Copyright © 2001 by the European Society of Cardiology.
Cardiovascular critical event pathways for the progression of heart failure; a report from the ATLAS study
a University of Hull, U.K.
b Aarhus University Hospital, Denmark
c University of Texas, Galveston, U.S.A.
d University of Alberta, Edmonton, Canada
e University of Adelaide, Adelaide, Australia
f University of California, San Francisco, U.S.A.
g Columbia University, New York, U.S.A.
h Imperial College School of Medicine, University of London, U.K.
i Karolinska Institutet, Stockholm, Sweden
revised December 4, 2000; accepted December 6, 2000
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- (2·5–5·0mg.day–1) or high-dose (32·5–35·0mg.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.
Key Words: Heart failure, lisinopril, ischaemia, arrhythymia, progression, critical events pathways
f1 Correspondence: Dr John G. F. Cleland, Department of Cardiology, Castle Hill Hospital, Castle Road, University of Hull, Kingston upon Hull, HU16 5JQ, U.K.
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