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Greater regression of electrocardiographic left ventricular hypertrophy during hydrochlorothiazide therapy in
Peter M Okin1, Darcy A Hille, Sverre E Kjeldsen
1Greenberg Division of Cardiology, Weill Cornell Medical College, New York, New York, USA. pokin@med.cornell.edu
Insights
Hydrochlorothiazide (HCTZ) use significantly improved electrocardiographic left ventricular hypertrophy (LVH) regression. This effect was more pronounced in patients receiving losartan compared to atenolol, independent of blood pressure changes.
Area of Science:
- Cardiology
- Pharmacology
- Hypertension Research
Background:
- Losartan-based regimens showed greater regression of electrocardiographic (ECG) left ventricular hypertrophy (LVH) than atenolol in the LIFE study, irrespective of blood pressure (BP) changes.
- The independent effect of concomitant hydrochlorothiazide (HCTZ) therapy on LVH regression and its interaction with treatment arms was not previously examined.
Purpose of the Study:
- To investigate whether hydrochlorothiazide (HCTZ) therapy enhances left ventricular hypertrophy (LVH) regression independently of blood pressure (BP) changes.
- To determine if the effect of HCTZ on LVH regression differs between losartan- and atenolol-based treatment regimens.
Main Methods:
- Assessed changes in Cornell product and Sokolow-Lyon voltage LVH in 9,193 hypertensive patients randomized to losartan or atenolol.
- Hydrochlorothiazide (HCTZ) was added as needed to achieve target blood pressure (BP) goals per protocol.
Main Results:
- Hydrochlorothiazide (HCTZ) therapy was associated with greater regression of both Cornell product and Sokolow-Lyon voltage LVH at year-4 follow-up, after adjusting for multiple clinical factors.
- This LVH regression effect of HCTZ was significantly more pronounced in patients treated with losartan compared to those on atenolol (P < 0.001 for interaction).
Conclusions:
- Hydrochlorothiazide (HCTZ) use promotes greater regression of ECG-defined LVH.
- The beneficial effect of HCTZ on LVH regression is significantly enhanced when combined with losartan-based therapy versus atenolol-based therapy, independent of BP control and baseline LVH severity.
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.
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