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Abstract & Commentary
By Michael H. Crawford, MD. Dr. Crawford is Professor of Medicine, Chief of Cardiology, University of California, San Francisco. Dr. Crawford is on the speaker's bureau for Pfizer. This article originally appeared in the March 2010 Clinical Cardiology Alert. It was peer reviewed by Ethan Weiss, MD. Dr. Weiss is Assistant Professor of Medicine, Division of Cardiology and CVRI, University of California, San Francisco. Dr. Weiss reports no financial relationships relevant to this field of study.
Source: Sharkey SW, et al. Natural history and expansive clinical profile of stress (Tako-Tsubo) cardiomyopathy. J Am Coll Cardiol. 2010;55: 333-341.
Stress-induced apical cardiomyopathy (tako-Tsubo) is a recently recognized reversible form of acute cardiomyopathy that may mimic acute myocardial infarction initially. Reported experience with this condition is limited to small observational studies with short follow-up periods. Thus, these investigators from Minneapolis and Boston assembled data on 136 consecutive cases of stress cardiomyopathy (SC) over a seven-year period. Diagnostic criteria included an acute chest pain event, typical LV contraction abnormality encompassing more than one coronary artery territory, and no significant coronary stenoses on angiography. A subgroup of 95 patients had cardiac MRI shortly after admission. Almost all the patients were women (96%), and the mean age was 68 years (range 32-94 years). In 89%, a distinct stressful event preceded the presentation within 12 hours. These events were emotional in 47% and physical (trauma, post surgical) in 42%. Among the physical triggers, use of catecholamines was common. An ECG mimicking acute ST elevation myocardial infarction was common (49%), and troponin was elevated in 92%. Ventricular wall motion abnormalities were variable, but most involved at least the apex of the left ventricle. Only one patient showed delayed enhancement on CMR consistent with scar. Acute mortality was 2%, but only one patient died of cardiogenic shock. The others died of intracranial causes. Apical ventricular thrombi were identified in five patients, two of whom had embolic events. LV function returned rapidly in 96%, although, in 5%, recovery was delayed more than two months. Nonfatal recurrences occurred in 5%. During the seven years of the study, the incidence of SC increased due to a shift to more events associated with physical trauma. The authors concluded that the clinical spectrum of SC was heterogeneous, and suggested that expanded surveillance strategies and anticoagulation should be considered.
This large observational study of patients with SC raises several interesting points about this unusual but serious condition. First, the investigators took an inclusive approach, combining those with emotionally triggered events and those with physical or pharmacologic triggers. Much has been written about the cardiomyopathy of subarachnoid hemorrhage, but it was included as another form of SC in this series. Second, in the later years of their experience, physical triggers predominated, suggesting that increased awareness led to more SC diagnoses in hospitalized patients with a variety of medical illnesses, surgical procedures, and, even, diagnostic tests (e.g., dobutamine stress echo). Third, despite the potential role of exogenous or endogenous catecholamines, beta-blocker therapy did not seem to prevent the occurrence of SC. Fourth, ventricular thrombus and systemic emboli were observed in a few patients, raising the issue of prophylactic anticoagulation. Since the majority of patients had normal LV function within a few days, perhaps prophylactic anticoagulation should be used in those with persistent apical akinesis and continued until LV function normalizes. Fortunately, mortality is low in SC and usually due to the underlying disease.