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Cardiovascular critical event pathways for the progression of heart failure; a report from the ATLAS study.

Abstract：

AIMS:To determine the sequence of critical cardiovascular events in the progression of heart failure, and whether aetiology or high-dose vs low-dose lisinopril affected these pathways. METHODS AND RESULTS:This was a post-hoc investigation of the ATLAS database, which comprised 3164 patients with chronic heart failure, randomized to low- (2.5-5.0 mg. day(-1)) or high-dose (32.5-35.0 mg. day(-1)) lisinopril, followed up for a median of 46 months. Two-thirds (64.3%) of patients had heart failure attributed to ischaemic heart disease. During the study, most patients (61.1%) had at least one cardiovascular hospitalization and 42.5% of all patients died: most deaths (88.2%) were cardiovascular. Nearly half (49.7%) of the cardiovascular deaths were considered sudden and 45.2% of cardiovascular deaths occurred as the first cardiovascular event. A third (30.2%) of deaths resulted from heart failure and were generally preceded by hospitalization, either for heart failure (85.5%), myocardial ischaemic events (21.7%) or arrhythmias (18.0%). Compared with low-dose, high-dose lisinopril was associated with a lower risk of death or hospitalization for any reason (P=0.002) and death or hospitalization with worsening heart failure (P<0.001). High-dose lisinopril delayed the time to all-cause mortality and hospitalization for chronic heart failure by 7.1 months. CONCLUSIONS:Vascular and arrhythmic events may not only be important precipitants of sudden death, but were also seen to contribute to the progression of heart failure. A reduction in vascular events, as well as benefits on ventricular remodelling, could account for the decrease in death or hospitalization with high-dose lisinopril.

journal_name

Eur Heart J

journal_title

European heart journal

authors

Cleland JG,Thygesen K,Uretsky BF,Armstrong P,Horowitz JD,Massie B,Packer M,Poole-Wilson PA,Rydén L,ATLAS investigators.

doi

10.1053/euhj.2000.2570

subject

Has Abstract

pub_date

2001-09-01 00:00:00

pages

1601-12

issue

17

eissn

0195-668X

issn

1522-9645

pii

S0195668X00925703

journal_volume

22

pub_type

杂志文章

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