Recent studies have shown that moderate and regular consumption of alcohol is associated with a reduction in the risk for coronary arterial disease, angina pectoris and acute myocardial infarction.1 Binge-drinking, in contrast, appears to have an unfavorable effect on the risks for coronary arterial disease and acute myocardial infarction.2 It has been reported that young people with normal coronary arteries are more likely to suffer from a myocardial infarction than older people.3 Although the aetiology, and the pathogenetic mechanisms, of the myocardial infarctions with normal coronary arteries is not well known, coronary vasospasm and concomitant thrombosis, endothelial dysfunction, and platelet dysfunction have been implicated.3 The therapeutic measures for myocardial infarction with normal coronary arteries, as yet, are not well documented. We report here a case of acute myocardial infarction with normal coronary arteries in a 19-year-old adolescent triggered by acute consumption of excessive amounts of alcohol.
Case report
A 19-year-old boy presented at about 11:00 am on Sunday morning to the emergency department of our hospital with complaints of severe retrosternal chest pain lasting three hours, diaphoresis and mild shortness of breath. He had previously been healthy, with no family history of premature coronary arterial disease, nor any history of smoking. One night prior to this event, he had drunk large amounts of alcohol, consisting of 0.70 litre of 45% ethanol, and four beers, approximately six hours prior to the onset of symptoms. After about six hours sleep, he was woken by a severe compressing chest pain radiating to the left shoulder and back. He was haemodinamically stable at the time of admission. Physical examination revealed his blood pressure to be 110 over 60 millimetres of mercury, the pulse rate was 105 beats per minute, and cardiac auscultation showed mild tachycardia, and a gallop rhythm with a third heart sound. There were no signs of pulmonary or peripheral congestion. His 12-lead electrocardiogram showed elevations of the ST segments, on average from 2 to 10 millimetres, in leads V1-6, DI, and aVL (Fig. 1). Laboratory examinations revealed high levels of enzymes consistent with acute myocardial infarction. Biochemical markers of myocardial necrosis showed a typical rise and fall. Troponin-T was positive. The levels of creatine kinase, and its myocardial band, on admission were 851 and 87 units, peaking at 1855 and 191 units, respectively, with normal ranges for our laboratory being from 23 to 132, and from 0 to 6 units per litre.
Figure 1. The electrocardiogram on admission.
Echocardiography performed immediately showed regional abnormalities of wall motion for the left ventricle, mild systolic dysfunction, and a low ejection fraction at 45%. The apical and septal segments were akinetic, while the anterior and lateral segments were hypokinetic. The patient was questioned for the use of cardiotoxic agents other than alcohol, but there was no history of other agents such as cocaine, ergot derivates, ephedrine-like alcaloids, or amphetamines. He was neither a regular drinker nor a smoker. The level of alcohol in the blood was measured at 0.59 grams per litre. We made the diagnosis of acute myocardial infarction triggered by acute ingestion of alcohol. Treatment started with acetylsalicylic acid, clopidogrel, diazepam, nitroglycerine given as an intravenous infusion, titrated up to 40 micrograms per minute, and unfractionated heparin given as an intravenous bolus of 5000 units and a subsequent controlled intravenous infusion. As there were no changes in the degree of ST elevation and symptoms after 15 minutes of infusion of nitroglycerine, we used thrombolytic therapy with tissue plasminogen activator. After the thrombolytic therapy, the chest pain was relieved, and the elevations of the ST segments regressed. After seven days of admission, the patient was referred to a centre for interventional cardiology cardiac catheterization. Coronary angiography demonstrated normal coronary arteries, with left coronary arterial dominance, but without any disturbance of blood flow, and no signs of coronary dissection or atherosclerosis (Fig. 2). Left ventriculography showed the left ventricle to be of normal size, with mild apical hypokinesia.
Figure 2. Angiographically normal coronary arteries.
Other laboratory tests revealed mild leucocytosis, at 12,200 per millimetre cubed, normal levels of platelets, haemoglobin, glucose, blood electrolytes, cholesterol, triglyceride, high density lipoprotein at 0.63 grams per litre, low density lipoprotein at 0.127 grams per litre, thyroid function tests, apoprotein-A-I, apoprotein-B, homocysteine, protein-C activity, protein-S activity, antitrombin-III activity, fibrinogen, erytrocyte sedimentation rate, rheumatoid factor, but high levels of cero-reactive protein, at 1.18 grams per litre, and Lipoprotein(a) at 0.5 grams per litre. Serological tests for infection with Clamidia pneumonia and Helicobacter pylori were negative, as were tests for factor-5 Leiden mutation. These tests were deemed to confirm our diagnosis of acute myocardial infarction triggered by prolonged coronary vasospasm and concomitant thrombosis due to acute consumption of large amounts of alcohol. On the 30th day after the infarction, the electrocardiogram showed persistant loss of R waves in leads I, aVL and V1-6. Echocardiography revealed mild apical hypokinesia of the left ventricle, but now with a nearly normal ejection fraction, at 55%.
Discussion
Mild-to-moderate and regular ingestion of alcohol is well known to be associated with a reduced risk for coronary arterial disease and acute myocardial infarction. In contrast, consumption of large amounts of alcohol, and binge-drinking, may be associated with high cardiovascular mortality, and may trigger acute myocardial infarction in patients with coronary arterial disease.4 Coronary vasospasm and formation of thrombus have been implicated in the pathogenesis of acute myocardial infarction with normal coronary arteries.5 Binge-drinking and excessive consumption of alcohol, however, are also known to cause acute myocardial infarction in the setting of normal coronary arteries, as in our very young patient.5, 6 The underlying mechanisms of infarction, nonetheless, have yet to be demonstrated. Several mechanisms have been suggested, such as coronary vasospasm, decreased fibrinolysis, and an enhanced prothrombotic state caused by the acute intoxication. Oda et al.7 reported that alcohol-induced coronary vasospasm may last nine hours after consumption, even if the levels of ethanol in the plasma return to zero levels. They also suggested that decreased levels of prostaglandin F1a and cyclic guanosin monophosphate play important roles. It has been demonstrated that relatively large doses of alcohol enhance thromboxane-mediated activation of platelets, and activate the inhibitors of plasminogen in the plasma, especially in subjects like ours not accustomed to consumption of alcohol.8 These effects seem to be independent of the circadian variation of the haemostatic system, and may change the balance of haemostasis in favor of thrombogenesis. Furthermore, alcohol has an acute inhibitory effect on fibrinolytic activity, which becomes apparent after consumption of about 40 to 50 grams of alcohol.9 Normally, the circadian variation of fibrinolysis is at its lowest in the morning. Thus, after excessive consumption of alcohol, an ongoing inhibition of fibrinolysis may be superimposed on the morning dip, so promoting life-threatening acute coronary arterial events in the morning hours, as in our case. There are very rare reports of acute myocardial infarction triggered by acute alcohol intoxication in young patients with normal coronary arteries.5 As far as we know, however, our patient is the youngest reported thus far. Binge-drinking, and excessive consumption of alcohol, therefore, increases the risk of myocardial infarction.10 Since consumption of alcohol is very common in the community, the triggering effect of binge-drinking and excessive consumption of alcohol on acute myocardial infarction should be considered as a crucial subject for public health, especially in young persons.
