Update of takotsubo syndrome in the era of COVID-19

Abstract

Takotsubo cardiomyopathy or takotsubo syndrome (TTS) has become a well-known disease not only in Japan but also in the rest of the world. Early reports suggested that TTS is a self-limiting disease with better prognosis than acute coronary syndrome. However, recent data showed that TTS is not a benign disease as compared with acute coronary syndrome. In addition to the apical ballooning, several other types of wall motion abnormalities have been classified as variants of TTS. In particular, right ventricular involvement, or biventricular TTS, is not uncommon and is associated with poor in-hospital as well as long-term outcomes. With respect to the pathophysiology, modulation (desensitization) of the beta-adrenergic receptor is suspected as a possible mechanism for transiently depressed myocardial contraction. Although specific treatments to improve prognosis of TTS are still uncertain, observational data suggest favorable impact of angiotensin-converting enzyme inhibitors or angiotensin receptor blockers. Finally, in the era of COVID-19, we should pay attention to a variety of cardiovascular conditions related to COVID-19. TTS is one of these conditions that can be triggered by both emotional and physical impact of the COVID-19 pandemic.

Keywords: COVID-19; Echocardiography; Takotsubo syndrome.

Fig. 1

Proposed mechanisms of wall motion abnormalities in patients with takotsubo syndrome. (A) With superphysiological catecholamine levels, β-arrestin2 internalization the β1-AR and GRK2 induces β1-AR uncoupling, resulting in desensitization and suppression of myocardial contraction. Adapted from Nakano et al. [19]. (B With superphysiological catecholamine levels, stimulation of β2-AR suppress myocardia contraction by switching Gs protein to Gi protein. Adapted from Paur et al. [17].

Fig. 2

Apical takotsubo syndrome. (A) Left ventriculography demonstrates typical apical ballooning, or “takotsubo”-like appearance. (B) Echocardiography demonstrates akinesis of the apical segment (arrows). LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle.

Fig. 3

Classification of takotsubo syndrome based on the location of wall motion abnormalities. Adapted from Kagiyama et al. [26], Citro et al. [28], Templin et al. [29], Uribarri et al. [30], and Arcari et al. [31].

Fig. 4

Mid-ventricular takotsubo syndrome. (A, B) Both left ventriculography and echocardiography demonstrated akinesis (arrows) of the mid-ventricular segment. Ao, aorta; LA, left atrium; LV, left ventricle.

Fig. 5

Biventricular takotsubo syndrome. Apical long-axis view of the echocardiography [end-diastole (A) and end-systole (B)] demonstrates akinesis of LV and RV (arrows). Ao, aorta; LA, left atrium; LV, left ventricle; RV, right ventricle.

Fig. 6

Left ventricular outflow tract obstruction (LVOTO) in takotsubo syndrome. (A) Left ventriculography shows apical ballooning. (B) Echocardiography shows LVOTO (arrow) and mitral regurgitation caused by systolic anterior motion (SAM) of the anterior mitral valve (arrow heads). Ao, aorta; LA, left atrium; LV, left ventricle.

Fig. 7

A case of takotsubo syndrome complicated with posterior myocardial infarction. (A) Coronary angiogram shows occlusion of the postero-lateral branch of the left circumflex coronary artery (arrows). (B, C) Echocardiography shows akinesis of the apical segment (arrows) that cannot be explained by the coronary artery occlusion. LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle.

Fig. 8

A case of takotsubo syndrome complicated with cardiac amyloidosis. (A, B) Echocardiography shows diffuse left ventricular hypertrophy and hypokinesis and akinesis of the left (arrows) and right ventricular (arrow heads) apical segments. (B) 99 m Tc-pyrophosphate (99 m Tc-PYP) myocardial scintigraphy demonstrates significant uptake (arrows), suggesting the diagnosis of transthyretin cardiac amyloidosis. LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle.