Literature DB >> 10933370

Circadian rhythm and sudden death in heart failure: results from Prospective Randomized Amlodipine Survival Trial.

P A Carson1, C M O'Connor, A B Miller, S Anderson, R Belkin, G W Neuberg, J H Wertheimer, D Frid, A Cropp, M Packer.   

Abstract

OBJECTIVE: The purpose of this study was to address the timing of sudden death in advanced heart failure patients.
BACKGROUND: Sudden death is a catastrophic event in cardiovascular disease. It has a circadian pattern prominent in the early AM, which has been thought to be due to a surge of sympathetic stimulation. We postulated that the distribution of events in advanced heart failure, with chronic sympathetic activation, would be more uniform implicating other potential mechanisms.
METHODS: We analyzed data from Prospective Randomized Amlodipine Survival Trial (PRAISE). Sudden deaths were analyzed by time of death in 4-h and 1-h blocks for uniformity of distribution in the entire cohort, and in the prespecified ischemic and nonischemic stratum. Further analyses were undertaken in the treatment groups of amlodipine and placebo, and among those receiving background therapy of aspirin and warfarin.
RESULTS: Sudden deaths in the overall cohort showed a nonuniform distribution with a PM peak but not an AM peak. The ischemic stratum also showed a PM peak, but sudden deaths within the nonischemic stratum were uniformly distributed. Neither amlodipine treatment nor aspirin or warfarin use altered the distribution.
CONCLUSIONS: Sudden death in advanced heart failure did not show an AM peak, suggesting that circadian sympathetic activation did not strongly influence these events. The PM peak noted is likely complex in origin and was not affected by antiischemic or antithrombotic medications.

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Year:  2000        PMID: 10933370     DOI: 10.1016/s0735-1097(00)00728-2

Source DB:  PubMed          Journal:  J Am Coll Cardiol        ISSN: 0735-1097            Impact factor:   24.094


  11 in total

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3.  Cardiomyocyte-specific Bmal1 deletion in mice triggers diastolic dysfunction, extracellular matrix response, and impaired resolution of inflammation.

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4.  Altered myocardial metabolic adaptation to increased fatty acid availability in cardiomyocyte-specific CLOCK mutant mice.

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Review 7.  Circadian rhythms in cardiac gene expression.

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Review 9.  Chronic heart failure: a disease of the brain.

Authors:  Ram B Singh; Krasimira Hristova; Jan Fedacko; Galal El-Kilany; Germaine Cornelissen
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Review 10.  Impact of sleep on arrhythmogenesis.

Authors:  Richard L Verrier; Mark E Josephson
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