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Year : 2021  |  Volume : 11  |  Issue : 1  |  Page : 29-31

Myocardial infarction following marijuana consumption in a young male

Department of Cardiology, Apollo Main Hospital, Chennai, Tamil Nadu, India

Date of Submission28-May-2020
Date of Decision14-Jun-2020
Date of Acceptance02-Jul-2020
Date of Web Publication18-Feb-2021

Correspondence Address:
Dr. Sathyamurthy Immaneni
Department of Cardiology, Apollo Main Hospital, Greams Lane, Off Greams Road, Chennai - 600 006, Tamil Nadu
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/JICC.JICC_42_20

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Recreational use of Marijuna smoking is on the rise among the young and adolescents. This can result in worsening of angina or acute myocardial infarction in those with underlying coronary artery disease (CAD) due to sympathetic nervous system stimulation. Even those without CAD can present with acute coronary syndromes due to coronary spasm which can be confirmed by Coronary angiography by ruling out obstructive lesions in these cases . There is fivefold increase in symptoms during 1st hour after consumption. High chances of recurrence of symptoms when the drug is reused and patients needs to be counselled.

Keywords: Acute myocardial infarction, cannabis, coronary vasospasm, marijuana

How to cite this article:
Immaneni S, Lavanya N, Kirubakaran K, Srinivasan K N. Myocardial infarction following marijuana consumption in a young male. J Indian coll cardiol 2021;11:29-31

How to cite this URL:
Immaneni S, Lavanya N, Kirubakaran K, Srinivasan K N. Myocardial infarction following marijuana consumption in a young male. J Indian coll cardiol [serial online] 2021 [cited 2021 Mar 6];11:29-31. Available from:

  Introduction Top

Cannabis sativa or Cannabis indica, commonly called as marijuana, is a psychotropic drug commonly used by adolescents for smoking. There is a surge in its usage globally and its consumption has been on the rise as it was legally permitted in few countries. Marijuana consists of delta 9-tetrahydrocannabinol as an active ingredient. It causes tachycardia, hypertension, and coronary spasm, leading to angina or acute myocardial infarction (AMI). Arrhythmias such as ventricular ectopics, atrial fibrillation, and ventricular tachycardia have been reported with marijuana intake.[1] Other recreational drugs known to induce AMI include cocaine, amphetamine, and ecstasy.[2] This article presents a patient who developed AMI after marijuana consumption.

  Case Report Top

A 27-year-old male student reported to a local hospital with severe retrosternal chest pain, diaphoresis, and dyspnea. A history revealed that he had consumed marijuana 2 h prior to the development of symptoms. There were no known risk factors such as diabetes, hypertension, or family history of coronary artery disease (CAD). He disclosed occasional use of marijuana during social gatherings and there was no intake of alcohol on the day of reporting.

On examination, he was tachycardic with loud S3 gallop and basal rales. Blood pressure was 160/100 mmHg. Electrocardiogram (ECG) showed acute anterior wall myocardial infarction [Figure 1]a. Troponin-I was elevated. Echocardiogram revealed regional wall motion abnormality (RWMA) involving anterior wall with mild left ventricular systolic dysfunction. An emergency coronary angiography showed normal coronaries with TIMI-3 flow. He was advised to continue medical management.

Three weeks after the index episode, the patient reported to us for seeking a second opinion. He remained asymptomatic after the initial event. His body mass index was 29; low-density lipoprotein-cholesterol (LDLc) level was 134 mg/dl. On routine examination, his ECG was normal [Figure 1]b, echocardiogram revealed RWMA with low normal left ventricular function (left ventricular ejection fraction-55'). Repeat coronary angiogram revealed normal coronaries with TIMI-3 flow [Figure 2]a and [Figure 2]b. The patient was reassured and was advised to continue medical treatment. He was counseled regarding abstinence from marijuana use.
Figure 1: (a) Electrocardiogram at first admission. (b) Electrocardiogram after 3 weeks

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Figure 2: (a) Coronary angiography revealing normal left main and its branches. (b) Coronary angiography revealing normal right coronary artery

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  Discussion Top

Acute effects of marijuana consumption are increase in heart rate and blood pressure, extreme sweating, orthostatic hypotension, and even presyncope due to sympathetic nervous system stimulation. The myocardial oxygen (O2) demand increases with decrease in O2 supply due to increased carboxyhemoglobin levels, which can result in worsening of preexisting angina or even result in AMI. Even in those without underlying CAD, it can produce AMI due to acute coronary spasm. The severity of symptoms can be less in chronic users compared to those who consume occasionally in large quantities. Hence, it is vital to delve at depth into the history, to ascertain whether the individual is acute or chronic user and the quantity of the drug consumed.

In vitro studies revealed that Cannabis exerts procoagulant effects through increased expression of glycoprotein IIb/IIIa, P-selectin, and platelets,[3],[4] which can precipitate or aggravate the CAD. The risk of AMI is found to increase five-fold during 1st-h after consumption and the effect slowly wanes off.[5] Concurrent consumption of alcohol has been shown to prolong the detrimental cardiovascular effects. It should be kept in mind that patients may not complain of chest pain due to the analgesic effect of Cannabis, which may mask symptoms.[6] Mittleman et al.[7] interviewed 3882 individual and found marijuana to be the cause for AMI in 3.2' of cases, suggesting that the incidence is low.

Our patient showed ECG evidence of AMI at admission. It has been reported that in some cases, dynamic ST-T changes with deep T-wave inversions in V2, V3 were observed and named as “Pseudo-Wellen's Syndrome,” which reverts back to normal with time.[8] Those with prior CAD can present with worsening angina or acute coronary syndromes (ACS). Individual without prior CAD can present with vasospastic angina or AMI due to coronary spasm as is evident in our patient. Our patient had elevated LDLc and increased BMI without any other comorbidity. CAG done twice did not show any obstructive coronary vascular disease, confirming that AMI could be due to vasospasm as expected with marijuana use.

Saffa et al.[9] reported marijuana-induced recurrent ACS with normal coronary anatomy. AMI has been reported with concomitant use of marijuana and sildenafil.[10] Hence, the physicians should caution the patients about this risk. As reuse of this agent can result in recurrence of symptoms, patients should be strictly counseled about avoidance of this agent.

Myocardial infarction with nonobstructive coronary arteries is a heterogeneous entity with a prevalence of 1'–13' in those diagnosed as AMI. It has several potential etiologies such as spontaneous coronary arterial dissection, vasospastic angina, coronary thromboembolism, and myocardial bridging which needs a detailed diagnostic workup. The treatment depends on the most probable mechanism of AMI [Figure 3].
Figure 3: Potential mechanisms of myocardial infarction with nonobstructive coronary artery

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  Conclusion Top

Marijuana consumption can result in AMI even without underlying CAD. Marijuana can cause angina, AMI due to coronary vasospasm. The acute exposure has higher chances of cardiovascular symptoms. Rarely, patients can be asymptomatic due to analgesic effect of marijuana. Physician should keep wide index of suspicion particularly when younger individual present with AMI without conventional risk factors. Cardiovascular symptoms can recur when this agent is reused and patients' needs to be cautioned about it to prevent future events.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

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Conflicts of interest

There are no conflicts of interest.

  References Top

Rezkalla SH, Sharma P, Kloner RA. Coronary no-flow and ventricular tachycardia associated with habitual marijuana use. Ann Emerg Med 2003;42:365-9.  Back to cited text no. 1
Lippi G, Plebani M, Cervellin G. Cocaine in acute myocardial infarction. Adv Clin Chem 2010;51:53-70.  Back to cited text no. 2
Deusch E, Kress HG, Kraft B, Kozek-Langenecker SA. The procoagulatory effects of delta-9-tetrahydrocannabinol in human platelets. Anesth Analg 2004;99:1127-30.  Back to cited text no. 3
Brantl SA, Khandoga AL, Siess W. Mechanism of platelet activation induced by endocannabinoids in blood and plasma. Platelets 2014;25:151-61.  Back to cited text no. 4
Jouaujus E, Raymond V, Laperpe-Mestre M, Wolff V. What is the current knowledge about CV risk for users of Cannabis based products? A systematic review. Curr Atherosclerosis Rep 2017;19:26.  Back to cited text no. 5
Singh A, Saluja S, Kumar A, Agrawal S, Thind M, Nanda S, et al. CV complications of Marijuana and related substances: A review. Cardiol Therapeut 2018;7:45-59.  Back to cited text no. 6
Mittleman MA, Lewis RA, Maclure M, Sherwood JB, Muller JE. Triggering myocardial infarction by marijuana. Circulation 2001;103:2805-9.  Back to cited text no. 7
Baboujian A, Patibandla S, Tsai KL, Monzidelis C Jr., Buddhavarapu S, Reddy S. Marijuana-related ECG changes: Case report of Pseudo-Wellen's syndrome. JACC 2019;73 supplement 1-2912.  Back to cited text no. 8
Saffa AM, Markham R, Jayasinghe R. Marijuana induced recurrent ACS with normal coronary angiograms. Drug Alcohol Rev 2012;31:91-4.  Back to cited text no. 9
McLeod AL, McKenna CJ, Northridge DB. Myocardial infarction following the combined recreational use of Viagra and Cannabis. Clin Cardiol 2002;25:133-4.  Back to cited text no. 10


  [Figure 1], [Figure 2], [Figure 3]


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