Stress-induced cardiomyopathy accounts for 2% to 3% of patients presenting with signs and symptoms of acute anterior MI.
2,5,6 It is characterized by minimal coronary artery obstruction, regional cardiomyopathy with wall-motion abnormalities extending beyond the distribution of a single vascular territory, and the occurrence of a precipitating stressor.
7 The following criteria are required to establish the diagnosis of stress-induced cardiomyopathy
8:
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transient, reversible akinesis or dyskinesis of the left ventricular apical and midventricular segments with regional wall-motion abnormalities extending beyond a single vascular territory at left ventriculography
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absence of obstructive coronary artery stenosis (>50% of the luminal diameter) or angiographic evidence of acute plaque rupture
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new electrocardiographic abnormalities consisting of ST-segment elevation or T-wave inversion
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absence of recent head trauma, intracranial bleeding, pheochromocytoma, obstructive epicardial coronary artery disease, myocarditis, and hypertrophic cardiomyopathy
Certain ECG criteria have been shown in combination to have a high sensitivity and specificity for differentiating between anterior MI and stress-induced cardiomyopathy. Kosuge et al
9 demonstrated that the combination of ST-segment depression in lead aVR and the absence of ST-segment elevation in lead V
1 identified stress-induced cardiomyopathy with 91% sensitivity, 96% specificity, and 95% predictive accuracy—superior to any other ECG criteria that have been studied. In an anterior MI, the perfusion territory of the left anterior descending artery generally does not extend into the apical and inferolateral regions of the myocardium; changes in the perfusion of these regions, as in stress-induced cardiomyopathy, would result in ST-segment depression in lead aVR. In opposite fashion, the wall-motion abnormalities of stress-induced cardiomyopathy rarely extend to the region faced by lead V
1, resulting in minimal—if any—ST-segment changes in that lead. Most patients with an anterior MI and subsequent anteroseptal ischemia have ST-segment elevation in lead V
1.
Elevations in serial cardiac biomarker measurements are small compared with the degree of wall-motion abnormality seen. In addition, cardiac biomarker measurements generally do not follow the kinetics seen with acute anterior MI, and a small proportion of patients do not have any rise in their troponin levels.
2 Wall-motion abnormalities generally return to normal within days of diagnosis, with nearly all patients returning to normal within 4 weeks.
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Treatment of patients with stress-induced cardiomyopathy involves initiation of an angiotensin-converting enzyme inhibitor (or angiotensin-II receptor blocker), β-blocker therapy, or both in patients with substantial left ventricular dysfunction who can tolerate therapy. Rarely, treatment will involve inotropic support if hemodynamic compromise is clinically significant. Acute complications (eg, cardiogenic shock, heart failure, pulmonary edema, arrhythmia, left ventricular thrombus formation, free wall rupture, death) occur in about 1 of 5 patients with stress-induced cardiomyopathy.
7,11 Mortality is uncommon, as is recurrence of the condition.
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