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Changing Characteristics and Mode of Death Associated With Chronic Heart Failure Caused by Left Ventricular Systolic Dysfunction A Study Across Therapeutic Eras

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Richard M. Cubbon, Christopher P. Gale, Lorraine C. Kearney, Clyde B. Schechter, W. Paul Brooksby, Jim Nolan, Keith A. A. Fox, Adil Rajwani, Wazir Baig, David Groves, Pauline Barlow, Anthony C. Fisher, Phillip D. Batin, Matthew B. Kahn, Azfar G. Zaman, Ajay M. Shah, Jon A. Byrne, Steven J. Lindsay, Robert J. Sapsford, Stephen B. Wheatcroft & 2 more Klaus K. Witte, Mark T. Kearney

Original languageEnglish
Pages (from-to)396-403
Number of pages8
JournalCirculation-Heart Failure
Issue number4
PublishedJul 2011

King's Authors


Background-Therapies for patients with chronic heart failure caused by left ventricular systolic dysfunction have advanced substantially over recent decades. The cumulative effect of these therapies on mortality, mode of death, symptoms, and clinical characteristics has yet to be defined. Methods and Results-This study was a comparison of 2 prospective cohort studies of outpatients with chronic heart failure caused by left ventricular systolic dysfunction performed between 1993 and 1995 (historic cohort: n = 281) and 2006 and 2009 (contemporary cohort: n = 357). In the historic cohort, 83% were prescribed angiotensin-converting enzyme inhibitors and 8.5% were prescribed beta-adrenoceptor antagonists, compared with 89% and 80%, respectively, in the contemporary cohort. Mortality rates over the first year of follow-up declined from 12.5% to 7.8% between eras (P = 0.04), and sudden death contributed less to contemporary mortality (33.6% versus 12.7%; P <0.001). New York Heart Association class declined between eras (P <0.001). QTc dispersion across the chest leads declined from 85 ms (SD, 2) to 34 ms (SD, 1) and left ventricular end-diastolic dimensions declined from 65 mm (SD, 0.6) to 59 mm (SD, 0.5) (both P <0.001). Conclusions-Survival has significantly improved in patients with chronic heart failure caused by left ventricular systolic dysfunction over the past 15 years; furthermore, sudden death makes a much smaller contribution to mortality, and noncardiac mortality is a correspondingly greater contribution. This has been accompanied by an improvement in symptoms and some markers of adverse electric and structural left ventricular remodeling. (Circ Heart Fail. 2011; 4: 396-403.)

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