Neurohormonal treatment in tako-tsubo cardiomyopathy precipitated by COVID-19. Response

To the Editor,

The neurohormonal treatment received by our patient comprised a beta-blocker, bisoprolol, and an angiotensin-converting enzyme inhibitor (ACE-I), enalapril. At 3 months of follow-up, he had no further episodes of chest pain or signs of heart failure.

As mentioned in the Letter, although treatment with beta-blockers may slow the effect of catecholamine release thought to be the pathophysiological mechanism behind tako-tsubo cardiomyopathy, clinical benefits have not been demonstrated. However, treatment with ACE-I, which has shown improved survival in a registry, could contribute to ventricular remodeling.

In the case of coronavirus disease 2019 (COVID-19), treatment with ACE-I has generated controversy. When the disease first emerged, animal studies¹ demonstrated that coronavirus uses angiotensin-converting enzyme 2 (ACE-2), an aminopeptidase with abundant expression in the lungs and heart, as a receptor for cell entry. Treatment with ACE-I increases the expression of ACE-2, leading to the hypothesis that it may affect susceptibility to the infection or its virulence. Later, a case-control study² with more than 6000 patients found no evidence of an association between these drugs and COVID-19; current protocols therefore recommend continuing treatment with ACE-I in patients with SARS-CoV-2 infection in the absence of other contraindications.

As tako-tsubo cardiomyopathy is a rare complication of SARS-CoV-2 infection, to date there are no specific studies on the recommended treatment. The only treatment with evidence on survival in COVID-19 is corticosteroids³ (dexamethasone), possibly due to its effect on the inflammatory cascade that occurs in this disease. Bearing in mind that the systemic inflammatory status could contribute to the development of tako-tsubo cardiomyopathy, treatment with dexamethasone may affect its onset and outcome, although specific studies are needed to assess this.