Left atrial systolic force and outcome in asymptomatic mild to moderate aortic stenosis. Academic Article uri icon

Overview

abstract

  • BACKGROUND AND AIMS: In patients with chronic pressure overload due to hypertension or aortic valve stenosis (AS), higher left atrial systolic force (LASF) is associated with a high-risk cardiovascular (CV) phenotype. We tested LASF as prognostic marker in patients with AS. METHODS: We used baseline and outcome data from 1,566 patients recruited in the Simvastatin and Ezetimibe in AS (SEAS) study evaluating the effect of placebo-controlled simvastatin and ezetimibe treatment on CV events. The primary outcome was a composite of major CV events, including CV death, aortic valve replacement, nonfatal myocardial infarction, hospitalization for unstable angina, heart failure caused by progression of AS, coronary artery bypass grafting, percutaneous coronary intervention, and nonhemorrhagic stroke. LASF was calculated by Manning's method. High LASF was defined as >95th percentile (50 Kdynes/cm(2)) of the distribution within the study population. RESULTS: During 4.3 years of follow-up, a major CV event occurred in 38 of 78 patients with high LASF (49%) and in 513 of 1,488 (34%) with normal LASF (P = 0.01). In multivariate Cox regression analysis, high LASF predicted higher rate of major CV events (Hazard ratio 1.43 [95% confidence interval 1.01-2.03] independent of aortic valve area and LV mass index. A simple risk score including absence or presence of these three variables allowed risk stratification into low, intermediate, high and very high risk for major CV events during follow-up (22%, 28%, 38%, and 53%, respectively). CONCLUSIONS: Higher LASF provides additional prognostic information in patients with asymptomatic mild-to-moderate AS.

publication date

  • June 7, 2012

Research

keywords

  • Aortic Valve Stenosis
  • Heart Atria
  • Hypolipidemic Agents

Identity

Scopus Document Identifier

  • 84867404398

Digital Object Identifier (DOI)

  • 10.1111/j.1540-8175.2012.01744.x

PubMed ID

  • 22676207

Additional Document Info

volume

  • 29

issue

  • 9