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Stress (Takotsubo) Cardiomyopathy -- A Novel Pathophysiological Hypothesis to Explain Catecholamine-induced Acute Myocardial Stunning : The Clinical Syndrome


The Clinical Syndrome

The characteristic clinical syndrome of stress cardiomyopathy is acute left ventricular dysfunction, usually after a sudden emotional or physical stress. Patients typically present with cardiac chest pain, which can mimic an acute coronary syndrome. Although the coronary arteries have no flow-limiting lesions, acute changes on the electrocardiogram, suggesting ischemia, and raised levels of cardiac enzymes, reflecting acute myocardial injury, are usually present. Left ventricular dysfunction and wall-motion abnormalities are typically seen, affecting the apical and, frequently, the midventricular myocardium, but sparing the basal myocardium. On left ventriculography, echocardiography or cardiac MRI, these functional abnormalities typically resemble a flask with a short, narrow neck and wide, rounded body (Figure 1; cardiac MRI movies recorded during the acute phase and follow-up period, respectively, are provided as Supplementary Movies 1 and 2 online). The shape of the ventricle at end systole resembles the Japanese fisherman's octopus pot—the tako-tsubo—from which the syndrome derives its original name. The hypercontractile basal myocardium can generate left ventricular outflow tract obstruction in the presence of apical and midwall hypokinesis. The final element of the syndrome is that left ventricular function and apical wall motion return to normal within days or weeks of the acute insult, in a similar manner to traditional myocardial stunning, providing no further acute cardiac events occur.[2]

Figure 1. (click image to zoom) Left ventricular end systolic cardiac MRI. (A) Acute phase with akinetic apical and mid-left ventricular wall and reduced or absent wall thickening (a cardiac MRI movie demonstrating the acute phase is provided as Supplementary Movie 1 online). (B) Follow-up image at 5 months, demonstrating normal left ventricular systolic function, with recovery of motion and wall thickening in all segments (a movie recorded during follow-up is provided as Supplementary Movie 2 online).

The long-term prognosis of patients with this syndrome is excellent. In one series of 13 cases, all patients who survived the acute event (n = 12) were alive at 5-year follow-up.[3] A clinical series from the US[4] and a detailed systematic review of case reports and cohort studies[5] have recently been reported. In 2006, the syndrome was renamed stress cardiomyopathy and reclassified within the subgroup of acquired cardiomyopathies.[6]

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