Acute myocardial infarction due to marijuana smoking in a young man: guilty should not be underestimated
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American Journal of Emergency Medicine
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American Journal of Emergency Medicine 33 (2015) 1114.e1-1114.e3
Acute myocardial infarction due to marijuana smoking in a young man: guilty should not be underestimated?
Abstract
Marijuana (cannabis) is a frequently used recreational drug that po- tentially imposes serious health problems. We present a case of acute myocardial infarction with chronic total occlusion of left main coronary artery due to marijuana smoking in a 27-year-old man, which was not previously reported. This case illustrate that marijuana abuse can lead to serious cardiovascular events.
Marijuana is the most widely used illicit drug among young adults because of its euphoric and addictive effects [1]. It has been proposed that marijuana is a risk factor for coronary heart disease and can trigger acute coronary syndrome (ACS) especially in Young individuals [2]. In this report, we present a case of acute myocardial infarction (AMI) with chronic total occlusion of left main coronary artery (LMCA) due to marijuana smoking in a 27-year-old man.
A 27-year-old man without previous medical history presented to the emergency department with typical chest pain for 5 hours. He had no any atheresclerotic risk factors, and there was no documented family history of premature ischemic heart disease. He was only a heavy (4 days per a week) marijuana (cannabis) smoker with approximately 10 years. On ad- mission, his arterial blood pressure was 125/75 mm Hg, and his heart rate was 53 beats per minute. Electrocardiography revealed mild sinus brady- cardia with poor R-wave progression in leads DII, DIII, aVF, and V1 to V3 and 0.5-mm ST depression in leads V5 to V6 (Fig. 1). Transthoracic echo- cardiography revealed mild mitral and tricuspid regurgitation and global hypokinesis of left ventricle with an ejection fraction of 30%. His serum biomarkers of myocardial injury were elevated, and his troponin I, creatine kinase (CK) , and creatine kinase-MB (CK-MB) levels were 33 (0-0.028), 600, and 114 ng/mL, respectively. After the administration of a loading dose of clopidogrel (600 mg) and acetylsalicylic acid (300 mg), he was taken to the catheterization laboratory for urgent angiogra- phy with a diagnosis of acute non-ST-segment elevation MI. Coronary an- giography revealed total occlusion of the LMCA with retrograde perfusion of left ventricle via a normal dominant right coronary artery (Fig. 2A and B; Movie 1). To identify the coronary anatomy, a multidetector row com- puted tomography was performed using an Aquillion 64 (64 detector row; Toshiba Medical, Osaka, Japan), which provideda spatial resolution of 0.5 mm and a temporal resolution of 350 milliseconds. Curved planner
? The authors declare that they have no commercial associations or sources of support that might pose a conflict of interest.
and volume rendering images showed total occlusion of the LMCA (Fig. 3). The patient underwent urgent coronary artery bypass graft sur- gery with distal anastomosis of the left internal mammary artery to the left anterior descending artery and an autologous saphenous vein graft bypassing the Circumflex artery.
Marijiuna is the most widely used illicit drug in the United States, and the European Monitoring Center for Drugs and Drug Addiction declared that 1 in 5 adults in Europe have used marijuana or related drugs like hashish at June 2008 report. Marijuana is known to contain at least 60 separate chemical products; the main biological effects of smoking mari- juana result from ?-9-tetrahydrocannabinol and other cannabinoids [1]. It has been proposed that marijuana is a risk factor for coronary heart dis- ease and can trigger ACS especially in young individuals without common risk factors. The strongest evidence implicating marijuana as a trigger MI was reported from a large epidemiologic study by Mittleman et al [2]. They identified 124 patients with ACS, who reported marijuana use and found a statistically significant 4.8-fold increase in the risk of MI in the first hour after marijuana use decreases as time progresses. However, we know that marijuana abuse can lead to coronary artery thrombosis, Spontaneous coronary artery dissection, coronary artery spasm, and coro- nary slow flow according to previous reports; there is not a case report about the total LMCA stenosis. Patients with ACS-associated marijuana abuse described in the literature are usually young and free of atheroscle- rotic risk factors [3-14,2,15]. Total occlusion of LMCA is very rare in pa- tients especially younger than the age of 30 years with coronary artery disease and defined as the complete absence of antegrade flow of contrast beyond the bifurcation of the LMCA. Total LMCA occlusion can be acute, which usually presents as sudden cardiac death, cardiogenic shock, and acute pulmonary edema. Chronic total occlusion like our case manifests more insidiously, usually over a period of more than 3 months, and pa- tients are often presented with acute coronary syndrome.
The exact mechanism of coronary atheresclerosis or ACS due to mari-
juana smoking is not well known. However, possible mechanisms include increased myocardial oxygen demand, which is due, in part, to an increase in Carboxyhemoglobin level and cardiac output, development of coronary atheresclerosis via endothelial damage, decrease Blood supply, marked vasoconstriction of the coronary arteries, and increasing platelet aggrega- tion via ?-9-tetrahydrocannabinol as a major pharmacologically active compound of cannabis [1,16-18].
In conclusion, increased reporting of ACS related to marijuana indicates marijuana as a potential risk factor for ACS in healthy young patients, and marijuana abuse can lead to serious cardiovascular events.
Supplementary data to this article can be found online at http://dx. doi.org/10.1016/j.ajem.2015.01.032.
0735-6757/(C) 2015
1114.e2 Y. Velibey et al. / American Journal of Emergency Medicine 33 (2015) 1114.e1-1114.e3
Fig. 1. Electrocardiography showing poor R-wave progression in leads DII, DIII, aVF, and V1 to V3 and 0.5-mm ST depression in leads V5 to V6.
Fig. 2. Selective left coronary angiogram (A) showing total occlusion of the LMCA (white arrow). Selective right coronary angiogram (B) showing retrograde perfusion of left ventricle via a normal dominant right coronary artery.
Yalcin Velibey, MD Department of Cardiology, Siyami Ersek Thoracic and Cardiovascular Surgery Center, Training and Research Hospital
Istanbul, Turkey Corresponding author. Dr Siyami Ersek Hospital, TibbiyeStr. No. 25 Uskudar/Istanbul,Turkey, Tel.: +90 2164445257
fax: +90 2163379719
E-mail address: [email protected]
Sinan Sahin, MD Department of Radiology, Siyami Ersek Thoracic and Cardiovascular Surgery Center, Training and Research Hospital, Istanbul, Turkey
Ozan Tanik, MD Muhammed Keskin, MD Osman Bolca, MD Mehmet Eren, MD
Department of Cardiology, Siyami Ersek Thoracic and Cardiovascular Surgery Center, Training and Research Hospital, Istanbul, Turkey
http://dx.doi.org/10.1016/j.ajem.2015.01.032
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Fig. 3. Curved planner (A) and volume rendering (B and C) images showing total occlusion of the LMCA (yellow arrow). Abbreviations: RCA, right coronary artery; LAD, left anterior de- scending artery; Cx, circumflex artery.
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