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Recurrent myocardial infarction caused by cocaine abuse
Volume
111
Number
4
Brief
Recurrent myocardial cocaine abuse
infarction
caused by
Robert J. Weiss, M.D. Salem, Mass. Recent experimental workIs2has shownthat the adrenergic nervous systemand norepinephrine can causeclinically significant constriction of coronary arteries. Cocaineinhibits norepinephrine reuptake into the nerve terminal (uptake-l) and thus can both prolong and potentiate its effect.3Tachycardia and an increasein blood pressurecanresult. This report presentsa patient who experienced3 myocardial infarctions temporally related to cocaineabuse. A 19-year-old man, who wasa frequent cocaineabuser, presentedon December 13, 1984,with 2 hours of substernal chest pain and an ECG diagnosticof an acute inferior infarction. He stated that for approximately 6 months he had been getting brief episodesof chest pain after most episodesof intranasal cocaine use. He had used cocaine just prior to this hospital visit. He denied any history of exertional chestpain. There wasno history of rest pain not associatedwith drug use,no complaint of cold sensitivity, and no early morning or nocturnal pain. His cardiac risk factors included a mother with a history of an infarction in her early 40’sand heavy cigarette use.Becauseof his age, he underwent cardiac catheterization at another hospital prior to discharge,that revealed apical and diaphragmatic hypokinesia and a 60% diameter lesion in the right coronary artery, a 40% lesion in the mid left anterior descendingartery, and a 60% lesion in the first diagonal vessel.The patient was dischargedon propanolol, 30 mg four times daily; aspirin, 325 mg per day; and dipyridamole, 50 mg thrice daily. The discharge ejection fraction was 58%. On January 17, 1985, again immediately after cocaine use, the patient was readmitted with a new inferior infarction confirmed by ECG and enzyme changes.He received intravenous streptokinase within 5 hours of the onset of chest pain, and the creatine phosphokinase (CPK) peaked at 12 hours at 261with a positive MB band. The patient declined a suggestedright coronary artery angioplasty and was dischargedon atenolol, 50 mg a day; nifedipine, 10mg four times daily; isosorbidedinitrate, 30 mg four times daily; and aspirin and dipyridamole. He again presented on February 15, 1985, after cocaine use, with chest pain and new inferolateral ECG changes.His CPK peaked at 1282. He subsequently underwent a predischargethallium exercisetest in which he attained a heart rate of 70% of predicted. No evidence of exertioninduced ischemia was noted on the ECG or thallium images. A fixed inferoapical defect was defined. The patient wasdischargedon isosorbidedinitrate, 20 mg four times daily; atenolol, 100mg a day; nifedipine, 20 mg four times daily; aspirin and dipyridamole, and was lost to follow-up. In April, 1985, the patient apparently comFrom Salem Hospital. Reprint requests: Robert 04240.
J. Weiss, M.D.,
95
Campus Ave., I,ewiston,
ME
Communications
793
plained to friends of severechest pain and then collapsed. He wasdead on arrival at the hospital. No reliable history of the episode could be obtained. He had undergone another exercisetest at a different hospital in the interim that again had not shown exercise-induced ischemia. It was not clear whether the patient died from another infarction or from an arrhythmia. No autopsy was performed. The is the first report of recurrent infarction and possible death caused by cocaine use. Other casesof cocaine-induced single infarctions have recently been reported.4 This caseextends the likelihood of a relationship between cocaine use and myocardial ischemia. Cocaine inhibits the reuptake of norepinephrine into the nerve terminal. This prolongs and potentiates the activity of norepinephrine, and can be manifest as tachycardia or vasoconstriction and increased blood pressure. Norepinephrine can alsobe removed from the synapseby smooth muscle(uptake-2). Cholesterolhasbeenshownto potentiate coronary artery vasoconstriction due to norepinephrine in dogs.5Although this patient did not have hypercholesterolemia,he did have significant atherosclerosis.It is theoretically possible that cholesterol plaque induced blockade of uptake-2 in the vascular smooth muscle,and the addition of cocaine induced blockade of uptake-l in the nerve. These additive effects may have potentiated norepinephrine’s vasoconstrictor effect enough to cause coronary artery spasm. It is possible that the cocaineinduced vasoconstriction worsened vasospastic angina; however, this diagnosiswasnot suggestedby the patient’s history. It is also possiblethat the sympathetically mediated tachycardia causedby cocaineuseincreasedmyocardial oxygen consumption enoughto causeinfarction. This would seem less likely in light of the lack of ischemia during exercise testing, that also resulted in tachycardia and an elevation in blood pressure.The lack of exertioninduced symptomsor ischemiaon the treadmill makesit most likely that cocaine-induced and sympatheticallymediated vasoconstriction played a causative role in this patient’s recurrent ischemia,infarctions, and possibly in his death. His underlying coronary artery diseasemay have caused his vessels to be more sensitive to the vasoconstrictor effects of norepinephrine. REFERENCES
1.
BuffingonCW, FeiglEO: Adrenergiccoronaryvasoconstriction in the presence of coronarystenosis in the dog.Circ Res
48:416, 1981. 2. Saeed M, Holtz
J, ElsnerD, Bassenge E:Sympatheticcontrol of myocardialoxygenbalancein dogsmediatedby activation
of vascular alpha, adrenoreceptors. J Cardiovasc Pharmacol 7:167, 1985. I Baum ‘3 T: Fundamental principles governing regulation of circulatory function. In Antonaccio MJ, editor: Cardiovascular Pharmacology. New York, 1984, RavenPress,p. 5. 4. Pasternack PF, Colvin SB, Baumann FG: Cocaine-induced angina pectoris and acute myocardial infarction in patients younger than 40 years. Am J Cardiol 55:847, 1985. 5. Rosendorff C, Hoffman JI, Verrier ED, Rouleau J, Boerboom LE: Cholesterol potentiated the coronary artery response to norepinephrine in anesthetized and conscious dogs. Circ Res 48:320, 1981.
111
Number
4
Brief
Recurrent myocardial cocaine abuse
infarction
caused by
Robert J. Weiss, M.D. Salem, Mass. Recent experimental workIs2has shownthat the adrenergic nervous systemand norepinephrine can causeclinically significant constriction of coronary arteries. Cocaineinhibits norepinephrine reuptake into the nerve terminal (uptake-l) and thus can both prolong and potentiate its effect.3Tachycardia and an increasein blood pressurecanresult. This report presentsa patient who experienced3 myocardial infarctions temporally related to cocaineabuse. A 19-year-old man, who wasa frequent cocaineabuser, presentedon December 13, 1984,with 2 hours of substernal chest pain and an ECG diagnosticof an acute inferior infarction. He stated that for approximately 6 months he had been getting brief episodesof chest pain after most episodesof intranasal cocaine use. He had used cocaine just prior to this hospital visit. He denied any history of exertional chestpain. There wasno history of rest pain not associatedwith drug use,no complaint of cold sensitivity, and no early morning or nocturnal pain. His cardiac risk factors included a mother with a history of an infarction in her early 40’sand heavy cigarette use.Becauseof his age, he underwent cardiac catheterization at another hospital prior to discharge,that revealed apical and diaphragmatic hypokinesia and a 60% diameter lesion in the right coronary artery, a 40% lesion in the mid left anterior descendingartery, and a 60% lesion in the first diagonal vessel.The patient was dischargedon propanolol, 30 mg four times daily; aspirin, 325 mg per day; and dipyridamole, 50 mg thrice daily. The discharge ejection fraction was 58%. On January 17, 1985, again immediately after cocaine use, the patient was readmitted with a new inferior infarction confirmed by ECG and enzyme changes.He received intravenous streptokinase within 5 hours of the onset of chest pain, and the creatine phosphokinase (CPK) peaked at 12 hours at 261with a positive MB band. The patient declined a suggestedright coronary artery angioplasty and was dischargedon atenolol, 50 mg a day; nifedipine, 10mg four times daily; isosorbidedinitrate, 30 mg four times daily; and aspirin and dipyridamole. He again presented on February 15, 1985, after cocaine use, with chest pain and new inferolateral ECG changes.His CPK peaked at 1282. He subsequently underwent a predischargethallium exercisetest in which he attained a heart rate of 70% of predicted. No evidence of exertioninduced ischemia was noted on the ECG or thallium images. A fixed inferoapical defect was defined. The patient wasdischargedon isosorbidedinitrate, 20 mg four times daily; atenolol, 100mg a day; nifedipine, 20 mg four times daily; aspirin and dipyridamole, and was lost to follow-up. In April, 1985, the patient apparently comFrom Salem Hospital. Reprint requests: Robert 04240.
J. Weiss, M.D.,
95
Campus Ave., I,ewiston,
ME
Communications
793
plained to friends of severechest pain and then collapsed. He wasdead on arrival at the hospital. No reliable history of the episode could be obtained. He had undergone another exercisetest at a different hospital in the interim that again had not shown exercise-induced ischemia. It was not clear whether the patient died from another infarction or from an arrhythmia. No autopsy was performed. The is the first report of recurrent infarction and possible death caused by cocaine use. Other casesof cocaine-induced single infarctions have recently been reported.4 This caseextends the likelihood of a relationship between cocaine use and myocardial ischemia. Cocaine inhibits the reuptake of norepinephrine into the nerve terminal. This prolongs and potentiates the activity of norepinephrine, and can be manifest as tachycardia or vasoconstriction and increased blood pressure. Norepinephrine can alsobe removed from the synapseby smooth muscle(uptake-2). Cholesterolhasbeenshownto potentiate coronary artery vasoconstriction due to norepinephrine in dogs.5Although this patient did not have hypercholesterolemia,he did have significant atherosclerosis.It is theoretically possible that cholesterol plaque induced blockade of uptake-2 in the vascular smooth muscle,and the addition of cocaine induced blockade of uptake-l in the nerve. These additive effects may have potentiated norepinephrine’s vasoconstrictor effect enough to cause coronary artery spasm. It is possible that the cocaineinduced vasoconstriction worsened vasospastic angina; however, this diagnosiswasnot suggestedby the patient’s history. It is also possiblethat the sympathetically mediated tachycardia causedby cocaineuseincreasedmyocardial oxygen consumption enoughto causeinfarction. This would seem less likely in light of the lack of ischemia during exercise testing, that also resulted in tachycardia and an elevation in blood pressure.The lack of exertioninduced symptomsor ischemiaon the treadmill makesit most likely that cocaine-induced and sympatheticallymediated vasoconstriction played a causative role in this patient’s recurrent ischemia,infarctions, and possibly in his death. His underlying coronary artery diseasemay have caused his vessels to be more sensitive to the vasoconstrictor effects of norepinephrine. REFERENCES
1.
BuffingonCW, FeiglEO: Adrenergiccoronaryvasoconstriction in the presence of coronarystenosis in the dog.Circ Res
48:416, 1981. 2. Saeed M, Holtz
J, ElsnerD, Bassenge E:Sympatheticcontrol of myocardialoxygenbalancein dogsmediatedby activation
of vascular alpha, adrenoreceptors. J Cardiovasc Pharmacol 7:167, 1985. I Baum ‘3 T: Fundamental principles governing regulation of circulatory function. In Antonaccio MJ, editor: Cardiovascular Pharmacology. New York, 1984, RavenPress,p. 5. 4. Pasternack PF, Colvin SB, Baumann FG: Cocaine-induced angina pectoris and acute myocardial infarction in patients younger than 40 years. Am J Cardiol 55:847, 1985. 5. Rosendorff C, Hoffman JI, Verrier ED, Rouleau J, Boerboom LE: Cholesterol potentiated the coronary artery response to norepinephrine in anesthetized and conscious dogs. Circ Res 48:320, 1981.