CASE REPORT * ETUDE DE CAS
Acute myocardial infarction associated with cocaine withdrawal Mitchell A.H. Levine, MD, MSc, FRCPC; Jim Nishikawa, MD, FRCPC C ase reports have emphasized a close temporal relation between cocaine use and acute cardiovascular events.' More recently there has been some evidence that silent myocardial ischemia frequently develops in cocaine users during the first weeks of withdrawal.2 We describe an unusual case of myocardial infarction that we felt was associated with cocaine withdrawal rather than with its use.
Case report A 21-year-old man presented to the Emergency Department with retrosternal chest discomfort of about 30 hours' duration. He admitted to having used cocaine, but the last time had been about 2 weeks before the onset of the chest pain. During the two nights before presentation he had been drinking large amounts of alcohol but denied any other drug or substance abuse. The patient had never experienced chest discomfort of this type, and his medical history was notable only for knee surgery. He stated that he was not taking any medication. His father had had a myocardial infarction at 46 years of age. The patient was a nonsmoker and did not have hypertension, diabetes mellitus or known hyperlipidemia. His pulse rate was 88 beats/min and his blood pressure 142/88 mm Hg. There were no signs of left or right heart failure. The remainder of the findings on physical examination were unremarkable. The total serum creatine kinase (CK) peak level 8 hours after admission was 487 (normally < 225) U/L and the CK-MB peak level 50 (normally < 20, 5% of total) U/L. Routine hematologic and biochemical test results were normal. No cocaine or benzoylecgonine was found in the urine.
The initial electrocardiogram showed a sinus rhythm of 65 beats/min and elevations of the ST segment in leads II, III, aVF, V5 and V6. There was no depression of the P-R interval. Inversion of the T wave in these leads evolved over the following 2 days. First-degree heart block also developed. The patient was admitted to the coronary care unit and given acetylsalicylic acid, propranolol, lidocaine (for an episode of ventricular tachycardia) and morphine but no thrombolytic agent. The pain recurred a number of times over the next few days but responded to therapy with nitrites. On the fourth day the patient underwent heart catheterization. The left ventriculogram showed that the distal lateral segment in the right anterior oblique plane was hypokinetic; no other wall motion abnormality was identified. The left and right coronary arteries were free of any sign of disease. There was no attempt to induce spasm. Nitroglycerin was infused throughout the procedure. It was felt that the patient had experienced myocardial ischemia involving the inferior and lateral walls that resulted in a small subendocardial infarction. The observed findings were presumed to be the consequence of coronary artery spasm.
Comments The patient's denial of recent cocaine use was supported by the negative result of the urine screen for cocaine and its metabolite benzoylecgonine. The latter is readily detected in urine within the first 72 hours after cocaine use and can be detected for up to 6 days after cessation of cocaine use.3 In light of the report by Nademanee and associates2 of a high incidence of spontaneous ischemic
From the departments of Clinical Epidemiology and Biostatistics and of Medicine, McMaster
University, Hamilton, Ont.
Reprint requests to: Dr. Mitchell A.H. Levine, Department of Clinical Epidemiology and Biostatistics, 1200 Main St. W, Hamilton, ON L8N 3Z5 MAY 1, 1991
CAN MED ASSOC J 1991; 144 (9)
1139
episodes in cocaine addicts during the early stages of withdrawal the myocardial ischemia and infarction observed in this patient may have been a more severe manifestation of that phenomenon. Most of the studies in the literature emphasize the close temporal relation between acute myocardial events and cocaine use. This selection bias results in the active exclusion of case reports that would identify the withdrawal period as an important time for inyocardial complications. The only other report of acute myocardial infarction during cocaine withdrawal involved a patient in whom a thrombus developed in his left anterior descending artery after 3 days of intermittent chest pain that had begun within 5 hours after cocaine ingestion.4 Unlike patients with Prinzmetal angina those with cocaine-related coronary vasospasm do not show evidence of ergonovine-induced vasospasm.' 24 Thus, there is no evidence of an inherent propensity for coronary vasospasm among these patients. Vasospasm occurring during cocaine withdrawal may be the result of dopamine depletion or receptor down-regulation and an increased sensitivity to a-adrenergic receptor stimulation.2 In the past propranolol has been recommended for the treatment of cocaine-related cardiac events.5 Recently it has been shown that cocaineinduced coronary vasoconstriction is potentiated by p-adrenergic blockade.6 Whether this is true for the withdrawal period is unknown, but the mechanism we have proposed for withdrawal-associated vasospasm in this case would suggest a similar problem with f-adrenergic blockade. In addition, the patient's episodes of postinfarction angina were limited to the 48-hour period in hospital during which he received propranolol.
This is only one case report, but together with the documentation of myocardial ischemia in other patients during cocaine withdrawal it should encourage physicians to consider cocaine use in the preceding month as a potential factor in acute myocardial ischemia and infarction. If cocaine withdrawal is suspected propranolol should probably be avoided and nitroglycerin or calcium-channel blockers used instead.
References 1. Inner J, Estes NA III, Thompson PD et al: Acute cardiac events temporally related to cocaine abuse. N Engi J Med 1986; 315: 1438-1443 2. Nademanee K, Gorelick DA, Josephson MA et al: Myocardial ischemia during cocaine withdrawal. Ann Intern Med 1989; 111: 876-880
3. Hamilton HE, Wallace JE, Shimek EL et al: Cocaine and benzoylecgonine excretion in humans. J Forensic Sci 1977; 22: 697-707 4. Zimmerman FH, Gustafson GM, Kemp HG Jr: Recurrent myocardial infarction associated with cocaine abuse in a young man with normal coronary arteries: evidence for coronary artery spasm culminating in thrombosis. J Am Coll Cardiol 1987; 91: 964-968
5. Rappolt RT Sr, Gay GR, Soman M et al: Treatment plan for acute and chronic adrenergic poisoning crisis utilizing sympatholytic effects of the f1-02 receptor site blocker propranolol (Inderal) in concert with diazepam and urine acidification. Clin Toxicol 1979; 14: 55-69
6. Lange RA, Cigarroa RG, Flores ED et al: Potentiation of cocaine-induced coronary vasoconstriction by beta-adrenergic blockade. Ann Intern Med 1990; 112: 897-903
Testing the soil Mlan is essentiall1 a bulb with manv thousands of roots. In himn the alone /eIe; the rest serves to hold themn together and to mnove themn ablout mnore convenient/v. WArhat wve see then is the pot in which the mnan (the nerves,) is planted. nerves
-
1140
CAN MED ASSOC J 1991; 144 (9)
Georg Christoph Lichtenberg (1742-1799)
LE Ier MAI 1991
Acute myocardial infarction associated with cocaine withdrawal Mitchell A.H. Levine, MD, MSc, FRCPC; Jim Nishikawa, MD, FRCPC C ase reports have emphasized a close temporal relation between cocaine use and acute cardiovascular events.' More recently there has been some evidence that silent myocardial ischemia frequently develops in cocaine users during the first weeks of withdrawal.2 We describe an unusual case of myocardial infarction that we felt was associated with cocaine withdrawal rather than with its use.
Case report A 21-year-old man presented to the Emergency Department with retrosternal chest discomfort of about 30 hours' duration. He admitted to having used cocaine, but the last time had been about 2 weeks before the onset of the chest pain. During the two nights before presentation he had been drinking large amounts of alcohol but denied any other drug or substance abuse. The patient had never experienced chest discomfort of this type, and his medical history was notable only for knee surgery. He stated that he was not taking any medication. His father had had a myocardial infarction at 46 years of age. The patient was a nonsmoker and did not have hypertension, diabetes mellitus or known hyperlipidemia. His pulse rate was 88 beats/min and his blood pressure 142/88 mm Hg. There were no signs of left or right heart failure. The remainder of the findings on physical examination were unremarkable. The total serum creatine kinase (CK) peak level 8 hours after admission was 487 (normally < 225) U/L and the CK-MB peak level 50 (normally < 20, 5% of total) U/L. Routine hematologic and biochemical test results were normal. No cocaine or benzoylecgonine was found in the urine.
The initial electrocardiogram showed a sinus rhythm of 65 beats/min and elevations of the ST segment in leads II, III, aVF, V5 and V6. There was no depression of the P-R interval. Inversion of the T wave in these leads evolved over the following 2 days. First-degree heart block also developed. The patient was admitted to the coronary care unit and given acetylsalicylic acid, propranolol, lidocaine (for an episode of ventricular tachycardia) and morphine but no thrombolytic agent. The pain recurred a number of times over the next few days but responded to therapy with nitrites. On the fourth day the patient underwent heart catheterization. The left ventriculogram showed that the distal lateral segment in the right anterior oblique plane was hypokinetic; no other wall motion abnormality was identified. The left and right coronary arteries were free of any sign of disease. There was no attempt to induce spasm. Nitroglycerin was infused throughout the procedure. It was felt that the patient had experienced myocardial ischemia involving the inferior and lateral walls that resulted in a small subendocardial infarction. The observed findings were presumed to be the consequence of coronary artery spasm.
Comments The patient's denial of recent cocaine use was supported by the negative result of the urine screen for cocaine and its metabolite benzoylecgonine. The latter is readily detected in urine within the first 72 hours after cocaine use and can be detected for up to 6 days after cessation of cocaine use.3 In light of the report by Nademanee and associates2 of a high incidence of spontaneous ischemic
From the departments of Clinical Epidemiology and Biostatistics and of Medicine, McMaster
University, Hamilton, Ont.
Reprint requests to: Dr. Mitchell A.H. Levine, Department of Clinical Epidemiology and Biostatistics, 1200 Main St. W, Hamilton, ON L8N 3Z5 MAY 1, 1991
CAN MED ASSOC J 1991; 144 (9)
1139
episodes in cocaine addicts during the early stages of withdrawal the myocardial ischemia and infarction observed in this patient may have been a more severe manifestation of that phenomenon. Most of the studies in the literature emphasize the close temporal relation between acute myocardial events and cocaine use. This selection bias results in the active exclusion of case reports that would identify the withdrawal period as an important time for inyocardial complications. The only other report of acute myocardial infarction during cocaine withdrawal involved a patient in whom a thrombus developed in his left anterior descending artery after 3 days of intermittent chest pain that had begun within 5 hours after cocaine ingestion.4 Unlike patients with Prinzmetal angina those with cocaine-related coronary vasospasm do not show evidence of ergonovine-induced vasospasm.' 24 Thus, there is no evidence of an inherent propensity for coronary vasospasm among these patients. Vasospasm occurring during cocaine withdrawal may be the result of dopamine depletion or receptor down-regulation and an increased sensitivity to a-adrenergic receptor stimulation.2 In the past propranolol has been recommended for the treatment of cocaine-related cardiac events.5 Recently it has been shown that cocaineinduced coronary vasoconstriction is potentiated by p-adrenergic blockade.6 Whether this is true for the withdrawal period is unknown, but the mechanism we have proposed for withdrawal-associated vasospasm in this case would suggest a similar problem with f-adrenergic blockade. In addition, the patient's episodes of postinfarction angina were limited to the 48-hour period in hospital during which he received propranolol.
This is only one case report, but together with the documentation of myocardial ischemia in other patients during cocaine withdrawal it should encourage physicians to consider cocaine use in the preceding month as a potential factor in acute myocardial ischemia and infarction. If cocaine withdrawal is suspected propranolol should probably be avoided and nitroglycerin or calcium-channel blockers used instead.
References 1. Inner J, Estes NA III, Thompson PD et al: Acute cardiac events temporally related to cocaine abuse. N Engi J Med 1986; 315: 1438-1443 2. Nademanee K, Gorelick DA, Josephson MA et al: Myocardial ischemia during cocaine withdrawal. Ann Intern Med 1989; 111: 876-880
3. Hamilton HE, Wallace JE, Shimek EL et al: Cocaine and benzoylecgonine excretion in humans. J Forensic Sci 1977; 22: 697-707 4. Zimmerman FH, Gustafson GM, Kemp HG Jr: Recurrent myocardial infarction associated with cocaine abuse in a young man with normal coronary arteries: evidence for coronary artery spasm culminating in thrombosis. J Am Coll Cardiol 1987; 91: 964-968
5. Rappolt RT Sr, Gay GR, Soman M et al: Treatment plan for acute and chronic adrenergic poisoning crisis utilizing sympatholytic effects of the f1-02 receptor site blocker propranolol (Inderal) in concert with diazepam and urine acidification. Clin Toxicol 1979; 14: 55-69
6. Lange RA, Cigarroa RG, Flores ED et al: Potentiation of cocaine-induced coronary vasoconstriction by beta-adrenergic blockade. Ann Intern Med 1990; 112: 897-903
Testing the soil Mlan is essentiall1 a bulb with manv thousands of roots. In himn the alone /eIe; the rest serves to hold themn together and to mnove themn ablout mnore convenient/v. WArhat wve see then is the pot in which the mnan (the nerves,) is planted. nerves
-
1140
CAN MED ASSOC J 1991; 144 (9)
Georg Christoph Lichtenberg (1742-1799)
LE Ier MAI 1991
