Prognostic Significance of Left Ventricular Mass Change During Treatment of Hypertension
- Richard B. Devereux, MD;
- Kristian Wachtell, MD, PhD;
- Eva Gerdts, MD, PhD;
- Kurt Boman, MD;
- Markku S. Nieminen, MD;
- Vasilios Papademetriou, MD;
- Jens Rokkedal, MD;
- Katherine Harris, DrPH;
- Peter Aurup, MD;
- Björn Dahlöf, MD, PhD
- Author Affiliations: Department of Medicine, Cornell Medical Center, New York, NY (Dr Devereux); Department of Medicine, Glostrup University Hospital, Glostrup, Denmark (Drs Wachtell and Rokkedal); Haukeland University Hospital, Bergen, Norway (Dr Gerdts); Skellefteå Lasarett and Umea University, Skellefteå, Sweden (Dr Boman); Department of Cardiology, Helsinki University Central Hospital, Helsinki, Finland (Dr Nieminen); Veterans Administration Hospital, Washington, DC (Dr Papademetriou); Merck Research Laboratories, West Point, Pa (Drs Harris and Aurup); and Department of Medicine, Sahlgrenska University Hospital, Östra, and University of Göteborg, Göteborg, Sweden (Dr Dahlöf).
- Corresponding Author: Richard B. Devereux, MD, New York Presbyterian Hospital-Weill Cornell Medical Center, 525 E 68th St, New York, NY 10021 (rbdevere{at}med.cornell.edu).
Abstract
Context Increased baseline left ventricular (LV) mass predicts cardiovascular (CV) complications of hypertension, but the relation between lower LV mass and outcome during treatment for hypertension is uncertain.
Objective To determine whether reduction of LV mass during antihypertensive treatment modifies risk of major CV events independent of blood pressure change.
Design, Setting, and Participants Prospective cohort substudy of the Losartan Intervention For Endpoint Reduction in Hypertension (LIFE) randomized clinical trial, conducted from 1995 to 2001. A total of 941 prospectively identified patients aged 55 to 80 years with essential hypertension and electrocardiographic LV hypertrophy had LV mass measured by echocardiography at enrollment in the LIFE trial and thereafter were followed up annually for a mean (SD) of 4.8 (1.0) years for CV events.
Main Outcome Measures Composite end point of CV death, fatal or nonfatal myocardial infarction, and fatal or nonfatal stroke.
Results The composite end point occurred in 104 patients (11%). The multivariable Cox regression model showed a strong association between lower in-treatment LV mass index and reduced rate of the composite CV end point (hazard ratio [HR], 0.78 per 1-SD (25.3) decrease in LV mass index; 95% confidence interval [CI], 0.65-0.94; P = .009) over and above that predicted by reduction in blood pressure. There were parallel associations between lower in-treatment LV mass index and lower CV mortality (HR, 0.62; 95% CI, 0.47-0.82; P = .001), stroke (HR, 0.76; 95% CI, 0.60-0.96; P = .02), myocardial infarction (HR, 0.85; 95% CI, 0.62-1.17, P = .33), and all-cause mortality (HR, 0.72; 95% CI, 0.59-0.88, P = .002), independent of systolic blood pressure and assigned treatment. Results were confirmed in analyses adjusting for additional CV risk factors, electrocardiographic changes, or when only considering events after the first year of study treatment.
Conclusion In patients with essential hypertension and baseline electrocardiographic LV hypertrophy, lower LV mass during antihypertensive treatment is associated with lower rates of clinical end points, additional to effects of blood pressure lowering and treatment modality.
