Absence of left ventricular hypertrophy in severe isolated aortic stenosis and preserved left ventricular systolic function.

BACKGROUND AND AIM OF THE STUDY: Recent evidence challenges the paradigm that left ventricular hypertrophy (LVH) is required to preserve left ventricular systolic performance in severe aortic stenosis (AS). The study aims were to determine the clinical, echocardiographic and prognostic implications in a cohort of patients with symptomatic severe AS, a preserved left ventricular ejection fraction (LVEF), and an absence of LVH. METHODS: Echocardiographic, clinical, aortic valve replacement (AVR)-related and all-cause death data were analyzed in 512 patients (253 males, 259 females; mean age 78.4 +/- 10.3 years) with severe AS and a preserved LVEF. Of these patients, 21% were enrolled prospectively, and the mean follow up was 40.4 +/- 32.5 months. RESULTS: By using the American Society of Echocardiography equation for left ventricular mass calculation, LVH was shown to be present in 330 patients (63%) and absent from 182 (36%). Typically, patients without LVH had a larger body surface area, were more often male, had a larger aortic valve area index (AVAi), and had similar LVEFs and rates of AVR as compared to those with LVH. A total of 59 deaths (32.4%) occurred among patients without LVH, and 134 (40.6%) among those with LVH (p = 0.07). When the left ventricular mass index (LVMi) was analyzed as a continuous variable, in both unadjusted and adjusted models for demographics, clinical characteristics, medications, AVAi, LVEF, and systemic vascular resistance, no association was found between LVMi and survival (p = 0.26). However, only patients with a normal LVMi and relative wall thickness had a survival benefit when compared to those with any pattern of abnormal left ventricular geometry (p = 0.01). CONCLUSION: LVH was absent in more than one-third of patients with severe AS, and was not associated with worse outcomes. A normal left ventricular geometry was associated with lower mortality rates, while AVR was associated with prolonged survival, regardless of LVMi. Mechanisms other than compensatory hypertrophy appear capable of offsetting the adverse effects of afterload excess in AS.