Tako-Tsubo cardiomyopathy following an allergic asthma attack after cephalosporin administration

Abstract

Tako-Tsubo (TT) syndrome is characterized by acute onset ofchest symptoms, ECG changes with elevated cardiac markers mim-icking acute myocardial infarction, left ventricular (LV) wall motionabnormalities in the apical region with preserved function of base,and normal coronary arteries [1]. Those affected are typically olderwomen presenting after a stressful trigger, either emotional orphysical.A 70-year-old woman with history of hypertension, diabetes,asthma and allergy, was admitted with chest pain and dyspnea,whichsuddenly appearedafter asingle 1 g doseof ceftriaxonei.m.as-sumed because of cough and fever. On physical examination, bloodpressure was 120/70 mm Hg, heart rate 110 bpm, respiratory rate22 breaths/min, and diffuse bilateral wheezes were found. ECGshowed sinus rhythm and mild ST-elevation in anterior leads(Fig. 1a); troponin-I levels were increased (1.09 m ng/ml (n.v.b0.03)). Trans-thoracic echocardiogram showed LV systolic dysfunc-tion (ejection fraction [EF] 25%) with both apical dyskinesis andbasal hyperkinesis (Fig. 1c), and right ventricular (RV) apical dyskin-esis (Fig. 1d). Mild mitral regurgitation and tricuspid regurgitationwere also detectable at color Doppler analysis. Total IgE circulatinglevels were increased (1270 I.U./ml (n.v. b240 I.U./ml). Coronary an-giography showed normal coronary arteries and confirmed LV apicalballooning (Fig. 1e–f). Medical treatment with furosemide,levosimendan,ramipril,andbisoprololwasthereforestarted.Thepatientgradually recovered, and was discharged a week later, when all ECGanomalies, after transient onset of negative T-waves ( Fig. 1b) disap-peared. Pre-discharge echocardiography showed both improved LV (EF55%) and RV systolic functions.We report a case of transient apical ballooning triggered by admin-istration of antibiotics (cephalosporin). We therefore hypothesize thatallergic activation induced by antibiotic and featured by increased IgElevels may be related to TT phenomenon, as previously reported [2].RV apical ballooning, as found in this patient, was reported in 25% ofcases with TT syndrome [3].The exact mechanism leading to transient apical systolic dysfunc-tion is still not well elucidated. Increased catecholamine levels werethoughas responsible [4] , but also coronaryspasm has been reportedin subjects showing TT phenomenon [5].Several prior reports linked TT syndrome to bronchial asthma [6]anaphylactic reaction [7,8] and even cephalosporin administration[9], although in all these cases apical systolic dysfunction usually fol-lowed administration of i.v. epinephrine. We therefore postulate inthis patient a catecholamine independent pathway leading to TT phe-nomenon. Direct histamine effect consequent to allergic activationmay be presumed as responsible for transient apical dysfunction.Two cases of profound reversible myocardial dysfunction occurring inthe setting of anaphylaxis, with histamine discussed as a potential myo-cardial depressor, were previously reported [10]. Raper et al. noted thatstimulation of histamine receptors in both animal and human hearts ex-perimentally leads to myocardial depression, providing a possibleexplaining mechanism for our findings.References