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

Journal Article (Journal Article)

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.

Full Text

Duke Authors

Cited Authors

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

Published Date

  • September 2001

Published In

Volume / Issue

  • 22 / 17

Start / End Page

  • 1601 - 1612

PubMed ID

  • 11492990

International Standard Serial Number (ISSN)

  • 0195-668X

Digital Object Identifier (DOI)

  • 10.1053/euhj.2000.2570


  • eng

Conference Location

  • England