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- Okin, P. M., et al.
(författare)
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Greater regression of electrocardiographic left ventricular hypertrophy during hydrochlorothiazide therapy in hypertensive patients
- 2010
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Ingår i: American Journal of Hypertension. - : Oxford University Press (OUP). - 0895-7061 .- 1941-7225. ; 23:7, s. 786-793
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Tidskriftsartikel (refereegranskat)abstract
- 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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- Wiik, B. P., et al.
(författare)
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Serum uric acid is associated with new-onset diabetes in hypertensive patients with left ventricular hypertrophy: The LIFE Study
- 2010
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Ingår i: American Journal of Hypertension. - : Nature Publishing Group. - 0895-7061 .- 1941-7225. ; 23:8, s. 845-851
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: It is unclear whether serum uric acid (SUA) is associated with development of new-onset diabetes (NOD) in patients with hypertension and left ventricular hypertrophy (LVH). The aim of the present investigation was to test the hypothesis that SUA predicts development of NOD in these patients. METHODS: In the Losartan Intervention For Endpoint reduction in hypertension (LIFE) study, a double-masked, parallel-group design, 9,193 patients with hypertension and electrocardiographic LVH were randomized to losartan- or atenolol-based antihypertensive treatment and followed for a mean of 4.9 years. At baseline, 7,489 patients with available SUA measurements did not have diabetes mellitus and were thus at risk of its development during the study. We used Cox regression analyses to investigate whether SUA predicted development of NOD. RESULTS: NOD developed in 522 of 7,489 patients. The association between baseline SUA and development of NOD was significant (hazard ratio (HR) 1.29 per s.d. (1.3 mg/dl), 95% confidence interval (CI) 1.18-1.42, P < 0.001) after adjustment for treatment with losartan vs. atenolol, baseline serum glucose, urinary albumin/creatinine ratio, estimated glomerular filtration rate and Framingham risk score, time-varying systolic and diastolic blood pressure, and time-varying LVH by Cornell voltage-duration product and Sokolow-Lyon voltage. In parallel analyses, baseline quartiles of SUA were significantly associated with increasing NOD (HR 1.28, 95% CI 1.18-1.40, P < 0.001). Time-varying SUA was also associated with NOD (HR 1.10 per s.d. [1.3 mg/dl], 95% CI 1.02-1.19, P = 0.015). CONCLUSION: Our analysis suggests that SUA is an independent risk marker for NOD in hypertensive patients with LVH.
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