10-45: Stress Cardiomyopathy

ESSENTIALS OF DIAGNOSIS

GENERAL CONSIDERATIONS

Stress cardiomyopathy (tako-tsubo syndrome) generally follows a high catecholamine surge. The resulting shape of the LV acutely suggests a rounded ampulla form similar to a Japanese octopus pot (tako-tsubo pot) (eFigure 10–77). Mid-ventricular ballooning has also been described. The key feature is that the myocardial stunning that occurs does not follow the pattern suggestive of coronary ischemia (even though about 15% of patients will have coexisting CAD, and some may have concomitant plaque rupture MI). Over two-thirds of patients report a prior stressful event, either emotional or physical, including hypoglycemia, lightning strikes, earthquakes, postventricular tachycardia, during alcohol withdrawal, following surgery, during hyperthyroidism, after stroke, and following emotional stress (“broken-heart syndrome”). Virtually any event that triggers excess catecholamines has been implicated in a wide number of case reports. Pericarditis and even tamponade have been described in isolated cases. Recurrences have also been described. In Western countries it predominantly affects women (up to 90%), primarily postmenopausal. Among patients with stress cardiomyopathy, compared to patients with acute coronary syndrome, there are more neurologic and psychiatric disorders. Patients with COPD, migraines, or affective disorders who take beta-agonists may have an increased risk of a poor outcome. The prognosis was initially thought to be benign, but subsequent studies have demonstrated that both short-term mortality and long-term mortality are higher than thought. Indeed, mortality reported during the acute phase in hospitalized patients is approximately 4–5%, a figure comparable to that of STEMI in the era of primary percutaneous coronary interventions. Approximately 10% of patients will have cardiac and neurologic adverse outcomes over the next year.

The structures that mediate the stress response are in both the central and autonomic nervous systems. Acute stressors induce brain activation, increasing bioavailability of cortisol and catecholamine. Both circulating epinephrine and norepinephrine released from adrenal medullary chromaffin cells and norepinephrine released locally from sympathetic nerve terminals are significantly increased. This catecholamine surge leads to myocardial damage through multiple mechanisms, including, direct catecholamine toxicity, adrenoceptor-mediated damage, epicardial and microvascular coronary vasoconstriction and/or spasm, and increased cardiac workload. The relative preponderance among postmenopausal women suggests that estrogen deprivation may be facilitating, possibly via endothelial dysfunction.

CLINICAL FINDINGS

A. Symptoms and Signs

The symptoms are ...