A Rare Case of Second Degree Mobitz Type II AV Block Associated with Cocaine Use

Pramod Theetha Kariyanna¹, Apoorva Jayarangaiah², Mohammed Al-Sadawi³, Rodaina Ahmed¹, Jason Green¹, Iya Dubson⁴ and Samy I. McFarlane^3,

¹Division of Cardiovascular Disease, Department of Internal Medicine, State University of New York, Downstate Medical Center, Brooklyn, New York, U.S.A- 11203

²Department of Internal Medicine, Wake Forest University, Baptist Health System, Winston-Salem, North Carolina, U.S.A-27157

³Department of Internal Medicine, State University of New York Downstate Medical Center, Brooklyn, New York, U.S.A- 11203

⁴Department of Internal Medicine NYC HHC Kings County Hospital, Brooklyn, New York, U.S.A- 11203

Cite this paper:
Pramod Theetha Kariyanna, Apoorva Jayarangaiah, Mohammed Al-Sadawi, Rodaina Ahmed, Jason Green, Iya Dubson and Samy I. McFarlane. A Rare Case of Second Degree Mobitz Type II AV Block Associated with Cocaine Use. American Journal of Medical Case Reports. 2018; 6(7):146-148. doi: 10.12691/ajmcr-6-7-7

Abstract

Cocaine is a commonly abused illicit drug in the United States. The complex effects of cocaine on the conduction system of the human heart has not been completely understood. Cocaine acts as a sympathomimetic by inhibition of reuptake of neuronal catecholamines, leading mostly to tachyarrhythmias on presentation. However, cocaine also exerts other effects on the conduction system including sympathomimetic, sino-bradycardic as well as local anesthetic properties. While Multiple cases of atrioventricular (AV) conduction blocks including first degree AV block, Mobitz type I and third degree AV blocks have been previously reported, we hereby present the first case report of cocaine- induced Mobitz type II second degree AV block. This case occurred in a 55 year old woman who presented with retrosternal chest pressure and tested positive for cocaine abuse as documented by urine toxicology test. Patient spontaneously converted to normal sinus rhythm the following day post admission to the hospital. Cocaine is known to inhibit sodium channels and thus has been known to decrease SA node automaticity and conduction via AV node. Electrophysiology studies have previously confirmed cocaine mediated delay in impulse conduction and repolarization. Though rare, physicians should be aware of the possibility of bradyarrhythmias associated with cocaine abuse in order to apply standard therapy such as pacemaker in the event of non-resolution of this serious arrhythmia.

Keywords:
cocaine second degree mobitz type II AV block

This work is licensed under a Creative Commons Attribution 4.0 International License. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/

References:

[1]	Center for Behavioral Health Statistics and Quality (CBHSQ). Behavioral Health Trends in the United States: Results from the 2014 National Survey on Drug Use and Health. Rockville, MD: Substance Abuse and Mental Health Services Administration; 2015. HHS Publication No. SMA 15-4927, NSDUH Series H-50.
[2]	Afonso, L.; Mohammad, T.; Thatai, D. Crack whips the heart: a review of the cardiovascular toxicity of cocaine. Am. J. Cardiol., 2007, 100(6), 1040-1043.
[3]	Maraj, S.; Figueredo, V.M.; Lynn Morris, D. Cocaine and the heart. Clin. Cardiol., 2010, 33(5), 264-269.
[4]	Vasica, G.; Tennant, C.C. Cocaine use and cardiovascular complications. Med. J. Aust., 2002, 177(5), 260-262.
[5]	Jacobsen TN, Grayburn PA, Snyder RW, Hansen J, Chavoshan B, Landau C, Lange RA, Hillis LD, Victor RG. Effects of intranasal cocaine on sympathetic nerve discharge in humans. The Journal of clinical investigation. 1997 Feb 15; 99(4):628-34.
[6]	Seelig MG. History of cocaine as a local anesthetic. Journal of the American Medical Association. 1941 Oct 11; 117(15):1284.
[7]	Magnano AR, Talathoti NB, Hallur R et al. Effect of acute cocaine administration on the QTc interval of habitual users. Am. J. Cardiol. 97, 1244-1246 (2006).
[8]	Javaid JI, Fischman MW, Schuster CR et al. Cocaine plasma concentration: relation to physiological and subjective effects in humans. Science 202, 227-228 (1978).
[9]	Orr D, Jones I. Anaesthesia for laryngoscopy. a comparison of the cardiovascular effects of cocaine and lignocaine. Anaesthesia 23, 194-202 (1968).
[10]	Hollander JE, Hoffman RS, Gennis P et al. Prospective multicenter evaluation of cocaine-associated chest pain. Cocaine Associated Chest Pain (COCHPA) Study Group. Acad. Emerg. Med. 1, 330-339 (1994).
[11]	Chakko S, Fernandez A, Mellman TA et al. Cardiac manifestations of cocaine abuse: a cross-sectional study of asymptomatic men chronically abusing ‘crack’ cocaine. J. Am. Coll. Cardiol. 20, 1168-1174 (1992).
[12]	Kalimullah EA, Bryant SM. Case files of the medical toxicology fellowship at the toxikon consortium in Chicago: cocaine-associated wide-complex dysrhythmias and cardiac arrest-treatment nuances and controversies. Journal of Medical Toxicology. 2008 Dec 1; 4(4): 277-83.
[13]	Weiner RB, Weiner SD, Yurchak PM. Removing the mask. The American journal of medicine. 2008 Feb 1; 121(2): 113-6.
[14]	Bertos-Polo J, Guti C. Aborted sudden death, transient Brugada pattern, and wide QRS dysrrhythmias after massive cocaine ingestion. Journal of electrocardiology. 2001 Oct 1; 34(4): 345-9.
[15]	Kerns II W, Garvey L, Owens J. Cocaine-induced wide complex dysrhythmia. The Journal of emergency medicine. 1997 May 1; 15(3): 321-9.
[16]	Grigorov V, Goldberg L, Foccard JP. Cardiovascular complications of acute cocaine poisoning: a clinical case report: case report. Cardiovascular Journal of South Africa. 2004 May 1; 15(3): 139-42.
[17]	Om A, Ellenbogen KA, Vetrovec GW. Cocaine-induced bradyarrhythmias. American heart journal. 1992 Jul 1; 124(1): 232-4.
[18]	Aryana A, Mooss AN. ST elevation alternans in presence of profound myocardial ischemia and injury induced by cocaine toxicity. Clinical Cardiology: An International Indexed and Peer-Reviewed Journal for Advances in the Treatment of Cardiovascular Disease. 2009 Jul; 32(7):E43-4.
[19]	Tanen DA, Greame KA, Curry SC, Curry S. Crack cocaine ingestion with prolonged toxicity requiring electrical pacing. Journal of Toxicology: Clinical Toxicology. 2000 Jan 1; 38(6): 653-7.
[20]	Isner JM, Estes III NM, Thompson PD, Costanzo-Nordin MR, Subramanian R, Miller G, Katsas G, Sweeney K, Sturner WQ. Acute cardiac events temporally related to cocaine abuse. New England Journal of Medicine. 1986 Dec 4; 315(23): 1438-43.
[21]	Stenberg RG, Winniford MD, Hillis LD, Dowling GP, Buja LM. Simultaneous acute thrombosis of two major coronary arteries following intravenous cocaine use. Archives of pathology & laboratory medicine. 1989 May; 113(5): 521-4.
[22]	Schwartz AB, Janzen D, Jones RT. Electrophysiologic effects of cocaine on the canine ventricle. Journal of cardiovascular pharmacology. 1989 Feb; 13(2): 253-7.
[23]	Temesy-Armos PN, Fraker JT, Brewster PS, Wilkerson RD. The effects of cocaine on cardiac electrophysiology in conscious, unsedated dogs. Journal of cardiovascular pharmacology. 1992 Jun; 19(6): 883-91.
[24]	Tracy CM, Bachenheimer L, Solomon A, Cohen MM, Kuhn FE, Jain R, Corr PB, Gillis RA. Evidence that cocaine slows cardiac conduction by an action on both AV nodal and His-Purkinje tissue in the dog. Journal of electrocardiology. 1991 Jul 1; 24(3): 257-62.
[25]	Przywara DA, Dambach GE. Direct actions of cocaine on cardiac cellular electrical activity. Circulation research. 1989 Jul 1; 65(1): 185-92.
[26]	Magnano AR, Talathoti NB, Hallur R, Jurus DT, Dizon J, Holleran S, Bloomfield DM, Collins E, Garan H. Effect of acute cocaine administration on the QTc interval of habitual users. American Journal of Cardiology. 2006 Apr 15; 97(8): 1244-6.
[27]	Kajdasz DK, Moore JW, Donepudi H, Cochrane CE, Malcolm RJ. Cardiac and mood-related changes during short-term abstinence from crack cocaine: the identification of possible withdrawal phenomena. The American journal of drug and alcohol abuse. 1999 Jan 1; 25(4): 629-37.
[28]	Hollander JE, Lozano M, Fairweather P, Goldstein E, Gennis P, Brogan GX, Cooling D, Thode HC, Gallagher EJ. “Abnormal” electrocardiograms in patients with cocaine-associated chest pain are due to “normal” variants. The Journal of emergency medicine. 1994 Mar 1; 12(2): 199-205.
[29]	Levin KH, Copersino ML, Epstein D, Boyd SJ, Gorelick DA. Longitudinal ECG changes in cocaine users during extended abstinence. Drug & Alcohol Dependence. 2008 May 1; 95(1): 160-3.