LAUSR

A 71-year-old woman was admitted to our secondary care hospital because of acute heart failure and high ventricular rate atrial fibrillation (AF). The ECG showed T-wave inversion in the anterior leads and the chest X-ray showed pulmonary congestion. The patient presented a history of paroxysmal AF on antiarrhythmic therapy with sotalol and partially effective anticoagulation with vitamin K antagonists (VKA) (time in therapeutic range (TTR) over the last year: 65%). VKA was replaced with weight-adjusted enoxaparin at admission. Echocardiography showed severe left ventricular (LV) dysfunction, ejection fraction (EF) 31%, due to midand apical akinesia, associated with apical right ventricular (RV) akinesia. Angiography excluded significant coronary artery disease, left ventriculography showed typical apical ballooning pattern. A first episode of persistent high ventricular rate AF was effectively converted with endovenous infusion of amiodarone on the first admission day with restoration of sinus rhythm. Clinical conditions improved after intravenous diuretic administration, but several symptomatic torsades de pointes (TdP) occurred on day 2, which were treated with DC-shocks and magnesium sulfate. Shortly after the TdP, the patient developed persistent AF. Trans-oesophageal echocardiography (TOE) revealed a large thrombus in the left atrial appendage (LAA) before attempting electrical cardioversion. Despite normal left atrial (LA) volumes (24 ml/m2), a subsequent echo-Doppler assessment of LAA was suggestive for mild dysfunction (peak emptying velocity 18 cm/s). Three days later, transthoracic echocardiography documented complete LV (EF 58%) and RV function recovery without regional wall motion abnormalities, as well as improvement of LAA function (peak emptying velocity 48 cm/s) (Fig. 1), despite high ventricular rate AF persistence during hospital stay. The patient was finally discharged on VKA therapy. An elective electrical cardioversion restored sinus rhythm 1 month later and the patient did well. LV thrombus is a possible complication of Tako-Tsubo cardiomyopathy (TTC) but, to our knowledge, this is the first report of isolated LAA thrombus during TTC. Buchholz et al. [1] previously reported a case of contemporary LV and LAA thrombus in a patient with TTC without AF history. Catecholamine release and related cardiotoxicity inducing myocardial stunning via beta adrenoceptors is one of the postulated mechanisms responsible for TTC [1]. Beta 1 and beta 2 adrenoceptors are present in the LA in the same proportion as in the LV, making LA involvement possible during TTC. Two mechanisms seem to be responsible for atrial dysfunction: an indirect effect on LA that occurs during LV dysfunction, or a direct effect of catecholamines at the level of the LA leading to regional stunning [2]. Atrial physiology constitutes of three components in rapid succession. The first two phases are passive: the reservoir and the conduit phase, whereas the contractile booster pump function is active. It is contrasting if only passive phases are depressed during acute and subacute TTC with [3] or without a compensatory work by the active phase, or if also the active phase is mildly reduced. There is evidence that patients affected by biventricular TTC have impaired active atrial contractility [4]. Anyhow, atrial function is completely restored in a relative brief time. It has been argued that the magnitude of the eventual effect of the catecholamines is unpredictable according to the heterogeneous distribution of beta receptors in the LA. Pathophysiology of thrombosis during TTC is multifactorial: endothelial stress is a cause of blood stasis and thrombus formation, as well as catecholaminergic platelet * Luca Donazzan [email protected]