We describe a case of a 76-year-old woman who presented with chest pain after a violent argument. On admission the electrocardiogram showed 1-mm ST segment elevation in II, III, aVF, V3-V6 leads; the subsequent electrocardiogram showed T-wave inversion in the same leads. Peak troponin I level was 7.3 ng/dl (normal < 0.4 ng/dl). Emergency angiography demonstrated the so-called "apical ballooning", in the absence of any obstructive coronary artery disease. A myocardial contrast echocardiogram performed 5 days later showed a large perfusion defect in the akinetic apical region of the left ventricle; at 1-month follow-up myocardial perfusion and left ventricular wall motion became completely normal. In patients with apical ballooning syndrome a catecholamine-mediated endothelial injury might be responsible of a microvascular coronary dysfunction which causes myocardial ischemia and subsequent myocardial stunning.
Transient impairment of myocardial perfusion in a patient with apical ballooning syndrome
GALASSI, ALFREDO;
2007-01-01
Abstract
We describe a case of a 76-year-old woman who presented with chest pain after a violent argument. On admission the electrocardiogram showed 1-mm ST segment elevation in II, III, aVF, V3-V6 leads; the subsequent electrocardiogram showed T-wave inversion in the same leads. Peak troponin I level was 7.3 ng/dl (normal < 0.4 ng/dl). Emergency angiography demonstrated the so-called "apical ballooning", in the absence of any obstructive coronary artery disease. A myocardial contrast echocardiogram performed 5 days later showed a large perfusion defect in the akinetic apical region of the left ventricle; at 1-month follow-up myocardial perfusion and left ventricular wall motion became completely normal. In patients with apical ballooning syndrome a catecholamine-mediated endothelial injury might be responsible of a microvascular coronary dysfunction which causes myocardial ischemia and subsequent myocardial stunning.File | Dimensione | Formato | |
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