hodge

stress cardiomyothapy  i was wondering if you could elaberate on this not hundred percent sure what were dealling with. Thankyou..

[Jack54]

Emotional Stress May Precipitate Severe, Reversible Left Ventricular Dysfunction  (stress-induced cardiomyopathy) CME
News Author: Laurie Barclay, MD
CME Author: Charles Vega, MD, FAAFP

Release Date: February 9, 2005; Reviewed and Renewed: February 9, 2006; Valid for credit through February 9, 2007

Feb. 9, 2004 — Emotional stress can precipitate severe but reversible left ventricular dysfunction caused by an exaggerated sympathetic response, according to the results of a study published in the Feb. 10 issue of the New England Journal of Medicine.

"The potentially lethal consequences of emotional stress are deeply rooted in folk wisdom, as reflected by phrases such as 'scared to death' and 'a broken heart,'" write Ilan S. Wittstein, MD, from Johns Hopkins University in Baltimore, Maryland, and colleagues. "In the past decade, cardiac contractile abnormalities and heart failure have been reported after acute emotional stress, but the mechanism remains unknown."

Using coronary angiography and serial echocardiography, the authors evaluated 19 patients presenting with left ventricular dysfunction after sudden emotional stress. Five patients underwent endomyocardial biopsy, and plasma catecholamine levels in 13 patients with stress-related myocardial dysfunction were compared with those in seven patients with Killip class III myocardial infarction.

Median age of patients with stress-induced cardiomyopathy was 63 years, and 95% were women. Presenting symptoms included chest pain, pulmonary edema, and cardiogenic shock, and most patients had diffuse T-wave inversion and a prolonged QT interval. Although 17 patients had mildly elevated serum troponin I levels, angiography revealed clinically significant coronary disease in only one of 19 patients.

On admission, all patients had severe left ventricular dysfunction (median ejection fraction, 0.20; interquartile range, 0.15-0.30), which resolved rapidly (ejection fraction at two to four weeks, 0.60; interquartile range, 0.55-0.65; P < .001). Endomyocardial biopsy revealed mononuclear infiltrates and contraction-band necrosis.

At presentation, patients with stress-induced cardiomyopathy had markedly higher plasma catecholamine levels than did those with Killip class III myocardial infarction (median epinephrine level, 1,264 pg/mL [interquartile range, 916-1,374] vs 376 pg/mL [interquartile range, 275-476]; norepinephrine level, 2,284 pg/mL [interquartile range, 1,709-2,910] vs 1,100 pg/mL [interquartile range, 914-1,320]; and dopamine level, 111 pg/mL [interquartile range, 106-146] vs 61 pg/mL [interquartile range, 46-77]; P < .005 for all comparisons).

Study limitations are those inherent in any small, observational case series, as well as inability to prove a causal relationship between sympathetic activation and stress cardiomyopathy.

"Emotional stress can precipitate severe, reversible left ventricular dysfunction in patients without coronary disease," the authors write. "Exaggerated sympathetic stimulation is probably central to the cause of this syndrome."

Because patients with stress cardiomyopathy typically present with clinical features resembling those of acute myocardial infarction, the authors recommend coronary angiography in most cases.

The Bernard A. and Rebecca S. Bernard Foundation partly supported this study, and the Donald W. Reynolds Foundation partly supported four of the authors.

N Engl J Med. 2005;352:539-548