Understanding Circadian Mechanisms of Sudden Cardiac Death: A Report From the National Heart, Lung, and Blood Institute Workshop, Part 2: Population and Clinical Considerations.

National Heart, Lung, and Blood Institute cardiovascular diseases circadian clock circadian rhythm genetics population sudden cardiac death

Journal

Circulation. Arrhythmia and electrophysiology
ISSN: 1941-3084
Titre abrégé: Circ Arrhythm Electrophysiol
Pays: United States
ID NLM: 101474365

Informations de publication

Date de publication:
11 2021
Historique:
pubmed: 2 11 2021
medline: 28 12 2021
entrez: 1 11 2021
Statut: ppublish

Résumé

Sudden cardiac death (SCD) is the sudden, unexpected death due to abrupt loss of heart function secondary to cardiovascular disease. In certain populations living with cardiovascular disease, SCD follows a distinct 24-hour pattern in occurrence, suggesting day/night rhythms in behavior, the environment, and endogenous circadian rhythms result in daily spans of increased vulnerability. The National Heart, Lung, and Blood Institute convened a workshop, Understanding Circadian Mechanisms of Sudden Cardiac Death to identify fundamental questions regarding the role of the circadian rhythms in SCD. Part 2 summarizes research gaps and opportunities in the areas of population and clinical research identified in the workshop. Established research supports a complex interaction between circadian rhythms and physiological responses that increase the risk for SCD. Moreover, these physiological responses themselves are influenced by several biological variables, including the type of cardiovascular disease, sex, age, and genetics, as well as environmental factors. The emergence of new noninvasive biotechnological tools that continuously measure key cardiovascular variables, as well as the identification of biomarkers to assess circadian rhythms, hold promise for generating large-scale human data sets that will delineate which subsets of individuals are most vulnerable to SCD. Additionally, these data will improve our understanding of how people who suffer from circadian disruptions develop cardiovascular diseases that increase the risk for SCD. Emerging strategies to identify new biomarkers that can quantify circadian health (eg, environmental, behavioral, and internal misalignment) may lead to new interventions and therapeutic targets to prevent the progression of cardiovascular diseases that cause SCD.

Identifiants

pubmed: 34719257
doi: 10.1161/CIRCEP.121.010190
pmc: PMC8865094
mid: NIHMS1749493
doi:

Types de publication

Journal Article Research Support, N.I.H., Extramural Review

Langues

eng

Sous-ensembles de citation

IM

Pagination

e010190

Subventions

Organisme : NIDDK NIH HHS
ID : R01 DK099512
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL141343
Pays : United States
Organisme : NHLBI NIH HHS
ID : R35 HL155681
Pays : United States
Organisme : NIDDK NIH HHS
ID : R01 DK102696
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL122010
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL153042
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL140574
Pays : United States
Organisme : NIDDK NIH HHS
ID : R01 DK105072
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL118601
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL111600
Pays : United States

Commentaires et corrections

Type : ErratumIn

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Auteurs

Brian P Delisle (BP)

Department of Physiology, University of Kentucky, Lexington (B.P.D.).

Alfred L George (AL)

Department of Pharmacology (A.L.G.), Northwestern University, Feinberg School of Medicine, Chicago, IL.

Jeanne M Nerbonne (JM)

Cardiovascular Division, and Developmental Biology, Departments of Medicine (J.M.N.), Washington University School of Medicine, St Louis, MO.

Joseph T Bass (JT)

Department of Medicine (J.T.B.), Northwestern University, Feinberg School of Medicine, Chicago, IL.

Crystal M Ripplinger (CM)

Department of Pharmacology, University of California, Davis (C.M.R.).

Mukesh K Jain (MK)

Department of Medicine, Case Western Reserve University, Cleveland, OH (M.K.J.).

Tracey O Hermanstyne (TO)

Department of Developmental Biology (T.O.H.), Washington University School of Medicine, St Louis, MO.

Martin E Young (ME)

Department of Medicine, University of Alabama, Birmingham (M.E.Y.).

Prince J Kannankeril (PJ)

Department of Pediatrics, Vanderbilt University Medical Center, Nashville, TN (P.J.K.).

Jeanne F Duffy (JF)

Department of Medicine (J.F.D.), Harvard Medical School, Boston, MA.

Joshua I Goldhaber (JI)

Department of Cardiology, Cedars-Sinai Medical Center, Los Angeles, CA (J.I.G.).

Martica H Hall (MH)

Department of Psychiatry, University of Pittsburgh, PA (M.H.H.).

Virend K Somers (VK)

Department of Medicine, Mayo Clinic, Rochester, MN (V.K.S.).

Michael H Smolensky (MH)

Department of Biomedical Engineering, University of Texas, Austin (M.H.S.).

Christine E Garnett (CE)

Food and Drug Administration, Silver Spring, MD (C.E.G.).

Ron C Anafi (RC)

Department of Medicine and Center for Sleep and Circadian Neurobiology, University of Pennsylvania Perelman School of Medicine, Philadelphia (R.C.A.).

Frank A J L Scheer (FAJL)

Division of Sleep Medicine (F.A.J.L.S.), Harvard Medical School, Boston, MA.

Kalyanam Shivkumar (K)

Departement of Medicine, David Greffen School of Medicine, University of California, Los Angeles (K.S.).

Steven A Shea (SA)

Oregon Institute of Occupational Health Sciences, Oregon Health and Science University, Portland (S.A.S.).

Ravi C Balijepalli (RC)

National Heart, Lung, and Blood Institute, Bethesda, MD (R.C.B.).

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