Background: Cocaine is responsible for LV systolic dysfunction
in patients (long-term users or with acute intoxication). The mechanism leading
to develop cocaine-induced cardiomyopathy is not completely understood, however
development of a coronary thrombus, increased oxidative stress, calcium flux sympathomimetic
effects are contributing factors in its pathophysiologic formation.
Case Report: A 23 year old B.Tech third year student from top of north
India was admitted in cardiac emergency department with complaint of severe breathlessness
and pink frothy sputum. ECG showed sinus tachycardia, hyperacute T waves without
any ST elevation and depression or T wave inversion. He denied previous history
of hypertension, diabetes, thyroid, asthma or tuberculosis and trauma or surgery.
He stated us his personal history about cocaine abuser almost 7 years 6 to 8 times
per month. On examination he was hypertensive and tachycardic with low Oxygen saturation
(70%). Lab data showed an elevated Brain natriuretic peptide; urine toxicology was
positive for cocaine. 2D-echocardiography showed dilated left ventricle with poor
LV systolic function LVEF-30%. Coronary angiography revealed LAD spasm without any
obstructive lesions, subsequently NTG infusion was given and final result was TIMI
3 flow in coronaries. He was managed medically and subsequently discharged with
drug rehabilitation. On follow-up diagnostic evaluation after 6 months of cocaine
cessation, his ejection function improved significantly.
Conclusion: Cocaine is a potent sympathomimetic agent associated with
the development of possible fatal cardiovascular complications. Hypertension,
Dilated cardiomyopathy, Dysrhythmias and Acute myocardial infarction are just some
of many cardiovascular effects related to the abuse of cocaine. The management is
like other forms of cardiomyopathy; however β-blockers should be avoided. Non-invasive
testing should be performed after several months to re-evaluate the treatment response.
Left Ventricle Systolic dysfunction, Heart Failure
Abraham JR, Butany J, Leong S, Luk A, Phillips K, Soor
GS. Cocaine cardiotoxicity a review of the pathophysiology, pathology, and
treatment options. Am J Cardiovasc Drugs. 2009;9(3):177–196. doi: 10.1007/BF03256574.
Afonso L, Mohammad T, Thatai D. Crack whips the heart: a
review of the cardiovascular toxicity of cocaine. Am J Cardiol. 2007;100:1040–1043. doi: 10.1016/j.amjcard.2007.04.049.
[3.] Arora S, Alfayoumi F,
Srinivasan V. Transient left ventricular apical ballooning after cocaine use:
is catecholamine cardiotoxicity the pathologic link? Mayo Clin Proc. 2006; 81:
[4.] Aslibekyan S, Levitan EB,
Mittleman M. Prevalent cocaine use and myocardial infarction. Am J Cardiol.
2008; 102: 966– 969.
[5.] Bertolet BD, Freund G,
Martin CA, Perchalski DL, Williams CM, Pepine CJ. Unrecognized left ventricular
dysfunction in an apparently healthy cocaine abuse population. Clin Cardiol.
1990; 13: 323– 328.
[6.] Brickner ME, Willard JE,
Eichhorn EJ, Black J, Grayburn PA. Left ventricular hypertrophy associated with
chronic cocaine abuse. Circulation. 1991; 84: 1130–1135.
Carrillo J, Marmol-Velez A, Martinez S, Restrepo CS,
Riascos R, Rojas CA, Vargas D. Cardiovascular complications of cocaine: imaging
findings. Emerg Radiol. 2009;16:11–19. doi: 10.1007/s10140-008-0762-x.
[8.] Diercks DB, Fonarow GC,
Kirk JD. Illicit stimulant use in a United States heart failure population
presenting to the emergency department (from the Acute Decompensated Heart
Failure National Registry Emergency Module). Am J Cardiol.2008; 102: 1216–
[9.] Egashira K, Morgan KG,
Morgan JP. Effects of cocaine on excitation-contraction coupling of aortic
smooth muscle from the ferret. J Clin Invest. 1991;87: 1322– 1328.
Figueredo VM. Chemical cardiomyopathies: the negative
effects of medications and nonprescribed drugs on the heart. Am J Med. 2011;124:480–488. doi: 10.1016/j.amjmed.2010.11.031.
Figueredo VM, Maraj S, Morris DL. Cocaine and the heart. Clin Cardiol. 2010;33(5):264–269. doi: 10.1002/clc.20746.
[12.] Fischman MW, Schuster CR,
Resnekov L, Shick JF, Krasnegor NA, Fennell W, Freedman DX. Cardiovascular and
subjective effects of intravenous cocaine administration in humans. Arch Gen
Psychiatry. 1976; 33: 983– 989.
[13.] Flores ED, Lange RA,
Cigarroa RG, Hillis L. Effect of cocaine on coronary artery dimensions in
atherosclerotic coronary artery disease: enhanced vasoconstriction at sites of
significant stenoses. J Am Coll Cardiol. 1990; 16: 74–79.
Fraker TD Jr, Madu EC, Mouhaffel AH, Satmary WA.
Cardiovascular complications of cocaine. Chest. 1995;107(5):1426–1434. doi: 10.1378/chest.107.5.1426.
[15.] Gardin JM, Wong N, Alker K,
Hale SL, Paynter J, Knoll M, Jamison B, PattersonM, Kloner R. Acute cocaine
administration induces ventricular regional wall motion and ultrastructural
abnormalities in an anesthetized rabbit model. Am Heart J. 1994; 128: 1117–
[16.] Hale SL, Alker KJ, Rezkalla
S, Figures G, Kloner RA. Adverse effects of cocaine on cardiovascular dynamics,
myocardial blood flow, and coronary artery diameter in an experimental model.
Am Heart J. 1989; 118: 927– 933.
[17.] Hale SL, Alker KJ, Rezkalla
SH, Eisenhauer AC, Kloner RA. Nifedipine protects the heart from the acute
deleterious effects of cocaine if administered before but not after cocaine.
Circulation. 1991; 83: 1437– 1443.
[18.] Hale SL, Lehmann MH, Kloner
RA. Electrocardiographic abnormalities after acute administration of cocaine in
the rat. Am J Cardiol. 1989; 63: 1529– 1530.
[19.] Havranek EP, Nademanee K,
Grayburn PA, Eichhorn EJ. Endothelium-dependent vasorelaxation is impaired in
cocaine arteriopathy. J Am Coll Cardiol.1996; 28: 1168– 1174.
[20.] Heesch CM, Wilhelm CR,
Ristich J, Adnane J, Bontempo FA, Wagner WR. Cocaine activates platelets and
increases the formation of circulating platelet containing microaggregates in
humans. Heart. 2000; 83: 688– 695.
[21.] Kelly RF, Sompalli V,
Sattar P, Khankari K. Increased TIMI frame counts in cocaine users: a case for
increased microvascular resistance in the absence of epicardial coronary disease
or spasm. Clin Cardiol. 2003; 26: 319– 22.
[22.] Kugelmass AD, Oda A,
Monahan K, Cabral C, Ware JA. Activation of human platelets by cocaine.
Circulation. 1993; 88: 876– 883.
[23.] Lange RA, Cigarroa RG,
Yancy CW Jr., Willard JE, Popma JJ, Sills MN, McBrideW, Kim AS, Hillis LD.
Cocaine-induced coronary-artery vasoconstriction. N Engl J Med. 1989; 321:
[24.] Mo W, Singh AK, Arruda JA,
Dunea G. Role of nitric oxide in cocaine-induced acute hypertension. Am J
Hypertens. 1998; 11: 708– 714.
[25.] Moliterno DJ, Willard JE,
Lange RA, Negus BH, Boehrer JD, Glamann DB, Landau C, Rossen JD, Winniford MD,
Hillis LD. Coronary-artery vasoconstriction induced by cocaine, cigarette
smoking, or both. N Engl J Med. 1994; 330: 454–459.
[26.] Moliterno DJ, Lange RA,
Gerard RD, Willard JE, Lackner C, Hillis LD. Influence of intranasal cocaine on
plasma constituents associated with endogenous thrombosis and thrombolysis. Am
J Med. 1994; 96: 492– 496.
[27.] Om A, Warner M, Sabri N,
Cecich L, Vetrovec G. Frequency of coronary artery disease and left ventricle
dysfunction in cocaine users. Am J Cardiol. 1992; 69:1549– 1552.
[28.] Pitts WR, Vongpatanasin W,
Cigarroa JE, Hillis LD, Lange RA. Effects of the intracoronary infusion of
cocaine on left ventricular systolic and diastolic function in humans. Circulation.
1998; 97: 1270– 1273.
[29.] Przywara DA, Dambach GE.
Direct actions of cocaine on cardiac cellular electrical activity. Circ Res.
1989; 65: 185– 192.
[30.] Rezkalla SH, Mazza JJ,
Kloner RA, Tillema V, Chang SH. Effects of cocaine on human platelets in
healthy subjects. Am J Cardiol. 1993; 72: 243– 246.
[31.] Rinder HM, Ault KA, Jatlow
PI, Kosten TR, Smith BR. Platelet alpha-granule release in cocaine users.
Circulation. 1994; 90: 1162– 1167.
[32.] Tazelaar HD, Karch SB,
Stephens BG, Billingham ME. Cocaine and the heart. Hum Pathol. 1987; 18: 195–
[33.] Tong W, Lima JA, Meng Q,
Flynn E, Lai S. Long-term cocaine use is related to cardiac diastolic
dysfunction in an African-American population in Baltimore, Maryland. Int J
Cardiol. 2004; 97: 25– 28.
[34.] Vita JA, Treasure CB, Fish
D, Yeung AC, Vekshtein VI, Ganz P Selwyn AP Endothelial dysfunction leads to
increased coronary constriction to catecholamines in patients with early
atherosclerosis. J Am Coll Cardiol. 1990; 15: 158A.
[35.] 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.
[36.] Vongpatanasin W, Mansour Y,
Chavoshan B, Arbique D, Victor RG. Cocaine stimulates the human cardiovascular system
via a central mechanism action. Circulation. 1999; 100: 497– 502.
[37.] Wilbert-Lampen U, Seliger C,
Zilker T, Arendt RM. Cocaine increases the endothelial release of immunoreactive
endothelin and its concentrations in human plasma and urine: reversal by coincubation
with sigma-receptor antagonists. Circulation. 1998; 98: 385– 390.
[38.] Weber JE, Hollander JE, Murphy
SA, Braunwald E, Gibson CM. Quantitative comparison of coronary artery flow and
myocardial perfusion in patients with acute myocardial infarction in the presence
and absence of recent cocaine use. J Thromb Thrombolysis. 2002; 14: 239– 245.
[39.] Willens HJ, Chakko SC, Kessler
KM. Cardiovascular manifestations of cocaine abuse: a case of recurrent dilated
cardiomyopathy. Chest. 1994; 106: 594– 600.