Thürmann P A, Kenedi P, Schmidt A, Harder S, Rietbrock N
Philipp Klee-Institute of Clinical Pharmacology, Hospital Wuppertal GmbH, Clinical Pharmacology, University Witten/Herdecke, Wuppertal, Germany.
Circulation. 1998 Nov 10;98(19):2037-42. doi: 10.1161/01.cir.98.19.2037.
Left ventricular hypertrophy (LVH) represents an independent risk factor in patients with essential hypertension. Because reversal of LVH may be associated with an improvement of prognosis, the influence of new antihypertensive compounds, such as angiotensin II AT1 receptor antagonists, on LVH should be determined.
In a randomized, double-blind trial, 69 predominantly previously untreated hypertensive patients with echocardiographically proven LVH, ie, left ventricular mass index (LVMI) >134 g/m2 in men and >110 g/m2 in women and/or end-diastolic septal thickness >12 mm, received either the angiotensin II antagonist valsartan or atenolol for 8 months. Echocardiographic data of 58 patients were available. After 8 months of valsartan treatment (n=29), LVMI decreased from 127+/-23 to 106+/-25 g/m2 (ratio [R]=0.83; 95% CI, 0.79 to 0.87; P<0.0001 versus baseline). Under atenolol (n=29), LVMI decreased to a smaller extent, from 127+/-25 to 117+/-27 g/m2 (R=0.92; 95% CI, 0.86 to 0.98; P=0.0082 versus baseline). The mean reduction of LVMI came to 21 g/m2 under valsartan and only to 10 g/m2 under atenolol (R=0.91; 90% CI, 0.85 to 0.97 versus atenolol). Baseline mean blood pressure values were determined to be 163+/-12/101+/-6 mm Hg before treatment with valsartan and 160+/-14/103+/-6 mm Hg before atenolol treatment. After 8 months of treatment, mean blood pressure decreased to 146+/-13/90+/-7 mm Hg with valsartan and to 147+/-18/90+/-7 mm Hg with atenolol. Nine patients in the valsartan group and 8 patients in the atenolol group required additional medication with hydrochlorothiazide.
Antihypertensive treatment with the angiotensin II antagonist valsartan for 8 months produced a significant regression of LVH in predominantly previously untreated patients with essential hypertension. The drug may be safely administered in this subset of hypertensive patients; however, the long-term benefit in terms of risk reduction has still to be evaluated in further trials.
左心室肥厚(LVH)是原发性高血压患者的一个独立危险因素。由于LVH的逆转可能与预后改善相关,因此应确定新型抗高血压药物(如血管紧张素II AT1受体拮抗剂)对LVH的影响。
在一项随机、双盲试验中,69例主要为未经治疗的高血压患者,经超声心动图证实存在LVH,即男性左心室质量指数(LVMI)>134 g/m2,女性>110 g/m2和/或舒张末期室间隔厚度>12 mm,接受血管紧张素II拮抗剂缬沙坦或阿替洛尔治疗8个月。58例患者的超声心动图数据可用。缬沙坦治疗8个月后(n = 29),LVMI从127±23降至106±25 g/m2(比值[R]=0.83;95%CI,0.79至0.87;与基线相比P<0.0001)。在阿替洛尔治疗组(n = 29)中,LVMI下降幅度较小,从127±25降至117±27 g/m2(R = 0.92;95%CI,0.86至0.98;与基线相比P = 0.0082)。缬沙坦治疗组LVMI平均降低21 g/m2,阿替洛尔治疗组仅降低10 g/m2(与阿替洛尔相比R = 0.91;90%CI,0.85至0.97)。缬沙坦治疗前基线平均血压值为163±12/101±6 mmHg,阿替洛尔治疗前为160±14/103±6 mmHg。治疗8个月后,缬沙坦组平均血压降至146±13/90±7 mmHg,阿替洛尔组降至147±18/90±7 mmHg。缬沙坦组9例患者和阿替洛尔组8例患者需要加用氢氯噻嗪。
血管紧张素II拮抗剂缬沙坦对主要为未经治疗的原发性高血压患者进行8个月的抗高血压治疗可使LVH显著消退。该药物可在这部分高血压患者中安全使用;然而,在降低风险方面的长期益处仍有待进一步试验评估。