Left Ventricular Hypertrophy in Asymptomatic Nonsevere Aortic Stenosis

Abstract

Barasch and Reichek Left Ventricular Hypertrophy in Aortic StenosisEffects of Rosuvastatin (ASTRONOMER) trial, which examined patients with mild to moderate AS and a mean age of 50 years, progression of LVH occurred only in those without LVH at baseline. 17 The older population enrolled in SEAS study and some differences in the baseline characteristics may explain this discrepancy. Asymmetrical septal hypertrophy present in 22% of patients enrolled in SEAS was not discussed. Efforts to refine evaluation of LV remodeling patterns using cardiac magnetic resonance have included proposals to distinguish asymmetrical septal remodeling and hypertrophy, 11 mixed hypertrophy, physiological hypertrophy, eccentric remodeling, 18 and dilated hypertrophy (concentric and eccentric).19 Indeterminate hypertrophy, which together with dilated hypertrophy has been proposed as an eccentric hypertrophic pattern, is reportedly associated with the lowest risk for adverse outcomes when compared with other remodeling patterns. Perhaps in this study, the impact of LV mass index on outcome variables was independent of concentricity because of predominance of eccentric hypertrophy of dilated subtype, which in the Dallas Heart Study was associated with an 8-fold increase in incidence of heart failure and cardiovascular death compared with the non-LVH group (16.7% versus 2%, respectively). 19In addition to hypertension, the presence of mild to moderate AS contributed to variations in LV geometry in SEAS. Despite similar AS severity by valve area, the LVH group had other echocardiographic variables suggestive of greater stenosis severity compared with the normal LV geometry group: higher transvalvular gradients and lower energy loss index. The latter takes into account the ascending aortic area at the sinotubular junction, and if aortic valve area was similar, the ascending aorta had to be smaller in the LVH than in the non-LVH group. Therefore, the higher prevalence of aortic regurgitation in patients with LVH was probably unrelated to ascending aortic dilatation. Considering the known limitations of echocardiographic aortic valve area calculation, especially measurement of the LV outflow tract area, and the known discrepancies between different echocardiographic indices reflecting AS severity, one cannot completely exclude a higher severity of AS in the LVH group. The association of elevated LV mass index with adverse outcomes in SEAS might be related to the presence of LVH itself, given known correlates including changes in myocardial matrix with increased collagen deposition and extracellular volume, increased coronary vascular resistance and reduced myocardial perfusion reserve, subclinical LV systolic dysfunction expressed as reduced systolic strain, altered diastolic filling, and increased risk of ventricular arrhythmias. Other contributors may include aortic valve calcification, which was shown to be associated with a 50% higher risk of cardiovascular events in the Multi-Ethnic Study of Atherosclerosis (MESA), 20 subclinical coronary...

The Incremental Effect of Obesity on Myocardial Fibrosis In Patients with Aortic Stenosis

“…To compensate for chronic pressure overload in these subjects, LV wall thickness gradually increases in order to normalize wall stress, leading to concentric LV remodeling and hypertrophy 11)12)13). Activation of several biological processes including various hormones, growth factors and cytokines also contribute to protein genesis by promoting muscle cell growth, leading to structural alterations and remodeling 14)…”