| Autor: |
Delisle BP; Department of Physiology, University of Kentucky, Lexington (B.P.D.)., George AL Jr; Department of Pharmacology (A.L.G.), Northwestern University, Feinberg School of Medicine, Chicago, IL., Nerbonne JM; Department of Medicine, Cardiovascular Division, and Developmental Biology, Washington University School of Medicine, St. Louis, MO (J.M.N.)., Bass JT; Department of Medicine (J.T.B.), Northwestern University, Feinberg School of Medicine, Chicago, IL., Ripplinger CM; Department of Pharmacology, University of California, Davis, CA (C.M.R.)., Jain MK; Department of Medicine, Case Western Reserve University, Cleveland, OH (M.K.J.)., Hermanstyne TO; Department of Developmental Biology, Washington University School of Medicine, St. Louis, MO (T.O.H.)., Young ME; Department of Medicine, University of Alabama, Birmingham (M.E.Y.)., Kannankeril PJ; Department of Pediatrics, Vanderbilt University Medical Center, Nashville, TN (P.J.K.)., Duffy JF; Department of Medicine, Harvard Medical School, Boston, MA (J.F.D.)., Goldhaber JI; Department of Cardiology, Cedars-Sinai Medical Center, Los Angeles, CA (J.I.G.)., Hall MH; Department of Psychiatry, University of Pittsburgh, PA (M.H.H.)., Somers VK; Department of Cardiovascular Medicine, Mayo Clinic, Rochester, MN (V.K.S.)., Smolensky MH; Department of Biomedical Engineering, University of Texas, Austin (M.H.S.)., Garnett CE; Food and Drug Administration, Silver Spring, MD (C.E.G.)., Anafi RC; Department of Medicine and Center for Sleep and Circadian Neurobiology, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA (R.C.A.)., Scheer FAJL; Division of Sleep Medicine, Harvard Medical School, Boston, MA (F.A.J.L.S.)., Shivkumar K; Departement of Medicine, David Greffen School of Medicine at UCLA, Los Angeles, CA (K.S.)., Shea SA; Oregon Institute of Occupational Health Sciences, Oregon Health and Science University, Portland (S.A.S.)., Balijepalli RC; National Heart, Lung, and Blood Institute, Bethesda, MD (R.C.B.). |
| Abstrakt: |
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. |
