Reversible cardiomyopathy provoked by focal ventricular arrhythmia originating from the base of the posterior papillary muscle

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A new distinct clinical syndrome comprising of ventricular tachycardia or frequent premature beats arising from the base of the posterior papillary muscle has recently been reported. The cardiac arrhythmia had a non-reentrant mechanism and none of the patients had left ventricular dysfunction. We report on a 55-year-old female patient presenting with a dilated cardiomyopathy and frequent ventricular premature beats (VPB). Ventricular arrhythmia was refractory to amiodarone. Eighteen months after the onset of palpitations the patient evolved from NYHA functional class I to class III, with a LVEF of 38%. VPB comprised 26% of the total number of QRS complexes during 24 h Holter monitoring, which also recorded 12 salvos of non-sustained VT. NT-pro BNP level was 1,080 mcg/ml. During electrophysiologic study LV geometry was reconstructed with Ensite NAVX system which allowed voltage and activation mapping. We found neither scar-like nor low-voltage tissue in the endocardial surface of the LV. VPB was mapped in a site at the base of the posterior papillary muscle, which was confirmed by LV angiography. Cool-tip catheter ablation successfully eliminated VPB. Three months later, the patient was in NYHA functional class I, NT-proBNP level was 98 mcg/ml, with partial LV reverse remodeling and LVEF of 58%. Twenty-four hours Holter monitoring showed only 24 single premature beats. Focal ventricular arrhythmia arising from the base of the left posterior papillary muscle can provoke significant left ventricular dysfunction. Left ventricular dysfunction reversed after elimination of the VPB.