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KEY POINTS

KEY POINTS

  • Catecholamine toxicity seems to be the key mechanism of takotsubo.

  • Emotional or physical triggers are almost always present in the history of takotsubo.

  • The dominant pattern is the apical ballooning form.

  • Takotsubo is a diagnosis of exclusion: myocardial infarction and myocarditis should be ruled out, generally requiring coronary angiography. MRI may also be useful.

  • Echocardiography is the main tool to diagnose, follow, and detect complications.

  • Severe cardiac failure and cardiogenic shock are the main causes of ICU hospitalization.

  • Left ventricular outflow tract obstruction is frequent in patients with takotsubo.

  • Management is based in very little evidence: anticoagulants, beta-blockers (in case of obstruction), levosimendan, and mechanical hemodynamical support have been advocated.

INTRODUCTION

In 1985, Tokioka and colleagues1 described transient asynergy on the echocardiogram along with electrocardiographic (ECG) changes simulating acute myocardial infarction following noncardiac surgery. Subsequently, Ryan and coauthors2 reported a 44-year-old woman with substernal pain and pulmonary edema after severe emotional stress. But the first true description of takotsubo cardiomyopathy was published3 from Hiroshima City Hospital delineating a mysterious stunned myocardium consisting of reversible, left ventricular (LV) apical wall-motion abnormalities without coronary artery disease (CAD), often associated with emotional or physical stress. The term “takotsubo-like left ventricular dysfunction” was proposed, referring to Japanese ceramic containers used by the Japanese to catch octopus,4 which have a bulbous bottom and narrow neck. Their shape resembles the most common LV conformation associated with this disorder: apical akinesis with basal hyperkinesis. By the 1980s, stress cardiomyopathy was described in patients with pheochromocytoma and in patients with subarachnoid haemorrhage.5,6 Later takotsubo syndrome (TTS) and stress cardiomyopathy were considered manifestations of a common process. After 2000, Kawai et al. and Ito et al. published papers in English, and the concept and name “takotsubo cardiomyopathy” became recognized worldwide.7,8 The expansion of echocardiography into critical care medicine has resulted in a blossoming of publications in the field.9

PATHOPHYSIOLOGY AND RISK FACTORS (FIG. 34-1)

Multiple pathophysiological processes are implicated in the etiology of TTS, but increased myocardial and circulating levels of catecholamines seems to be the principal mechanism. Other associated abnormalities that could play a role include endothelial dysfunction, estrogen deficiency, and microvascular spasm.10–13 Evidence suggests that TTS is caused by an acutely elevated catecholamine levels, released from sympathetic nerves or the adrenal medulla, or infused therapeutically. TTS occurs primarily in subjects with increased susceptibility of the coronary microcirculation and cardiac myocytes to stress hormones leading to prolonged, but transient, LV dysfunction and secondary myocardial inflammation.

FIGURE 34-1

Pathophysiology of takotsubo syndrome (TTS). LV, left ventricle.

The most recent evidence supports the concept that, in the acute phase of TTS, increased concentrations of catecholamines directly induce myocardial injury and coronary spasm, mostly at the microvascular level. Together ...

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