Hostname: page-component-745bb68f8f-b95js Total loading time: 0 Render date: 2025-01-14T20:00:03.467Z Has data issue: false hasContentIssue false
  • English
  • Français

The role of illicit drug use in sudden death in the young

Published online by Cambridge University Press:  13 January 2017

Peter Fischbach
Peter Fischbach*
Affiliation:
Children’s Pediatric Cardiology Fellowship Program, Sibley Heart Center Cardiology and Emory University, Atlanta, Georgia, United States of America
*
Correspondence to: P. Fischbach, Chief Academic Officer, Children’s Pediatric Cardiology Fellowship Program, Sibley Heart Center Cardiology and Emory University, 1405 Clifton Road NE, Atlanta, GA 30322, United States of America. Tel: 404 256 2593; Fax: 678 547 1494; E-mail: fischbachp@kidsheart.com
Get access Rights & Permissions [Opens in a new window]

Abstract

The recreational use of illicit drugs remains an enormous and growing problem throughout the United States of America and around the world. Cocaine is most frequently thought of when considering the cardiovascular toxicity of illicit drugs. The association of cocaine use with sudden death due to myocardial ischaemia and infarction is well recognised, and this risk appears to be amplified by concomitant cigarette smoking and alcohol consumption. Like cocaine, amphetamine and its derivatives lead to indirect stimulation of the autonomic nervous system through the release of norepinephrine, dopamine, and serotonin in nerve terminals of the central and autonomic nervous systems. However, amphetamine lacks the ion channel-blocking properties of cocaine. Also similar to cocaine, coronary artery spasm may be induced in individuals with or without atherosclerotic disease and may lead to myocardial infarction. With the movement across the United States of America to legalise marijuana, or cannabis, for medicinal and recreational purposes, it is important to consider its potential deleterious effects. Marijuana has long been thought to have very few adverse effects with the exception of long-term dependence. There are, however, scattered reports of acute adverse events up to and including sudden death. These appear to be due to myocardial infarction. In conclusion, the incidence of sudden death associated with the use of these drugs varies from rare in the case of marijuana use to not infrequent with some drugs such as cocaine. It is important for care providers to recognise the potential for drug abuse when caring for a sudden cardiac arrest survivor.

Keywords

Recreational drug usecocaineamphetamineheroinsudden cardiac death
Type
Original Articles
Information
Cardiology in the Young , Volume 27 , Supplement S1: Sudden Cardiac Arrest in the Young: A Contemporary Perspective , January 2017 , pp. S75 - S79
Copyright
© Cambridge University Press 2017 

Access options

Get access to the full version of this content by using one of the access options below. (Log in options will check for institutional or personal access. Content may require purchase if you do not have access.)

References

1. Johnston, LD, Miech, RA, O’Malley, PM, Bachman, JG, Schulenberg, JE. Use of ecstasy, heroin, synthetic marijuana, alcohol, cigarettes declined among US teens in 2015. University of Michigan News Service, Ann Arbor, MI, December 16, 2015. Retrieved 14 May 2016 from http://www.monitoringthefuture.org.Google Scholar
2. National Institute on Drug Abuse. High school and youth trends, 2014. Retrieved 14 May 2016 from https://www.drugabuse.gov/publications/drugfacts/high-school-youth-trends.Google Scholar
3. Lucena, J, Blanc, M, Jurado, C, et al. Cocaine-related sudden death: a prospective investigation in south-west Spain. Eur Heart J 2010; 31: 318–329.CrossRefGoogle ScholarPubMed
4. Littmann, L, Monroe, MH, Svenson, RH. Brugada-type electrocardiographic pattern induced by cocaine. Mayo Clin Proc 2000; 75: 845–849.CrossRefGoogle ScholarPubMed
5. Ferreira, S, Crumb, WJ Jr, Carlton, CG, Clarkson, CW. Effects of cocaine and its major metabolites on the HERG-encoded potassium channel. J Pharmacol Exp Ther 2001; 299: 220–226.Google Scholar
6. Lange, RA, Hillis, LD. Cardiovascular complications of cocaine use. N Engl J Med 2001; 345: 351–358.Google Scholar
7. Vongpatanasin, W, Mansour, Y, Chavoshan, B, Arbique, D, Victor, RG. Cocaine stimulates the human cardiovascular system via a central mechanism of action. Circulation 1999; 100: 497–502.Google Scholar
8. Hobbs, WE, Moore, EE, Penkala, RA, Bolgiano, DD, Lopez, JA. Cocaine and specific cocaine metabolites induce von Willebrand factor release from endothelial cells in a tissue-specific manner. Arterioscler Thromb Vasc Biol 2013; 33: 1230–1237.CrossRefGoogle Scholar
9. Siegel, AJ, Mendelson, JH, Sholar, MB, et al. Effect of cocaine usage on C-reactive protein, von Willebrand factor, and fibrinogen. Am J Cardiol 2002; 89: 1133–1135.Google Scholar
10. Mo, W, Singh, AK, Arruda, JA, Dunea, G. Role of nitric oxide in cocaine-induced acute hypertension. Am J Hypertens 1998; 11: 708–714.Google Scholar
11. Mouhaffel, AH, Madu, EC, Satmary, WA, Fraker, TD Jr. Cardiovascular complications of cocaine. Chest 1995; 107: 1426–1434.Google Scholar
12. Togna, G, Tempesta, E, Togna, AR, Dolci, N, Cebo, B, Caprino, L. Platelet responsiveness and biosynthesis of thromboxane and prostacyclin in response to in vitro cocaine treatment. Haemostasis 1985; 15: 100–107.Google Scholar
13. Brickner, ME, Willard, JE, Eichhorn, EJ, Black, J, Grayburn, PA. Left ventricular hypertrophy associated with chronic cocaine abuse. Circulation 1991; 84: 1130–1135.Google Scholar
14. Kolodgie, FD, Virmani, R, Cornhill, JF, Herderick, EE, Malcom, GT, Mergner, WJ. Cocaine: an independent risk factor for aortic sudanophilia. A preliminary report. Atherosclerosis 1992; 97: 53–62.CrossRefGoogle ScholarPubMed
15. Virmani, R, Robinowitz, M, Smialek, JE, Smyth, DF. Cardiovascular effects of cocaine: an autopsy study of 40 patients. Am Heart J 1988; 115: 1068–1076.CrossRefGoogle ScholarPubMed
16. Willens, HJ, Chakko, SC, Kessler, KM. Cardiovascular manifestations of cocaine abuse. A case of recurrent dilated cardiomyopathy. Chest 1994; 106: 594–600.Google Scholar
17. Wilson, LD, Henning, RJ, Suttheimer, C, Lavins, E, Balraj, E, Earl, S. Cocaethylene causes dose-dependent reductions in cardiac function in anesthetized dogs. J Cardiovasc Pharmacol 1995; 26: 965–973.Google Scholar
18. Xu, YQ, Crumb, WJ Jr, Clarkson, CW. Cocaethylene, a metabolite of cocaine and ethanol, is a potent blocker of cardiac sodium channels. J Pharmacol Exp Ther 1994; 271: 319–325.Google Scholar
19. Jatlow, P, Hearn, WL, Elsworth, JD, Roth, RH, Bradberry, CW, Taylor, JR. Cocaethylene inhibits uptake of dopamine and can reach high plasma concentrations following combined cocaine and ethanol use. NIDA Res Monogr 1990; 105: 572–573.Google Scholar
20. Moliterno, DJ, Willard, JE, Lange, RA, et al. Coronary-artery vasoconstriction induced by cocaine, cigarette smoking, or both. N Engl J Med 1994; 330: 454–459.Google Scholar
21. Bashour, TT. Acute myocardial infarction resulting from amphetamine abuse: a spasm-thrombus interplay? Am Heart J 1994; 128: 1237–1239.CrossRefGoogle ScholarPubMed
22. Derlet, RW, Rice, P, Horowitz, BZ, Lord, RV. Amphetamine toxicity: experience with 127 cases. J Emerg Med 1989; 7: 157–161.Google Scholar
23. Schifano, F, Oyefeso, J, Corkery, J, et al. Death rates from ecstasy (MDMA, MDA) and polydrug use in England and Wales 1996-2002. Hum Psychopharmacol 2003; 18: 519–524.CrossRefGoogle ScholarPubMed
24. Setola, V, Hufeisen, SJ, Grande-Allen, KJ, et al. 3,4-methylenedioxymethamphetamine (MDMA, “Ecstasy”) induces fenfluramine-like proliferative actions on human cardiac valvular interstitial cells in vitro. Mol Pharmacol 2003; 63: 1223–1229.Google Scholar
25. Casier, I, Vanduynhoven, P, Haine, S, Vrints, C, Jorens, PG. Is recent cannabis use associated with acute coronary syndromes? An illustrative case series. Acta Cardiol 2014; 69: 131–136.Google Scholar
26. Miller, RH, Dhingra, RC, Kanakis, C Jr, Amat-y-Leon, F, Rosen, KM. The electrophysiological effects of delta-9-tetrahydrocannabinol (cannabis) on cardiac conduction in man. Am Heart J 1977; 94: 740–747.Google Scholar
27. Fisher, BAC, Ghuran, A, Vadamalai, V, Antonios, TF. Cardiovascular complications induced by cannabis smoking: a case report and review of the literature. Emerg Med J 2005; 22: 679–680.CrossRefGoogle ScholarPubMed
28. Mir, A, Obafemi, A, Young, A, Kane, C. Myocardial infarction associated with use of the synthetic cannabinoid K2. Pediatrics 2011; 128: e1622–e1627.CrossRefGoogle ScholarPubMed
29. Lipski, J, Stimmel, B, Donoso, E. The effect of heroin and multiple drug abuse on the electrocardiogram. Am Heart J 1973; 86: 663–668.CrossRefGoogle ScholarPubMed
30. Anchersen, K, Clausen, T, Gossop, M, Hansteen, V, Waal, H. Prevalence and clinical relevance of corrected QT interval prolongation during methadone and buprenorphine treatment: a mortality assessment study. Addiction 2009; 104: 993–999.Google Scholar