Incomplete leaflet coaptation and tricuspid regurgitation mechanism in right ventricular Tako-Tsubo cardiomyopathy

Abstract

Tako-Tsubo cardiomyopathy (TTC) is a well-known form of acuteand reversible heart failure due to either an emotional or a physicalstressor,whichinvolvesmainlytheleftventriclewithatypicalechocar-diographic pattern (apical ballooningand basal hyperkinesis) [1].Rightventricular(RV)involvementhasaprevalenceof25%[2].Aclinicalcase,a short literature review and possible explaining mechanism areprovided.An86-yearoldwoman,withoutcardiovascularriskfactorsandwithhistory of bipolardisorder [3] cameto the emergency department afteran episode of syncope. At admission blood pressure was 70/50 mm Hg,ECG showed atrial fibrillation and ST-elevation in anterior and lateralleads (V2–V4, DI, aVL) (Fig. 1). Troponin I levels were increased(4.54 ng/ml, n.v. b 0.10). Trans-thoracic echocardiogram showed leftventricular (LV) systolic dysfunction (ejection fraction of 25%),akinesisofLVmidventricularsegments,dyskinesisofRVapicalsegmentsandin-complete coaptation of tricuspid leaflets (Video 1). At color-Dopplermild mitral regurgitation and severe tricuspid regurgitation werefound (Figs. 2 and 3, Video 2). Coronary angiography showed diffuseatherosclerosis not needing coronary intervention. Echocardiographyanomalies gradually recovered and the patient was discharged after acouple of weeks (Figs. 4 and 5) (Video 3). Discharge electrocardiogramshowed negative T-waves in anterior leads previously interested byST-elevation and diffuse decrease in QRS amplitude [4].Despite TTC affects mainly left ventricle, RV involvement is presentinoneoutoffourpatientsaffectedbyTTC.Severalechocardiographicstudies described acute mitral regurgitation and its clinical impor-tance in TTC[5], but, to the best of our knowledge, possible mecha-nism of tricuspid regurgitationduring RV TTC was never describedbefore.We report a case of RV apical dyskinesis causing traction of thepostero-lateral papillary muscle and consequent compromised coapta-tion of thetricuspid valve leaflets (Fig. 2);that could have led to severetricuspid regurgitation completely reversible after RV recovery.The mechanism of RV regurgitation seems to be different from thatwe have previously described in the left ventricle. LV basal hyperkinesis, consequent mitral valve area reduction and mitral leafletsredundancy may lead to LV outflow tract obstruction, increased intraventricular pressure and mitral regurgitation [6,7]. Systolic anteriormotion and tethering have been shown as independent predictors ofacute mitral regurgitation in patients with TTC [8].In thecaseof mid-LVballooning, rightward movement of midseptalsegmentsmayhaveincreasedRVpressure,thusimpairingRVgeometryand kinesis, and precipitating RV ballooning.Tricuspid regurgitation has not yet been evaluated as a marker ofprognosisinTTC;however,inacutemyocardialinfarctionoftheinferiorwall, moderate tricuspid regurgitation, affecting about one third ofpatients, is a predictor of rehospitalization at one-year follow-up [9].Although no in-hospital complication was present in our case, RVsystolic dysfunction represents an independent predictor of worseprognosis and is associated with a higher rate of in-hospital complica-tion both in inferior myocardial infarction [10] and TTC [2].Haghiet al. found in 34 patients with TTC that RV involvement is associatedwith a severe impairment in LV systolic function and a higher rate ofbilateral pleural effusion [2]. Elesber et al. showed in a population of30patientswithTTCthatRVinvolvementcarriesahigherriskofseverecongestive heart failure and longer in-hospital stay [11].We therefore believe that a systematic evaluation of RV function byechocardiogram is recommended for an optimal management of pa-tients with TTC. When an impaired LVEF is associated with abnormalRV function, there is a higher risk of hemodynamic complications.Therefore a strict monitoring is required and an early therapeuticstrategy including diuretics, levosimendan infusion and intra-aorticballoon pump counterpulsation should be considered [12–14].In conclusion, RV involvement in TTC may lead to severe tricuspidregurgitationduetoincompletecoaptationofvalveleaflets.This finding