Abstract 14719: Left Ventricular Hypertrophy With Strain is Associated With Increased Myocardial Injury and Fibrosis in Patients With Aortic Stenosis
OBJECTIVES: In patients with aortic stenosis (AS), left ventricular hypertrophy (LVH) with strain on electrocardiogram (ECG) is associated with an adverse prognosis. However the mechanism for this pattern is unknown. We sought to investigate the association of LVH strain with structural abnormalities on cardiovascular magnetic resonance (CMR) and serum cardiac troponin I (cTnI) concentrations.
METHODS: Patients with AS and no prior myocardial infarction were prospectively recruited. LVH on ECG was defined by Sokolow-Lyon and Cornell voltage criteria, and strain was identified by ST depression or T wave inversion in leads V4-V6. Standard echocardiographic indices were used to assess AS severity (iE33, Philips Medical Systems). Indexed left ventricular mass (LVMi) and volumes were measured using 3T CMR (MAGNETOM Verio, Siemens AG). Myocardial late gadolinium enhancement (LGE) was performed using inversion recovery gradient echo and phase sensitive inversion recovery sequences. Presence of LGE was evaluated by two independent observers 8-15 min following gadobutrol 0.1 mmol/kg. Serum cTnI concentrations were determined using the ARCHITECT STAT high-sensitive troponin I assay (Abbott Laboratories).
Results: Seventy patients were recruited (44 males; 72 years old; aortic jet velocity 3.6±0.8m/s). Patients with LVH with strain (n=8) had higher LVMi and more severe AS (both p<0.01) than subjects without LVH (n=40) and those with LVH but no strain (n=22). All patients with strain had mid-wall LGE (negative and positive predictive values of 73% and 100%, respectively). Moreover serum cTnI concentrations in patients with strain were 4-fold higher compared to other groups [median cTnI concentration, ng/L (IQR): LVH with strain, 18.6 (9.5, 49.2); LVH without strain, 4.5 (3.5, 7.8); no LVH, 4.7 (2.6, 9.9) p<0.01].
Conclusions: Patients with AS and LVH with strain have evidence of increased myocardial injury and fibrosis, which may explain their adverse prognosis.
- © 2013 by American Heart Association, Inc.