Stress-induced (Takotsubo) cardiomyopathy develops into a long-lasting heart failure syndrome

Reference to the original article

Persistent long-term structural, functional, and metabolic changes after stress-induced (Takotsubo) cardiomyopathy. Scally C et al. DOI 10.1161/CIRCULATIONAHA.117.031841

Comment

Takotsubo cardiomyopathy has a dramatic clinical presentation, mimicking an acute myocardial infarction (1). Until recently, the commonly accepted belief was that Takotsubo cardiomyopathy is a transient and self-limiting condition. Previous work showed the absence of demonstrable myocardial damage on routine cardiac magnetic resonance imaging (2). In a detailed cross-sectional study, new work reports for the first time that a proportion of patients who experienced an episode of acute Takotsubo cardiomyopathy 2 years previously go on to develop a heart failure with preserved ejection fraction phenotype. Compared with age, gender and cardiovascular morbidity-matched controls, patients with prior Takotsubo had objective reductions in peak VO2 because of cardiac limitation on cardiopulmonary exercise testing (increased VE/VCO2 slope) and a reduced cardiac energetic status (decreased in vivo PCr/ATP ratio in the myocardium). These were further accompanied by myocardial microscopic fibrosis and impaired left ventricular strain patterns alongside patients reporting persistent symptoms of heart failure because of physical rather than emotional disability.
These findings demonstrate a substantial and persistent adverse alteration in long-term cardiac morbidity associated with Takotsubo cardiomyopathy and define a new clinical phenotype in this population. This new report reverses the previously accepted concept of “rapid and complete recovery” post-Takotsubo cardiomyopathy and calls for a better understanding of the mechanisms and the development of therapeutic interventions, which are urgently required to improve the outcome of these patients.

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