Background
Treatment of hypertensive patients with a losartan-based regimen was associated with greater regression of electrocardiographic (ECG) left ventricular hypertrophy (LVH) than atenolol-based therapy in the Losartan Intervention for Endpoint Reduction in Hypertension (LIFE) study, independent of blood pressure (BP) changes. However, whether concomitant hydrochlorothiazide (HCTZ) therapy in >70% of LIFE patients was associated with greater regression of LVH independent of BP changes and whether this effect differed between treatment arms has not been examined.
Methods
Changes in Cornell product and Sokolow–Lyon voltage LVH were assessed in 9,193 hypertensive patients randomly assigned to treatment with losartan or atenolol, with additional HCTZ therapy added as necessary to achieve target BP goal per study protocol.
Results
After controlling for baseline and change in systolic and diastolic pressure, age, sex, race, prior antihypertensive treatment, baseline and year-4 body mass index and baseline LVH by either Cornell product or Sokolow–Lyon voltage, at year-4 follow-up HCTZ therapy was associated with greater regression of Cornell product LVH (−244 ± 788 vs. −172 ± 771 mm·msec, P < 0.05) and Sokolow–Lyon voltage (−4.2 ± 6.7 vs. −3.0 ± 7.0 mm, P < 0.001) and this effect was significantly greater in patients on losartan (−341 ± 743 vs. −189 ± 775 mm·msec and −5.2 ± 6.6 vs. −3.3 ± 6.6 mm) than in patients on atenolol (−142 ± 822 vs. −158 ± 765 mm·msec and −3.1 ± 6.6 vs. −2.7 ± 7.4 mm; both P < 0.001 for interaction of HCTZ with losartan vs. atenolol therapy).
Conclusions
HCTZ use was associated with greater regression of ECG LVH and this effect was greater in patients on losartan- than atenolol-based therapy, independent of baseline severity of ECG LVH and hypertension and changes in BP.