Marijuana-associated ST-elevation myocardial infarction: is this a benign drug

Abstract

Marijuana is the most commonly used psychoactive drug in the USA. A 35-year-old man with a medical history of marijuana abuse is admitted to the hospital due to crushing substernal chest pain. ECG shows evolving ST-segment elevation with a rise in cardiac enzymes, consistent with ST-elevation myocardial infarction. A urine toxicology screen is positive for cannabis and negative for cocaine and other stimulant drugs. An emergent cardiac catheterisation reveals no evidence of coronary artery disease or thrombosis. A diagnosis of coronary vasospasm is strongly considered, and the patient is started on calcium channel blocker, with a resolution of symptoms and ECG changes. Marijuana-induced coronary spasm causing myocardial infarction has rarely been reported. Marijuana is becoming a social norm in adolescents and there remains a misconception that it is harmless and even beneficial. Increasing drug abuse remains a public health concern, necessitating population education by physicians for safer healthcare practices.

Background

Marijuana is the most common psychoactive drug used in the USA, with over 22 million people consuming marijuana in a month according to the 2015 National Survey on Drug Use and Health. The majority of the users are young with more than 11 million young adults between ages 18 and 25 years having consumed marijuana in 1 year.¹ Medical emergencies related to marijuana use have also increased. According to the Drug Abuse Warning Network in 2011, there were up to 456 000 drug-related emergency department (ED) visits in the USA with marijuana use mentioned in the medical records (increase of 21% compared with 2009).² Marijuana use has been related to a miscellany of cardiovascular effects. We report a case of ST-elevation myocardial infarction (STEMI) after marijuana use in a patient with normal coronary angiography.

Case presentation

A 35-year-old man with a medical history of marijuana abuse and no previous history of cardiac disease presented to the ED with crushing left-sided chest pain. He denied traditional risk factors for coronary artery disease. He reported several episodes of emesis and decreased oral intake after increasing marijuana consumption lately. Vital signs were normal and physical examination was unremarkable on arrival. A CT angiogram was negative for pulmonary embolism. ECG on arrival revealed evolving ST-segment elevation in lateral leads (figure 1). Initial troponin was elevated at 5.6 ng/mL (normal <0.04 ng/mL). Urine toxicology screen was positive for marijuana and negative for other substances including cocaine. He underwent emergent cardiac catheterisation, revealing no evidence of coronary thrombosis or underlying coronary artery disease (figure 2). A transthoracic echocardiogram was also normal with preserved ejection fraction and no evidence of other echocardiographic abnormalities. Coronary artery spasm (CAS) was considered the likely aetiology and he was started on calcium channel blockers (CCBs) with prompt resolution of symptoms and ECG abnormalities. The patient was discharged from the hospital in 3 days on CCB therapy and counselled regarding ill effects of cannabinoids abuse.

Figure 1.

ECG on arrival showing ST-elevation in lateral leads (V5, V6, aVL and lead I)

Figure 2.

Cardiac catheterization showing normal coronary angiogram.

Investigations

ECG was performed (figure 1) and cardiac enzymes are obtained to rule out acute coronary syndrome.

Coronary angiography was performed as shown in figure 2.

Differential diagnosis

Pulmonary embolism was considered in the differential diagnosis given the age and absence of typical risk factors for coronary artery disease in this patient. However, a CT pulmonary angiogram was negative for pulmonary embolism. Coronary artery thrombosis and coronary spasm were also considered in this patient and coronary angiography was performed conceding the diagnosis as described.

Treatment

The patient was started on CCB therapy with resolution of ECG changes and symptoms.

Outcome and follow-up

The patient was discharged from the hospital on the third day of hospitalisation on CCB therapy. He had prompt resolution of his chest pain and ECG changes after CCB therapy. He was counselled regarding the ill effects of cannabinoids abuse before discharge.

Discussion

The use of tetrahydrocannabinol (THC), the active component of marijuana, has been temporally associated with myocardial ischaemia, cardiomyopathy, arrhythmia and sudden cardiac death.³ Smoked marijuana comprises a variety of chemical components, with delta-9-THC causing the majority of adverse cardiovascular effects.⁴

Marijuana has traditionally been considered a benign drug in the population, but a variety of cardiovascular effects have been reported. It affects haemodynamic parameters by altering heart rate and blood pressure responses. It can cause a dose-dependent increase in the heart rate up to 100%. There is a triphasic response of blood pressure.⁵ Marijuana-associated arrhythmias have also been reported.^{6 7} There is an alteration in the anginal threshold after a single marijuana cigarette consumption.^{8 9} The majority of patients with reported MIs had some form of atherosclerotic disease.⁸

Cases of marijuana-related STEMI have been reported in the literature.¹⁰ The precise mechanism of marijuana-related MI is difficult to determine. Enhanced platelet aggregation, increased factor VII levels and increased carboxyhaemoglobin content causing decreased oxygen carrying capacity have all been reported and could potentially contribute to ischaemia.^{11 12} Additionally, cannabis can induce CAS, especially in the presence of underlying atherosclerotic plaques.^{13 14} Marijuana use is associated with increased chances of plaque rupture in high-risk lesions.⁸ Nonetheless, not all cases of cannabis-induced MI involved atherosclerotic plaques.¹⁵

CAS is reported with various drugs, including cocaine and other direct sympathomimetic activators of the coronary vasculature. Rare cases of marijuana-induced coronary spasm have been reported.¹⁶ The exact mechanism of marijuana-related CAS remains unknown. Marijuana has been associated with emesis-related hypovolemic states, which can induce CAS due to coronary underfilling.¹⁷ We postulate that our patient had likely developed vasospasm worsened by hypovolaemia due to increased marijuana usage. Diagnosis of CAS is usually done with clinical and ECG features.¹⁸

Recent studies on the younger population with MI (Partners Young MI registry) have reported higher all-cause and cardiovascular mortality among patient with drug abuse. Marijuana use was more prevalent than cocaine in this study.¹⁹ With legalisation of marijuana by many states, we may be on the verge of a marijuana epidemic. Marijuana is becoming a social norm in adolescents and there remains a misperception that it is harmless and even beneficial. Marijuana is a major evolving public health concern and is now more prevalent than tobacco use in adolescents. The question remains regarding its safety as drug abuse, in general, is under-reported subject. Healthcare professional should be aware of potential adverse cardiovascular effects and should educate patients regarding this emerging public health issue.

Learning points.

• Cardiovascular mortality is elevated among patients with drug abuse with marijuana being the most prevalent drug in young population.

• Smoked marijuana has been associated with myocardial ischaemia, cardiomyopathy, arrhythmia and sudden cardiac death.

• Marijuana-induced coronary spasm has been reported which may lead to myocardial ischaemia and infarction.

• Healthcare professional should be aware of potential adverse cardiovascular effects of marijuana and should educate patients regarding this emerging public health issue.