Effects of losartan or atenolol in hypertensive patients without clinically evident vascular disease:: A substudy of the LIFE randomized trial

被引:50
作者
Devereux, RB
Dahlöf, B
Kjeldsen, SE
Julius, S
Aurup, P
Beevers, G
Edelman, JM
de Faire, U
Fyhrquist, F
Berg, SH
Ibsen, H
Kristianson, K
Lederballe-Pedersen, O
Lindholm, LH
Nieminen, MS
Omvik, P
Oparil, S
Snapinn, S
Wedel, H
机构
[1] Cornell Univ, Weill Med Coll, New York, NY USA
[2] Sahlgrenska Ostra Univ Hosp, Gothenburg, Sweden
[3] Nord Sch Publ Hlth, Gothenburg, Sweden
[4] Ullevaal Univ Hosp, Oslo, Norway
[5] Univ Michigan, Ann Arbor, MI 48109 USA
[6] Merck & Co Inc, Whitehouse Stn, NJ USA
[7] City Hosp, Birmingham, W Midlands, England
[8] Karolinska Univ Hosp, Stockholm, Sweden
[9] Univ Helsinki, Cent Hosp, FIN-00014 Helsinki, Finland
[10] Glostrup Univ Hosp, Glostrup, Denmark
[11] Viborg Hosp, Viborg, Denmark
[12] Umea Univ, S-90187 Umea, Sweden
[13] Haukeland Hosp, N-5021 Bergen, Norway
[14] Univ Alabama Birmingham, Birmingham, AL USA
关键词
LEFT-VENTRICULAR HYPERTROPHY; END-POINT REDUCTION; CONVERTING-ENZYME-INHIBITOR; CARDIOVASCULAR MORBIDITY; ELECTROCARDIOGRAPHIC IDENTIFICATION; MYOCARDIAL-INFARCTION; BLOOD-PRESSURE; SWEDISH TRIAL; OLD PATIENTS; MORTALITY;
D O I
10.7326/0003-4819-139-3-200308050-00006
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Background: Cardiovascular morbidity and mortality are reduced by treatment with the angiotensin II AT(1)-receptor antagonist losartan compared with conventional treatment with the beta-blocker atenolol in patients with hypertension and electrocardiogram-defined left ventricular hypertrophy, many of whom had known vascular disease. Objective: To determine whether losartan reduces cardiovascular event rates in lower-risk hypertensive patients without clinically evident vascular disease. Design: Subgroup analysis of a randomized trial. Setting: The Losartan Intervention for Endpoint reduction in hypertension (LIFE) study. Patients: 6886 men and women (57% women) 55 to 80 years of age (average, 66 years) with essential hypertension (sitting blood pressure, 160 to 200/95 to 115 mm Hg [average, 174/98 mm Hg]) and electrocardiogram-defined left ventricular hypertrophy who did not have clinically evident vascular disease. Intervention: Patients were randomly assigned to once-daily double-blind treatment with losartan or atenolol. Measurements: An end point committee ascertained end points (cardiovascular death, stroke, or myocardial infarction). Results: Blood pressure was reduced similarly by losartan and atenolol. The primary composite end point occurred in 282 losartan-treated patients (17.5 per 1000 patient-years) and 355 atenolol-treated patients (21.8 per 1000 patient-years; relative risk, 0.81 [95% CI, 0.69 to 0.95]; P = 0.008). Cardiovascular death occurred in 103 losartan-treated patients and 132 atenolol-treated patients (relative risk, 0.80 [CI, 0.62 to 1.04]; P = 0.092), stroke (nonfatal and fatal) occurred in 125 losartan-treated patients and 193 atenolol-treated patients (relative risk, 0.66 [CI, 0.53 to 0.82]; P < 0.001), and myocardial infarction (nonfatal and fatal) occurred in 110 losartan-treated patients and 100 atenolol-treated patients (relative risk, 1.14 [CI, 0.87 to 1.49]; P > 0.2). New-onset diabetes occurred less often in patients treated with losartan (n = 173) than in patients treated with atenolol (n = 254) (relative risk, 0.69 [CI, 0.57 to 0.84]; P < 0.001). Benefits of losartan treatment were numerically smaller, but not significantly so, in patients with preexisting vascular disease. Conclusion: In hypertensive patients without clinically evident vascular disease, losartan was more effective than atenolol in preventing cardiovascular morbidity and death, predominantly stroke, independent of blood pressure reduction.
引用
收藏
页码:169 / 177
页数:9
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