valvular obstruction. LV hypertrophy may be maladaptive rather than beneficial in AS in man.

Selective homocysteine-lowering gene transfer attenuates pressure overload-induced cardiomyopathy via reduced oxidative stress

“…In patients with severe aortic stenosis, the degree of left ventricular hypertrophy independently predicts heart failure regardless of the degree of flow restriction imposed by the valve pathology [28]. Taken together, less pronounced left ventricular hypertrophy as observed following homocysteine lowering may be beneficial and may contribute to the improved cardiac function.…”

Left ventricular mass regression after sutureless implantation of the Perceval S aortic valve bioprosthesis: Preliminary results

“…Left ventricular (LV) hypertrophy is a recognized risk factor for cardiac morbidity and mortality [1,2]. Prognostic studies have given rise to the hypothesis that regression of LV hypertrophy is the underlying determinant of longevity after aortic valve replacement (AVR) for aortic stenosis (AS) [3][4][5][6].…”

Noninvasive cardiac output monitoring during general anesthesia for Cesarean delivery in a patient with severe aortic stenosis

“…13 In AS, an increase in left ventricular wall thickness and mass, i.e., ventricular hypertrophy, to maintain normal wall stress and unimpaired contractions may bring adverse consequences, such as a potential for cardiac ischemia and diastolic dysfunction. 15 Our patient had an elevated left ventricular mass index, but she did not meet established criteria for ventricular hypertrophy. 16 In the study by Tzemos et al, 40% of pregnant patients with AS had Fig.…”

“…This result contrasts with findings in older patients with AS where ventricular hypertrophy was associated with adverse outcomes. 15,17 Severe AS is thought to lead to a relatively fixed CO with an inability to increase stroke volume. Cardiac output is thus determined primarily by HR.…”