Effect of left ventricular hypertrophy on long-term survival of patients with coronary artery disease following percutaneous coronary intervention

The impact of left ventricular hypertrophy (LVH) on survival among patients with established coronary artery disease (CAD) is not well understood. We sought to evaluate the effect of LVH on the survival of patients with CAD following percutaneous coronary intervention (PCI). Three hospitals in New York City contributed prospectively defined data on 4284 consecutive patients undergoing PCI. Allcause mortality at a mean follow-up of three years was the primary endpoint. LVH was present in 383 patients (8.9%). LVH patients had a greater prevalence of hypertension (88% vs. 68%, p<0.001), vascular disease (21% vs. 6.6%, p=0.001), and prior heart failure (10% vs. 5.5%, p<0.001). LVH patients presented less often with one-vessel disease (38% vs. 50%, p=0.040) and more often with two- (34% vs. 29%, p=0.014) or three-vessel (22% vs. 18%, p=0.044) disease. Ejection fractions and angiographic success were similar in both groups. In-hospital mortality did not differ between groups. At three-year follow-up, the survival rate for patients with LVH was 86% vs. 91% in patients without LVH (log-rank p=0.001). However, after adjustment for differences in baseline characteristics using Cox proportional hazards analysis, LVH was found not to be an independent predictor of mortality (hazard ratio, 0.93; 95% confidence interval, 0.68–1.28; p=0.67). We conclude that LVH at the time of PCI is not independently associated with an increase in the hazard of death at three years

Gender differences in left ventricular structure and function during antihypertensive treatment: the Losartan Intervention for Endpoint Reduction in Hypertension Study

Abstract—In hypertensive patients with left ventricular hypertrophy, antihypertensive treatment induces changes in left ventricular structure and function. However, less is known about gender differences in this response. Baseline and annual echocardiograms until the end of study or a primary end point occurred were assessed in 863 hypertensive patients with electrocardiographic left ventricular hypertrophy aged 55 to 80 years (mean: 66 years) during 4.8 years of randomized losartan- or atenolol-based treatment in the Losartan Intervention for Endpoint Reduction in Hypertension Echocardiography substudy. Left ventricular hypertrophy was diagnosed as left ventricular mass divided by height2.746.7 g/m2.7 and 49.2 g/m2.7 in women and men, respectively, and systolic function as ejection fraction and stress-corrected midwall fractional shortening. Women included more patients with obesity, isolated systolic hypertension, and mitral regurgitation (all P0.01). Ejection fraction, stress-corrected midwall shortening, and prevalence of left ventricular hypertrophy were higher in women at baseline and at the end of study (all P0.01). In particular, more women had residual eccentric hypertrophy (47 % versus 32%; P0.01) in spite of similar in-treatment reduction in mean blood pressure. In logistic regression, left ventricular hypertrophy at study end was more common in women (odds ratio: 1.61; 95 % CI: 1.16 to 2.26; P0.01) independent of other significant covariates. In linear regression analyses, female gender also predicted 2 % higher mean in-treatment ejection fraction and 2% higher mean stress-corrected midwall shortening (both 0.07; P0.01). Hypertensive women in this study retained higher left ventricular ejection fraction and stress-corrected midwall shortening in spite of less hypertrophy regression durin