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Valsartan in a Japanese population with hypertension and other cardiovascular disease (Jikei Heart Study): a randomised, open-label, blinded endpoint morbidity-mortality study
Oleh:
Mochizuki, Seibu
;
Dahlöf, Björn
;
Shimizu, Mitsuyuki
;
Ikewaki, Katsunori
;
Yoshikawa, Makoto
;
Taniguchi, Ikuo
;
Ohta, Makoto
;
Yamada, Taku
;
Ogawa, Kazuhiko
;
Kanae, Kiyoshi
;
Kawai, Makoto
;
Seki, Shingo
;
Okazaki, Fumiko
;
Taniguchi, Masayuki
;
Yoshida, Satoru
;
Tajima, Naoko
Jenis:
Article from Journal - ilmiah internasional
Dalam koleksi:
The Lancet (keterangan: ada di Proquest) vol. 369 no. 9571 (Apr. 2007)
,
page 1431.
Ketersediaan
Perpustakaan FK
Nomor Panggil:
L01.K.2007.02
Non-tandon:
1 (dapat dipinjam: 0)
Tandon:
tidak ada
Lihat Detail Induk
Isi artikel
Background: Drugs that inhibit the renin–angiotensin–aldosterone system benefit patients at risk for or with existing cardiovascular disease. However, evidence for this effect in Asian populations is scarce. We aimed to investigate whether addition of an angiotensin receptor blocker, valsartan, to conventional cardiovascular treatment was effective in Japanese patients with cardiovascular disease. Methods: We initiated a multicentre, prospective, randomised controlled trial of 3081 Japanese patients, aged 20–79 years, (mean 65 [SD 10] years) who were undergoing conventional treatment for hypertension, coronary heart disease, heart failure, or a combination of these disorders. In addition to conventional treatment, patients were assigned either to valsartan (40–160 mg per day) or to other treatment without angiotensin receptor blockers. Our primary endpoint was a composite of cardiovascular morbidity and mortality. Analysis was by intention to treat. The study was registered at clintrials.gov with the identifier NCT00133328. Findings: After a median follow-up of 3·1 years (range 1–3·9) the primary endpoint was recorded in fewer individuals given valsartan than in controls (92 vs 149; absolute risk 21·3 vs 34·5 per 1000 patient years; hazard ratio 0·61, 95% CI 0·47–0·79, p=0·0002). This difference was mainly attributable to fewer incidences of stroke and transient ischaemic attack (29 vs 48; 0·60, 0·38–0·95, p=0·028), angina pectoris (19 vs 53; 0·35, 0·20–0·58, p<0·0001), and heart failure (19 vs 36; 0·53, 0·31–0·94, p=0·029) in those given valsartan than in the control group. Mortality or tolerability did not differ between groups. Interpretation: The addition of valsartan to conventional treatment prevented more cardiovascular events than supplementary conventional treatment. These benefits cannot be entirely explained by a difference in blood pressure control.
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