Aspirin is key to the treatment of acute myocardial infarction, particularly if stent implantation is considered. In patients with a history of hypersensitivity to aspirin, the optimal management of ST-segment elevation acute myocardial infarction is unclear. We suggest a strategy for addressing this problem by performing percutaneous coronary intervention with antiplatelet therapy by intravenous glycoprotein IIb/IIIa receptor blockers and performing rapid oral desensitization in the ensuing hours, once the patient has stabilized.
Sir: The myocardial dysfunction which is sometimes observed in severe heat stroke does not necessary imply necrosis but seems to be integrated into a systemic inflammatory response syndrome (SIRS). We report a case of favourable evolution after heat stroke in a young man whose electrocardiogram (ECG) and increasing myocardial enzymes suggested acute myocardial infarction.A 24-year-old recruit without personal or family past medical history, collapsed during physical exercise. The systolic blood pressure was 60 mmHg and heart rate 170 bpm. Agitated coma was observed and the core temperature (t C) measured with a rectal probe was 42 C. The symptomatic treatment included controlled ventilation after endotracheal intubation and fluid administration (8 l of colloid and crystalloid solutions over 24 h). Intravenous cooling decreased the core temperature to 39.6 C after 1.5 h. The patient was admitted in our unit 48 h after his collapse. Hyperthermia was controlled, but several organ dysfunctions were noted: respiratory failure, renal insufficiency, rhabdomyolysis (creatine phosphokinase [CK]: 7265 IU; CK[MB fraction]: 0.9 %), fulminant hepatic failure (PT < 10 %; Factor V: 4 %), disseminated intravascular coagulation [DIC]. Simplified Acute Physiology Score (SAPS) II was 35. On admission, the ECG clearly showed an inferolateral subepicardial injury (ST segment elevation more than 2 mm) which persisted during 2 days. There was no prolonged QT interval or U wave (Fig. 1). Troponin Ic was measured at 0.73 IU/l (normal range inferior to 0.1). The transthoracic echocardiography, performed on admission, revealed global hypokinesis (LVEF: 28 %). On account of heart failure, positive inotropic agents such as dopamine (5 mg/kg per minute) and dobutamine (5 mg/ kg per minute) were started and then stopped on the 7th day, whereas a new echocardiographic examination demonstrated an improvement in LV function (LVEF: 42 %). The patient's condition evolved favourably; extubation was performed on the 11th day. Myocardial perfusion scintigraphy (with technetium 99) performed on the 16th day revealed an inferior and apical fixed defect. Coxsackie virus and arbovirus serologies were negative. The coronary arteriography performed on the 18th day showed a normal arteriogram. The patient left the unit on the 23rd day without apparent sequelae. One month after the initial event, a scintigraphy examination revealed the same exertional defect. The exertional test was negative at the clinical examination but changes in T waves appeared during the test and after recovery. A cardiac nuclear magnetic resonance test was performed to check for widening of interventricular septum and subendocardial left ventricular walls. The LVEF was preserved (67 %).
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