Int J Angiol. 2021 Jul 19;30(4):271-276. doi: 10.1055/s-0041-1729629. eCollection 2021 Dec.
Sudden Cardiac Death in the General Population: Can We Improve Risk Stratification and Prevention?.
The International journal of angiology : official publication of the International College of Angiology, Inc
Gary L Murray, Joseph Colombo
Affiliations
Affiliations
- Department of Cardiology, The Heart and Vascular Institute, Germantown, Tennessee.
- Department of Cardiology, Physio PS, INC, Atlanta, Georgia.
- Department of Cardiology, Autonomic Dysfunction and POTS Center, Sicklersville, New Jersey.
PMID: 34853574
PMCID: PMC8608466 DOI: 10.1055/s-0041-1729629
Abstract
A total of 15 to 20% of deaths worldwide are sudden (within 1 hour of symptom onset). Our ability to predict and prevent sudden cardiac death (SCD) in the general population, in which 85% have no known organic heart disease (OHD) or stable OHD with left ventricular ejection fraction >40%, is limited to poor. The purpose of this commentary is to suggest a new approach to SCD in this population. Oxidative stress is a common thread in development and progression of the major cardiac diseases associated with SCD. It has a profound adverse effect upon heart rate variability (HRV), sympathetic tone (S), and parasympathetic tone (P). Recently, developed technology finally has allowed accurate measures of S and P. Using this technique, the general population can be screened, those at risk for SCD can be identified with a higher degree of success, and preventative measures instituted. For example, in 133 geriatric type 2 diabetics with S and/or P abnormalities upon screening, the potent and natural antioxidant (r)α lipoic acid reduced SCD (relative risk reduction) 43% (
International College of Angiology. This article is published by Thieme.
Keywords: acute myocardial infarction; diabetes; oxidative stress; prevention; sudden cardiac death; ventricular fibrillation; α lipoic acid
Conflict of interest statement
Conflict of Interest None declared.
References
- Science. 1981 Jul 10;213(4504):220-2 - PubMed
- Int J Angiol. 2019 Sep;28(3):188-193 - PubMed
- Annu Int Conf IEEE Eng Med Biol Soc. 2007;2007:5047-50 - PubMed
- J Cardiovasc Electrophysiol. 2001 Nov;12(11):1295-301 - PubMed
- Am J Physiol. 1985 Oct;249(4 Pt 2):H867-75 - PubMed
- Acta Diabetol. 2010 Dec;47 Suppl 1:161-8 - PubMed
- Eur Heart J. 2014 Jul 1;35(25):1642-51 - PubMed
- Curr Diabetes Rev. 2017;13(5):488-497 - PubMed
- Int J Angiol. 2016 Sep;25(3):159-64 - PubMed
- Heart Int. 2014 Dec 22;9(2):66-73 - PubMed
- Mayo Clin Proc. 2002 Jan;77(1):45-54 - PubMed
- Am J Physiol. 1987 Jul;253(1 Pt 2):H176-83 - PubMed
- Circulation. 1996 Dec 1;94(11):2850-5 - PubMed
- Diabetes Metab Res Rev. 2011 Oct;27(7):639-53 - PubMed
- Free Radic Res. 2003 May;37(5):471-80 - PubMed
- Trends Pharmacol Sci. 1988 Jan;9(1):6-9 - PubMed
- Jpn Circ J. 1999 Jul;63(7):503-8 - PubMed
- Nutr Metab Cardiovasc Dis. 2018 Jun;28(6):543-556 - PubMed
- Toxicol Appl Pharmacol. 2006 Apr 15;212(2):167-78 - PubMed
- Hum Mol Genet. 2009 Jan 15;18(2):347-57 - PubMed
- Diabetol Metab Syndr. 2014 Jul 28;6(1):80 - PubMed
- Cardiovasc Drugs Ther. 2004 Jan;18(1):13-22 - PubMed
- Auton Neurosci. 2016 Aug;199:29-37 - PubMed
- Auton Neurosci. 2003 Oct 31;108(1-2):32-44 - PubMed
- J Trauma. 2008 Dec;65(6):1364-73 - PubMed
- Q J Med. 1980 Winter;49(193):95-108 - PubMed
- Aging (Albany NY). 2018 Feb 23;10(2):166-177 - PubMed
Publication Types