Myocardial infarction in a woman with no apparent risk factors

Abstract

In November, 2006, a 40-year-old woman presented to the Emergency Department of Beijing Chaoyang Hospital, with anterior chest pain, which she experienced as pressure. The chest pain had been triggered 4 h previously, by emotional excitement, and was unrelieved by sublingual glyceryl trinitrate. She had no history of hypertension, diabetes, or hyperlipidaemia; she was a non-smoker, and drank no alcohol. She had no previous history of heart disease, and had no other medical history of note. The patient’s heart rate was 61 beats per min, and her blood pressure was 110/80 mm Hg. The rest of the physical examination revealed nothing of note—except for a diastolic murmur, grade 3 (loud but not palpable), which was heard over the apex of the heart, and became louder when the patient changed from a supine to a left lateral position, or to sitting upright. Chest radiography showed no abnormality. On the ECG, there was ST-segment elevation in leads V2–V5, II, III, and aVF. The serum concentrations of troponin I and creatine kinase cardiac isoenzyme were both increased, at 23·06 μg/L and 57 U/L respectively, confi rming the diagnosis of myocardial infarction. The concentrations of total cholesterol and triglycerides were normal. Coronary arteriography showed only one arterial blockage: a total, distal occlusion of the left anterior descending artery (LAD). Repeated balloon dilation did not improve the fl ow through this artery. Echocardiography showed normal chamber sizes, but hypokinesis of the left ventricular apex and interventricular septum. The density of the septum was increased. A mass, measuring 33×21·5 mm, was observed to move between the left atrium and the left ventricle. In diastole, the mass caused mitral stenosis (fi gure). Other than an episode of ventricular tachycardia, lasting less than 30 s, with no resulting haemodynamic abnormalities, the patient’s recovery from her infarction was uneventful. 24 h after admission, she was no longer in pain. The mass was resected surgically: histopathological analysis established that it was a myxoma. When last seen, in June, 2007, the patient was well, and taking no cardiac medications. 30–50% of all primary cardiac tumours are myxomas. About three-quarters of cardiac myxomas are found in the left atrium, although they can occur in any chamber or on any valve. Clinical manifestations of cardiac tumours are determined by their location and size. Small tumours, causing obstruction of fl ow, can produce symptoms earlier than large, infi ltrative tumours. Up to 40% of left atrial myxomas form emboli, of which the majority lodge in the cerebral circulation. Myocardial infarction caused by coronary embolism of cardiac tumours is rare. However, in this case, it is likely, in our opinion, that the occlusion seen on arteriography was an embolus from the myxoma. The patient lacked risk factors for ischaemic heart disease, and had no previous history of heart disease. Arteriography indicated that the occlusion was isolated—and repeated balloon dilation did not improve fl ow through the LAD, implying that there was no pre-existing atheroma. Moreover, although the ECG indicated that the infarction was of the anterior and inferior walls of the heart, the blockage was in the distal LAD. Movement of an embolus could account for this discrepancy—and for the patient’s recovery. Although rare, cardiac myxoma should be considered as a cause of myocardial infarction or stroke, particularly in patients with no apparent risk factors.