Cardiovascular critical event pathways for the progression of heart failure: A report from the ATLAS study

John G F Cleland, K. Thygesen, B. F. Uretsky, P. Armstrong, J. D. Horowitz, B. Massie, M. Packer, P. A. Poole-Wilson, L. Rydén

Research output: Contribution to journalArticle

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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.

Original languageEnglish (US)
Pages (from-to)1601-1612
Number of pages12
JournalEuropean Heart Journal
Volume22
Issue number17
DOIs
StatePublished - 2001

Fingerprint

Critical Pathways
Lisinopril
Heart Failure
Hospitalization
Blood Vessels
Ventricular Remodeling
Sudden Death
Myocardial Ischemia
Cardiac Arrhythmias
Databases
Mortality

Keywords

  • Arrhythymia
  • Critical events pathways
  • Heart failure
  • Ischaemia
  • Lisinopril
  • Progression

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

Cleland, J. G. F., Thygesen, K., Uretsky, B. F., Armstrong, P., Horowitz, J. D., Massie, B., ... Rydén, L. (2001). Cardiovascular critical event pathways for the progression of heart failure: A report from the ATLAS study. European Heart Journal, 22(17), 1601-1612. https://doi.org/10.1053/euhj.2000.2570

Cardiovascular critical event pathways for the progression of heart failure : A report from the ATLAS study. / Cleland, John G F; Thygesen, K.; Uretsky, B. F.; Armstrong, P.; Horowitz, J. D.; Massie, B.; Packer, M.; Poole-Wilson, P. A.; Rydén, L.

In: European Heart Journal, Vol. 22, No. 17, 2001, p. 1601-1612.

Research output: Contribution to journalArticle

Cleland, JGF, Thygesen, K, Uretsky, BF, Armstrong, P, Horowitz, JD, Massie, B, Packer, M, Poole-Wilson, PA & Rydén, L 2001, 'Cardiovascular critical event pathways for the progression of heart failure: A report from the ATLAS study', European Heart Journal, vol. 22, no. 17, pp. 1601-1612. https://doi.org/10.1053/euhj.2000.2570
Cleland, John G F ; Thygesen, K. ; Uretsky, B. F. ; Armstrong, P. ; Horowitz, J. D. ; Massie, B. ; Packer, M. ; Poole-Wilson, P. A. ; Rydén, L. / Cardiovascular critical event pathways for the progression of heart failure : A report from the ATLAS study. In: European Heart Journal. 2001 ; Vol. 22, No. 17. pp. 1601-1612.
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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.",
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