Related Experiment Videos
Left ventricular mass regression in the LIFE study: effect of previous antihypertensive treatment
Gerard P Aurigemma1, Richard B Devereux, Kristian Wachtell
1Department of Medicine, Division of Cardiology, University of Massachusetts Medical School, Worcester, Massachusetts, USA. aurigemg@ummhc.org
Insights
Prior hypertension treatment does not affect baseline left ventricular (LV) mass or its reduction. Excluding previously treated patients in clinical trials for LV mass reduction is unnecessary when left ventricular hypertrophy is the criterion.
Area of Science:
- Cardiology
- Clinical Trials
- Hypertension Research
Background:
- Controversy exists regarding the inclusion of previously treated hypertensive patients in clinical trials for left ventricular (LV) mass reduction.
- The Losartan Intervention For Endpoint reduction (LIFE) study provides data to address this question.
Purpose of the Study:
- To investigate the relationship between prior hypertension treatment and baseline LV mass.
- To assess the impact of prior treatment on LV mass reduction over one year.
Main Methods:
- Analysis of clinical and echocardiographic data from 960 patients with electrocardiographically confirmed left ventricular hypertrophy in the LIFE study.
- LV mass was remeasured after one year in 847 patients, with 75% having prior hypertension treatment.
Main Results:
- Multivariable regression showed prior antihypertensive treatment was not associated with greater baseline LV mass or relative wall thickness.
- No significant differences were observed in the reduction of blood pressure, LV mass, or LV mass/body surface area between previously treated and untreated groups.
Conclusions:
- Prior hypertension treatment does not influence baseline LV mass or its reduction in patients with left ventricular hypertrophy.
- Future clinical trial designs do not need to restrict inclusion to previously untreated patients if left ventricular hypertrophy is the selection criterion.
Background:
Whether to include only those patients who have not had prior hypertension treatment in clinical trials of left ventricular (LV) mass reduction is controversial. Accordingly, our aim was to study the relationship between prior treatment and both baseline and 1-year echocardiographic LV mass in subjects enrolled in the Losartan Intervention For Endpoint reduction (LIFE) study.
Methods:
We studied clinical and baseline echocardiographic data on 960 patients with electrocardiographically confirmed left ventricular hypertrophy enrolled in the electrocardiographic substudy of the LIFE study, 847 of whom had LV mass remeasured after 1 year of blinded treatment. The majority (75%) of these patients had prior medical treatment for hypertension.
Results:
In multivariable regression analysis, controlling for age, sex, blood pressure (BP), body mass index, and indices of pump and myocardial function, prior antihypertensive treatment was not associated with either greater LV mass or relative wall thickness on the baseline study. Moreover, there was no significant difference between the 637 subjects who were previously treated and the 210 who were not treated with regard to the mean reduction in systolic or diastolic pressures (-25 +/- 17 v -24 +/- -16 and -13 +/- 9 mm Hg v -12 +/- 9 mm Hg), LV mass (-27 +/- 38 v -29 +/- 34 g), or LV mass/body surface area (-14 +/- 20 v -15 +/- 18 g/m(2)), all P >.05.
Conclusions:
Prior treatment is not associated with either greater LV mass or greater relative wall thickness when age, body mass index, sex, systolic BP, heart rate, or indices of LV volume load and systolic function are taken into account. In addition, prior treatment is not associated with lesser degrees of LV mass reduction. For design of future clinical trials, restriction of inclusion criteria to only previously untreated patients does not appear to be necessary when the selection criterion is electrocardiographically determined left ventricular hypertrophy.