Understanding Circadian Mechanisms of Sudden Cardiac Death: A Report From the National Heart, Lung, and Blood Institute Workshop, Part 1: Basic and Translational Aspects

Brian P. Delisle, Alfred L. George, Jeanne M. Nerbonne, Joseph T. Bass, Crystal M. Ripplinger, Mukesh K. Jain, Tracey O. Hermanstyne, Martin E. Young, Prince J. Kannankeril, Jeanne F. Duffy, Joshua I. Goldhaber, Martica H. Hall, Virend K. Somers, Michael H. Smolensky, Christine E. Garnett, Ron C. Anafi, Frank A.J.L. Scheer, Kalyanam Shivkumar, Steven A. Shea, Ravi C. Balijepalli

Research output: Contribution to journalReview articlepeer-review

6 Scopus citations


Sudden cardiac death (SCD), the unexpected death due to acquired or genetic cardiovascular disease, follows distinct 24-hour patterns in occurrence. These 24-hour patterns likely reflect daily changes in arrhythmogenic triggers and the myocardial substrate caused by day/night rhythms in behavior, the environment, and endogenous circadian mechanisms. To better address fundamental questions regarding the circadian mechanisms, the National Heart, Lung, and Blood Institute convened a workshop, Understanding Circadian Mechanisms of Sudden Cardiac Death. We present a 2-part report of findings from this workshop. Part 1 summarizes the workshop and serves to identify research gaps and opportunities in the areas of basic and translational research. Among the gaps was the lack of standardization in animal studies for reporting environmental conditions (eg, timing of experiments relative to the light dark cycle or animal housing temperatures) that can impair rigor and reproducibility. Workshop participants also pointed to uncertainty regarding the importance of maintaining normal circadian rhythmic synchrony and the potential pathological impact of desynchrony on SCD risk. One related question raised was whether circadian mechanisms can be targeted to reduce SCD risk. Finally, the experts underscored the need for studies aimed at determining the physiological importance of circadian clocks in the many different cell types important to normal heart function and SCD. Addressing these gaps could lead to new therapeutic approaches/molecular targets that can mitigate the risk of SCD not only at certain times but over the entire 24-hour period.

Original languageEnglish
Pages (from-to)E010181
JournalCirculation: Arrhythmia and Electrophysiology
Issue number11
StatePublished - Nov 1 2021

Bibliographical note

Funding Information:
The views expressed in this article are those of the authors and do not necessarily represent the views of the National Heart, Lung, and Blood Institute; the National Institutes of Health; or the US Department of Health and Human Services. Dr Delisle was supported by National Institutes of Health (NIH) grants R01HL153042 and R01HL141343. Dr George was supported by NIH grant R01HL122010. Dr Scheer was supported by NIH grants R01HL118601, R01DK099512, R01DK102696, R01DK105072, and R01HL140574. Dr Shea was supported by NIH grant R35 HL155681. Several of the images were prepared using BioRender.com.

Publisher Copyright:
© 2021 Lippincott Williams and Wilkins. All rights reserved.


  • National Heart, Lung, and Blood Institute
  • cardiovascular disease
  • circadian clocks
  • circadian rhythm
  • sudden cardiac death

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)


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