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Diffuse coronary ectasia and acute coronary syndrome in a young man. Who is guilty? Cannabis, smoking or dyslipidemia?/Genc bir erkekte yaygin koroner ektazi ve akut koroner sendrom. Suclu kim? Esrar, sigara ya da dislipidemi?

A 30-year-old male admitted to our emergency department with chest pain. He was a heavy smoker and also a cannabis user. Electrocardiogram showed QS in leads III, aVF, and dominant R in lead V2. Peak troponin-I and creatine kinase-MB levels were 0.879 ng/mL and 17.75 ng/mL, respectively. He also had dyslipidemia (low density lipoprotein: 214 mg/dL, high density lipoprotein: 35 mg/dL, total cholesterol: 293 mg/dL, triglyceride: 230 mg/dL). Coronary angiography showed diffuse ectasia and plaques in left anterior descending (LAD) and circumflex arteries (Fig. 1a, b, Video 1a, b. See video/movie images at www.anakarder.com). He also had coronary slow flow in LAD. Right coronary artery (RCA) was diffusely ectatic and occluded from proximal segment (Fig. 2a, Video 2a). Since his chest pain resolved, RCA intervention following medical therapy was performed. He had been given acetylsalicylic acid 300 mg, clopidogrel 75 mg, tirofiban 0.15pg/kg/min, enoxaparin bid 60 mg, metoprolol 50 mg, ramipril 5 mg, and atorvastatin 80 mg for 3 days. Control coronary angiogram showed a patent proximal RCA which was diffusely ectatic with abundant plaques (Fig. 2b, Video 2b). Distal RCA was totally occluded. Follow-up with medical therapy was planned.

Cannabis is produced from flower seeds and dried leaves of the plant "cannabis sativa". Active substance responsible from pharmacologic effects of cannabis is [DELTA]9-tetrahydrocannabinol. Cardiovascular effects of cannabis have been well defined. It increases heart rate (1). It causes supine hypertension, while it may cause upright hypotension (1). In addition to its hemodynamic effects, it significantly disrupts blood's oxygen carrying capacity by increasing carboxyhemoglobin level (2). Cannabis use has also been associated with coronary thrombosis (3). It has also been shown to cause coronary vasospasm (4). All of these effects may lead to myocardial ischemia and infarction (MI) by impairing myocardial oxygen demand-supply balance. Adverse hemodynamic changes may cause rupture of vulnerable coronary plaques. It has been shown that risk of MI increases within one hour after cannabis use (5). However, mechanism of MI following cannabis use is not entirely known. There are many case reports in literature about MI associated with cannabis use. Those cases were young and heavy smokers, like our patient. The main difference of our patient from others in literature was the diffuse ectatic coronaries. Coronary artery ecstasies are commonly associated with atherosclerosis. The main pathogenetic mechanism is thinning of the medial layer of the vessel. This leads to a vicious cycle by causing wall stress. The resulting is progressive dilatation and diffuses ectasia. As we previously mentioned, adverse hemodynamic effects associated with cannabis use may lead to ectasia development by increasing wall stress. We did not find any report in literature reporting cannabis and coronary ectasia association. Our case is the first in this respect. However, one also should take into consideration that he also was a heavy smoker and had dyslipidemia. Nevertheless, in clinical practice, clinicians do not encounter such severely ectatic vessels in young patients no matter how many and severe risk factors such patients have. This fact may suggest contribution of cannabis to development of diffuse ectasia. In conclusion, possible cannabis use should be remembered in young patients having diffuse ectatic coronary arteries with abundant plaques.

Muhammet Rasit Sayin, Ibrahim Akpinar, Mehmet Ali Cetiner [1], Turgut Karabag

Department of Cardiology, Faculty of Medicine, Bulent Ecevit University, Zonguldak-Turkey

[1] Clinic of Cardiology, Karadeniz Eregli State Hospital, Zonguldak-Turkey

Video 1. a, b. Left coronary angiogram

Video 2. a, b. Pre-treatment and post-treatment of right coronary angiograms

References

(1.) Weiss JL, Watanabe AM, Lemberger L, Tamarkin NR, Cardon PV. Cardiovascular effects of delta-9-tetrahydrocannabinol in man. Clin Pharmacol Ther 1972; 13: 671-84.

(2.) Hollister LE. Health aspects of cannabis. Pharmacol Rev 1986; 38: 1-20.

(3.) Tatli E, Yilmaztepe M, Altun G, Altun A. Cannabis-induced coronary artery thrombosis and acute anterior myocardial infarction in a young man. Int J Cardiol 2007; 120: 420-2. [CrossRef]

(4.) Basnet S, Mander G, Nicolas R. Coronary vasospasm in an adolescent resulting from marijuana use. Pediatr Cardiol 2009; 30: 543-5. [CrossRef]

(5.) Mittleman MA, Lewis RA, Maclure M, Sherwood JB, Muller JE. Triggering myocardial infarction by marijuana. Circulation 2001; 103: 2805-9. [CrossRef]

Address for Correspondence/Yazisma Adresi: Dr. Muhammet Rasit Sayin Bulent Ecevit Universitesi Tip Fakultesi, Kardiyoloji Anabilim Dali, Zonguldak-Turkiye

Phone: +90 372 261 21 62

E-mail: sayinmr@mynet.com

Available Online Date/Cevrimici Yayin Tarihi: 10.09.2013

doi: 10.5152/akd.2013.212
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Article Details
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Author:Sayin, Muhammet Rasit; Akpinar, Ibrahim; Cetiner, Mehmet Ali; Karabag, Turgut
Publication:The Anatolian Journal of Cardiology (Anadolu Kardiyoloji Dergisi)
Article Type:Letter to the editor
Date:Sep 1, 2013
Words:738
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