Key result
Stress-induced cardiomyopathy is triggered by emotional or somatic stressors, with catecholamines believed to play a pivotal role in its pathophysiology.
This review highlights the pathophysiology of stress-induced cardiomyopathy, emphasizing the pivotal role of catecholamines and the brain-heart connection.
Supports stress recognition in cardiomyopathy care; leaves open catecholamine-targeted therapies for prospective trials.
Stress-induced cardiomyopathy (SIC), also known as Takotsubo cardiomyopathy, is characterized by severe but potentially reversible regional left ventricular wall motion abnormalities, ie, akinesia, in the absence of explanatory angiographic evidence of a coronary occlusion. The typical pattern is that of an akinetic apex with preserved contractions in the base, but other variants are also common, including basal or midmyocardial akinesia with preserved apical function. The pathophysiology of SIC remains largely unknown but catecholamines are believed to play a pivotal role. The diverse array of triggering events that have been linked to SIC are arbitrarily categorized as either emotional or somatic stressors. These categories can be considered as different elements of a continuous spectrum, linked through the interface of neurology and psychiatry. This paper reviews our current knowledge of SIC, with focus on the intimate relationship between the brain and the heart.
No takes yet. Share an insight, caveat, or question.
Ömerovic et al. (2013) conducted a review in Stress-induced cardiomyopathy (Takotsubo cardiomyopathy). Stress-induced cardiomyopathy is triggered by emotional or somatic stressors, with catecholamines believed to play a pivotal role in its pathophysiology.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: