Understanding stress cardiomyopathy

A 76-year-old woman loses a close friend. Several hours later, she has chest pain, diaphoresis, and shortness of breath. She presents to the emergency department, where an ECG shows deep T wave inversion across the precordium. Cardiac troponin is elevated. This presentation is classic for myocardial ischemia and for stress cardiomyopathy. Recognition of stress cardiomyopathy, and its distinction from acute coronary syndrome (ACS), is crucial for the clinician, since their pathophysiology and treatment are quite different. Stress cardiomyopathy is an acute reversible syndrome with characteristic wall motion abnormalities, consisting of apical hypokinesis or dyskinesis with sparing of the basal ventricular segments. Although the final outcome is generally good, early in their clinical course, patientsmay have cardiogenic shock (4 %), malignant ventricular arrhythmias (1–2 %), and death (1–1.5 %) [1]. Stress cardiomyopathy can complicate other conditions in the ICU, notably including subarachnoid hemorrhage. Patients with these more complex presentations often present clinical challenges. This manuscript aims to increase understanding of the identification and pathophysiology of stress cardiomyopathy to help practitioners manage this interesting syndrome.