European Heart Journal (1985) 6, 637-638
Myocardial infarction during marijuana smoking in a young female
J. S. A. COLLINS*, J. D. S. HIGGINSON, D. MCC. BOYLE AND S. W. WEBB|
The Cardiology Department, Ulster Hospital, Dundonald and'f Regional Medical Cardiology Centre,
Royal Victoria Hospital, Belfast, U.K.
KEY WORDS: Cannabis, normal coronary arteries.
Although marijuana smoking is popular among young adults, hospital admissions due to adverse effects of this drug are uncommon". We report a case of a young female who developed an acute myocardial infarction while smoking the drug.
Case report
A previously healthy 33-year old secretary was admitted to the Casualty Department with severe central chest pain radiating to both arms. The pain had started one hour before, while smoking marijuana at a party. She had smoked 20 tobacco cigarettes per day for 16 years. There was no past history of cardiac disease, hypertension or diabetes. A paternal uncle had died of myocardial infarction age 59 years. She had taken marijuana on 3 occasions in the previous 3 years with no ill effects. She was not taking the oral contraceptive pill.
On examination, she was euphoric, pale and sweating profusely. Heart rate was 96 min " ' and blood pressure 110 mmHg. Heart sounds were normal and there were no signs of cardiac failure. The electrocardiograph showed ST elevation in leads 2,3 and aVF with reciprocal ST depression in leads V2-V6 (Fig. 1). Chest X-ray was within normal limits.
Fifteen minutes after admission, she developed ventricular fibrillation which responded to a 200 joule DC shock. She then developed 2:1 heart block, followed by complete heart block and a temporary transvenous pacing wire was inserted.
On the first admission day, serum creatine kinase and aspartate transaminase levels were elevated to 883 IU1"' (normal 0-180IU1"') and 78IU1"1 (normal 6-35 IU I"1), rising to 1701 I U r 1 and 208 IU1"1 on the second day, respectively. There was a corresponding rise in serum creatine kinase (MB) levels to 73 IU I"1 and 123 IU1"1 on these days. Blood urea, electrolytes and glucose were normal. Toxicological assay of the patient's urine within 6 h of admission, using a sensitive radioimmunoassay, showed S-Sngml"1 of total cross-reacting cannabinoids. Electrocardiographs showed evolving changes of acute inferior infarction over the next week, but there were no further arrhythmias and she was discharged on the twelfth hospital day.
Three months later, she underwent treadmill exercise testing and completed stage 7 of Bruce Protocol, achieving a heart rate of 190min"1 (>85% predicted maximal) with no haemodynamic or electrocardiographic abnormality. Random (non-fasting) serum cholesterol was 6-4mmoir' (normal 3-4-7-8) and random serum triglycerides level was l-58mmoir' (normal 0-34-2-26) at this time. Subsequent selective coronary arteriography and left ventriculography showed normal coronary arteries with posterior hypokinesis of the left ventricle.
Comment
Marijuana smoking has been shown to affect the electrocardiograph of normal subjects and a study in patients with ischaemic heart disease showed a significantly decreased exercise time to angina with the drug compared to high-nicotine cigarettes'31. Two previous cases of acute myocardial infarction in close association with marijuana smoking have been reported. In the most recent report, coronary atheroma was demonstrated at post-mortem. In neither case was toxicological evidence of marijuana exposure produced.
In this case, the evidence of myocardial infarction is indisputable with classical electrocardiographic change, rise in cardiac enzymes and ventricular wall hypokinesis. The radiologically normal coronary arteries would suggest that coronary spasm was the cause of infarction in this case, in the absence of predisposing causes for thrombosis other than cigarette smoking. It was felt that ergometrine or marijuana challenge during angiography was not ethical in this case.
Although the close relationship of drug exposure to acute infarction does not necessarily imply causation, an individual sensitivity to marijuana or an impurity in the preparation may have been present. Further non-invasive methods of investigation of myocardial perfusion in users of the drug would be of interest.
References
[1] Lundberg GD, Adelson J, Prosnitz EH. Marijuana-induced hospitalisation. JAMA 1971; 2151 121.
[2] Kochar MS, Hasko MJ. Electrocardiographic effects of marijuana. JAMA 1973; 225: 25-7.
[3] Aronow WS, Cassidy J. Effect of smoking marijuana and of a high-nicotine cigarette on angina pectoris. Clin
Pharmacol Ther 1975; 17: 549-54.
[4] Charles R, Holt S, Kirkhan N. Myocardial infarction and marijuana. Clin Toxicol 1979; 14 (4): 433-8.
[5] Macinnes DC, Miller KM. Fatal coronary artery thrombosis associated with cannabis smoking. J R Coll Gen Pract 1984; 34: 575-6.
•Currently Senior Registrar in Gastrocnterology, Royal Victoria Hospital
Received for publication on 8 February 1985 and in reviled form 27 March 1985.
Address for correspondence: Dr J. S. A. Collins, Senior Registrar in Gastroenterology, Department of Medicine, The Queen's University
of Belfast, Institute of Clinical Science, Grosvenor Road, Belfast BTI2 6BJ, U.K.
0195-668X/85/070637 + 02 $02.00/0 © 1985 The European Society of Cardiology
Downloaded from http://eurheartj.oxfordjournals.org/ by guest on July 10, 2014
Myocardial infarction during marijuana smoking in a young female
J. S. A. COLLINS*, J. D. S. HIGGINSON, D. MCC. BOYLE AND S. W. WEBB|
The Cardiology Department, Ulster Hospital, Dundonald and'f Regional Medical Cardiology Centre,
Royal Victoria Hospital, Belfast, U.K.
KEY WORDS: Cannabis, normal coronary arteries.
Although marijuana smoking is popular among young adults, hospital admissions due to adverse effects of this drug are uncommon". We report a case of a young female who developed an acute myocardial infarction while smoking the drug.
Case report
A previously healthy 33-year old secretary was admitted to the Casualty Department with severe central chest pain radiating to both arms. The pain had started one hour before, while smoking marijuana at a party. She had smoked 20 tobacco cigarettes per day for 16 years. There was no past history of cardiac disease, hypertension or diabetes. A paternal uncle had died of myocardial infarction age 59 years. She had taken marijuana on 3 occasions in the previous 3 years with no ill effects. She was not taking the oral contraceptive pill.
On examination, she was euphoric, pale and sweating profusely. Heart rate was 96 min " ' and blood pressure 110 mmHg. Heart sounds were normal and there were no signs of cardiac failure. The electrocardiograph showed ST elevation in leads 2,3 and aVF with reciprocal ST depression in leads V2-V6 (Fig. 1). Chest X-ray was within normal limits.
Fifteen minutes after admission, she developed ventricular fibrillation which responded to a 200 joule DC shock. She then developed 2:1 heart block, followed by complete heart block and a temporary transvenous pacing wire was inserted.
On the first admission day, serum creatine kinase and aspartate transaminase levels were elevated to 883 IU1"' (normal 0-180IU1"') and 78IU1"1 (normal 6-35 IU I"1), rising to 1701 I U r 1 and 208 IU1"1 on the second day, respectively. There was a corresponding rise in serum creatine kinase (MB) levels to 73 IU I"1 and 123 IU1"1 on these days. Blood urea, electrolytes and glucose were normal. Toxicological assay of the patient's urine within 6 h of admission, using a sensitive radioimmunoassay, showed S-Sngml"1 of total cross-reacting cannabinoids. Electrocardiographs showed evolving changes of acute inferior infarction over the next week, but there were no further arrhythmias and she was discharged on the twelfth hospital day.
Three months later, she underwent treadmill exercise testing and completed stage 7 of Bruce Protocol, achieving a heart rate of 190min"1 (>85% predicted maximal) with no haemodynamic or electrocardiographic abnormality. Random (non-fasting) serum cholesterol was 6-4mmoir' (normal 3-4-7-8) and random serum triglycerides level was l-58mmoir' (normal 0-34-2-26) at this time. Subsequent selective coronary arteriography and left ventriculography showed normal coronary arteries with posterior hypokinesis of the left ventricle.
Comment
Marijuana smoking has been shown to affect the electrocardiograph of normal subjects and a study in patients with ischaemic heart disease showed a significantly decreased exercise time to angina with the drug compared to high-nicotine cigarettes'31. Two previous cases of acute myocardial infarction in close association with marijuana smoking have been reported. In the most recent report, coronary atheroma was demonstrated at post-mortem. In neither case was toxicological evidence of marijuana exposure produced.
In this case, the evidence of myocardial infarction is indisputable with classical electrocardiographic change, rise in cardiac enzymes and ventricular wall hypokinesis. The radiologically normal coronary arteries would suggest that coronary spasm was the cause of infarction in this case, in the absence of predisposing causes for thrombosis other than cigarette smoking. It was felt that ergometrine or marijuana challenge during angiography was not ethical in this case.
Although the close relationship of drug exposure to acute infarction does not necessarily imply causation, an individual sensitivity to marijuana or an impurity in the preparation may have been present. Further non-invasive methods of investigation of myocardial perfusion in users of the drug would be of interest.
References
[1] Lundberg GD, Adelson J, Prosnitz EH. Marijuana-induced hospitalisation. JAMA 1971; 2151 121.
[2] Kochar MS, Hasko MJ. Electrocardiographic effects of marijuana. JAMA 1973; 225: 25-7.
[3] Aronow WS, Cassidy J. Effect of smoking marijuana and of a high-nicotine cigarette on angina pectoris. Clin
Pharmacol Ther 1975; 17: 549-54.
[4] Charles R, Holt S, Kirkhan N. Myocardial infarction and marijuana. Clin Toxicol 1979; 14 (4): 433-8.
[5] Macinnes DC, Miller KM. Fatal coronary artery thrombosis associated with cannabis smoking. J R Coll Gen Pract 1984; 34: 575-6.
•Currently Senior Registrar in Gastrocnterology, Royal Victoria Hospital
Received for publication on 8 February 1985 and in reviled form 27 March 1985.
Address for correspondence: Dr J. S. A. Collins, Senior Registrar in Gastroenterology, Department of Medicine, The Queen's University
of Belfast, Institute of Clinical Science, Grosvenor Road, Belfast BTI2 6BJ, U.K.
0195-668X/85/070637 + 02 $02.00/0 © 1985 The European Society of Cardiology
Downloaded from http://eurheartj.oxfordjournals.org/ by guest on July 10, 2014