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Previous Volume 352:539-548 February 10, 2005 Number 6 Next

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ABSTRACT

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.

Source Information

From the Division of Cardiology, Department of Medicine (I.S.W., D.R.T., J.A.C.L., S.P.S., G.G., K.C.W., J.J.R., H.C.C.), and the Brady Urological Institute (T.J.B.), Johns Hopkins University School of Medicine, Baltimore; the Department of Epidemiology, Johns Hopkins University School of Public Health, Baltimore (D.R.T.); and the Cardiovascular Division, Department of Medicine, Brigham and Women's Hospital, Boston (K.L.B.).

Address reprint requests to Dr. Wittstein at the Division of Cardiology, Johns Hopkins Hospital, Carnegie 568, 600 N. Wolfe St., Baltimore, MD 21287, or at iwittste{at}jhmi.edu.

Full Text of this Article

Related Letters:

Myocardial Stunning Due to Sudden Emotional Stress
Maseri A., Kurisu S., Inoue I., Kawagoe T., Kadhiravan T., Wittstein I. S., Champion H. C.
Extract | Full Text | PDF  
N Engl J Med 2005; 352:1923-1925, May 5, 2005. Correspondence

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