Abstract 11940: Impact of Sarcomere Gene Mutations on Clinical Outcome of Left Ventricular Hypertrophy: Evidence from Comparison with Hypertension-related Hypertrophy
Background: Left ventricular hypertrophy (LVH) is known to be an independent risk factor for cardiovascular events. However, few data exist regarding the role of sarcomere gene mutations frequently associated with hypertrophic cardiomyopathy as an additional factor for the cardiovascular events in subjects with LVH. Therefore, we investigated the impact of sarcomere gene mutations of subjects with LVH on the incidence of cardiovascular events in multi-center prospective trial.
Methods and Results: We enrolled 256 subjects with LVH defined as maximal left ventricular wall thickness > 13 mm. All subjects underwent screening of sarcomere gene mutations. We divided the subjects into three groups; LVH with sarcomere gene mutations (group G, n=90, mean age 56 years), LVH with only hypertension (group NG, n=47, mean age 67), and LVH without sarcomere gene mutations nor hypertension (group U, n=103, mean age 62). Group G included gene mutations such as 29 subjects with MYBPC3, 23 with TNNI3, 10 with MYH7 and 4 with TNNT2. The follow-up survey was performed at the time of the enrollment and a year after. We compared the occurrence of cardiovascular events such as sudden cardiac death, ventricular tachycardia/fibrillation, admission for heart failure, and atrial fibrillation. With Kaplan-Meier analysis of subjects ≥ 50 years, the subjects in group G showed significantly more cardiovascular events and more admission for heart failure than those in group NG (log rank test p = 0.042 and p = 0.034, respectively, Figure), although there was no significant difference between these groups in all patients.
Conclusions: These results demonstrate that the sarcomere gene mutations aggravate the prognosis of subjects with LVH ≥ 50 years in the presence or absence of hypertension, probably due to extension of myocardial fibrosis.
- © 2012 by American Heart Association, Inc.