Acute myocardial infarction

Abstract

A 62-year-old man was woken by a prolonged and very intensive episode of retrosternal pain. His past medical history included a prostate cancer treated 2 years before with radical prostatectomy and radiation therapy. Thirty minutes after the onset of symptoms, his wife called the regulatory centre of medical emergency (Service d’Aide Medicale d’Urgence). Before the arrival of the physician-staffed ambulance, she noted that her husband became apparently confused and no more complained of chest pain. She did not witness a transient loss of consciousness. When the rescue staff arrived to patient’s home, vital signs were as follows: blood pressure 155/95 mmHg, heart rate 95 beats/min, respiration rate 18 breaths/min and oxygen saturation 96%. Physical examination ruled out focal neurological and congestive heart failure signs. A 12-lead ECG showed a marked ST-segment elevation in anterior leads associated with an inferior ST-segment depression. Sublingual nitrates were ineffective on these ST-segment alterations. Despite neurological symptoms and the absence of persistent chest pain, he was treated like a ST-segment elevation myocardial infarction. Consequently, he received 250 mg of intravenous aspirin, 3000 UI of intravenous enoxaparin and 600 mg of clopidogrel. He arrived to catheterization laboratory 45 min after the first medical contact. Coronary angiogram performed via a right transradial approach demonstrated a culprit lesion on the mid-left anterior descending artery (LAD) coronary artery segment (Fig. 1). The blood flow was thrombolysis in myocardial infarction (TIMI 1) in the distal LAD segment. The remaining coronary tree was free from noticeable plaque. Thrombus aspiration followed by a direct bare-metal stent stenting restored a TIMI 3 blood flow. The brain computed tomography (CT) scan performed immediately after percutaneous coronary intervention was normal. At admission to the ICU of cardiology, haemodynamic status was stable. It remains an anterograde and a mild retrograde amnesia. He remembered the last evening, but did not remember having chest pain or coronary angiogram. He repeated continuously the same questions. Personal knowledge was spared; he was able to provide information about his past history. Physical examination did not find other cognitive impairment, focal neurological or cardiac signs. A second 12-lead ECG revealed a resolve of ST-segment alterations and the emergence of Q waves on anterior leads. Transthoracic echocardiography evaluated left ventricular ejection fraction at 45% with an area at risk concerning apical and mid (anterior, septal and lateral) segments of the left ventricle. Biological parameters ruled out hypoglycemia and unknown diabetes or dyslipidemia. Troponin peak rose to 29mg/l (normal less than 0.1mg/l) and B-type natriuretic peptide was in the normal range. The amnesic gap resolved within 12 h from the onset of symptoms. A transient global amnesia following anterior ST-segment elevation myocardial infarction was finally diagnosed. The patient was discharged from hospital on the third day with a usual postmyocardial infarction treatment. The transient neurological symptoms were explored by a cerebral MRI performed 4 weeks later, which excluded any ischemic event in the vertebrobasilar territory (Fig. 2).