摘要
BACKGROUND: Reversible left ventricular dysfunction precipitated by emotional stress has been reported, but the mechanism remains unknown. METHODS: We evaluated 19 patients who presented with left ventricular dysfunction after sudden emotional stress. All patients underwent coronary angiography and serial echocardiography; five underwent endomyocardial biopsy. Plasma catecholamine levels in 13 patients with stress-related myocardial dysfunction were compared with those in 7 patients with Killip class III myocardial infarction. RESULTS: The median age of patients with stress-induced cardiomyopathy was 63 years, and 95 percent were women. Clinical presentations included chest pain, pulmonary edema, and cardiogenic shock. Diffuse T-wave inversion and a prolonged QT interval occurred in most patients. Seventeen patients had mildly elevated serum troponin I levels, but only 1 of 19 had angiographic evidence of clinically significant coronary disease. Severe left ventricular dysfunction was present on admission(median ejection fraction, 0.20; interquartile range, 0.15 to 0.30) and rapidly resolved in all patients(ejection fraction at two to four weeks, 0.60; interquartile range, 0.55 to 0.65; P< 0.001). Endomyocardial biopsy showed mononuclear infiltrates and contraction-band necrosis. Plasma catecholamine levels at presentation were markedly higher among patients with stress-induced cardiomyopathy than among those with Killip class III myocardial infarction(median epinephrine level, 1264 pg per milliliter[interquartile range, 916 to 1374] vs. 376 pg per milliliter[interquartile range, 275 to 476]; norepinephrine level, 2284 pg per milliliter[interquartile range, 1709 to 2910] vs. 1100 pg per milliliter[interquartile range, 914 to 1320]; and dopamine level, 111 pg per milliliter[interquartile range, 106 to 146] vs. 61 pg per milliliter[interquartile range, 46 to 77]; P< 0.005 for all comparisons). CONCLUSIONS: Emotional stress can precipitate severe, reversible left ventricular dysfunction in patients without coronary disease. Exaggerated sympathetic stimulation is probably central to the cause of this syndrome.
BACKGROUND: Reversible left ventricular dysfunction precipitated by emotional stress has been reported, but the mechanism remains unknown. METHODS: We evaluated 19 patients who presented with left ventricular dysfunction after sudden emotional stress. All patients underwent coronary angiography and serial echocardiography; five underwent endomyocardial biopsy. Plasma catecholamine levels in 13 patients with stress-related myocardial dysfunction were compared with those in 7 patients with Killip class III myocardial infarction. RESULTS: The median age of patients with stress-induced cardiomyopathy was 63 years, and 95 percent were women. Clinical presentations included chest pain, pulmonary edema, and cardiogenic shock. Diffuse T-wave inversion and a prolonged QT interval occurred in most patients. Seventeen patients had mildly elevated serum troponin I levels, but only 1 of 19 had angiographic evidence of clinically significant coronary disease. Severe left ventricular dysfunction was present on admission(median ejection fraction, 0.20; interquartile range, 0.15 to 0.30) and rapidly resolved in all patients(ejection fraction at two to four weeks, 0.60; interquartile range, 0.55 to 0.65; P< 0.001). Endomyocardial biopsy showed mononuclear infiltrates and contraction-band necrosis. Plasma catecholamine levels at presentation were markedly higher among patients with stress-induced cardiomyopathy than among those with Killip class III myocardial infarction(median epinephrine level, 1264 pg per milliliter[interquartile range, 916 to 1374] vs. 376 pg per milliliter[interquartile range, 275 to 476]; norepinephrine level, 2284 pg per milliliter[interquartile range, 1709 to 2910] vs. 1100 pg per milliliter[interquartile range, 914 to 1320]; and dopamine level, 111 pg per milliliter[interquartile range, 106 to 146] vs. 61 pg per milliliter[interquartile range, 46 to 77]; P< 0.005 for all comparisons). CONCLUSIONS: Emotional stress can precipitate severe, reversible left ventricular dysfunction in patients without coronary disease. Exaggerated sympathetic stimulation is probably central to the cause of this syndrome.
