Letter to the Editor Alcohol induced myocardial infarction in two young brothers J.C. Murphy ⁎ , N.P.S. Campbell, P.P. McKeown Regional Medical Cardiology Centre, Royal Victoria Hospital, Grosvenor Road, Belfast, Northern Ireland, BT12 6BA, United Kingdom Received 29 January 2007; accepted 23 April 2007 Available online 24 July 2007 Keywords: Alcohol induced myocardial infarction; Ischaemic heart disease; Alcohol Dear Sir, We present the cases of two brothers who had myocardial infarction at a young age in the setting of excess alcohol ingestion. Both brothers had normal epicardial arteries on coronary angiography. Their father had died suddenly at the age of 42 without a prior history of cardiac disease. The brothers had no other traditional risk factors for developing ischaemic heart disease. 1. Case 1 A 37 year old male presented to his local hospital in June 1995 with a 3 h history of central crushing chest pain. The patient had been consuming alcohol for several hours prior to the onset of symptoms. An electrocardiogram (ECG) showed ST elevation in the infero-lateral leads (Fig. 1) and he received thrombolysis. His subsequent cardiac enzyme assay (CK 1384 U/l, CK-MB12%) confirmed myocardial necrosis. Within 6 h of presentation he developed systemic hypoten- sion and severe pulmonary oedema. He was transferred to a tertiary referral centre where he required inotrope treatment and the placement of an intra-aortic balloon pump. Echocar- diography showed moderately impaired LV function. At angiography his epicardial coronary arteries appeared entire- ly normal. He subsequently improved and was discharged. Three years later the same patient had a further myo- cardial infarction in the setting of acute alcohol intoxication. ECG suggested a non-ST elevation myocardial infarction and cardiac enzymes (CK 1674 U/l, CK-MB12%) confirmed the diagnosis. He was treated conservatively and made an uncomplicated recovery. He failed to attend for subsequent out-patient appointments, including coronary angiography. Two years later the patient had a third myocardial infarc- tion in the setting of alcohol intoxication. Alcohol level was 282 mg/l at presentation. ECG changes were in keeping with an anterior wall non-ST elevation myocardial infarction and myocardial damage was confirmed by biochemical testing (Troponin I 22 μg/l, CK 1682 U/l, CK-MB 10%). Echocar- diography at that time revealed a mildly dilated left ventricle with diffuse left ventricular hypokinesis. He underwent co- ronary angiography, which revealed normal epicardial coro- nary arteries, although flow appeared to be of an unusually slow pattern in the left circumflex artery. However, a follow- up study two weeks later was unequivocally normal. In recent years the patient has reduced his alcohol intake, remaining abstinent for long periods. He has had no further myocardial infarctions. 2. Case 2 In July 1989 a 26 year old male, who is the younger brother of the patient outlined in Case 1, was admitted to his local hospital with acute chest pain which had developed at rest. His symptoms had started in the setting of acute alcohol ingestion and a concurrent diarrheal illness. A non-ST elevation myo- cardial infarction was diagnosed on the initial ECG and con- firmed by a subsequent rise in cardiac enzymes (CK 6316 U/l, CK-MB 11%). He was treated appropriately and made an unremarkable recovery. At subsequent coronary angiography his epicardial coronary arteries appeared normal. Some years late the patient presented with evidence of heart failure and echocardiography showed severe left ven- tricular dysfunction. As part of the diagnostic process, the patient underwent endomyocardial biopsy. This revealed no evidence of myonecrosis, inflammatory cells, granulomata, International Journal of Cardiology 271 (2008) e145 – e147 www.elsevier.com/locate/ijcard ⁎ Corresponding author. Tel.: +44 2890 634065. E-mail address: conleth_m@hotmail.com (J.C. Murphy). 0167-5273/$ - see front matter © 2007 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.ijcard.2007.04.144