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cially in the parts of tissues with the highest demand for oxygen and the lowest metabolic stores, such as the brain and heart, which are therefore more vulnerable. CO in- toxications are usually expressed as neurological events, but cardiological events can also occur (2). Myocardial in- jury may arise via electrical, functional, and morphologi- cal changes in the heart through severe general tissue hy- poxia; there may be a direct toxic eect on the myocardial mitochondria promptly after exposure, or this may be de- layed for several days (3). CO can induce a tendency toward coronary vasospasm and thrombus formation by slowing the bloodstream, increasing the permeability of the ves- sel walls, and increasing platelet aggregability and poly- cythemia; these factors are also responsible for myocar- dial damage in patients with CO poisoning (4). In addi- tion, oxygen radical formation and subsequent lipid per- oxidation, as well as induction of cellular apoptosis, are also potential explanations for the cardiotoxicity of CO (2, 5). Cardiac involvement encompassing angina attack, my- ocardial infarction, heart failure, cardiogenic shock, and arrhythmias, such as ventricular extrasystoles, atrial fibril- lation, bradycardia, and atrioventricular block in CO poi- soning was first noted by Lippi (5). However, 50% or more of the circulating form of carboxyhemoglobin can lead to patchy myocardial necrosis, a CO-Hb level of 25% is con- sidered an indication for the use of hyperbaric oxygen or advanced treatment (6, 7). Acute myocardial infarction (AMI) is a clinical condition occurring suddenly but result- ing from a long-term decrease in the amount of oxygen present in the myocardium. Its most common cause is atherosclerotic disease of the coronary arteries. AMI asso- ciated with CO poisoning occurs very rarely.

Myocardial Infarction in a Young Patient After Acute Exposure to Carbon Monoxide