BACKGROUND: 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. CASE REPORT: 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. CONCLUSION: 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.
BACKGROUND: 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. CASE REPORT: 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. CONCLUSION: 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.
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Authors: Edmond M Cronin; Frank M Bogun; Philippe Maury; Petr Peichl; Minglong Chen; Narayanan Namboodiri; Luis Aguinaga; Luiz Roberto Leite; Sana M Al-Khatib; Elad Anter; Antonio Berruezo; David J Callans; Mina K Chung; Phillip Cuculich; Andre d'Avila; Barbara J Deal; Paolo Della Bella; Thomas Deneke; Timm-Michael Dickfeld; Claudio Hadid; Haris M Haqqani; G Neal Kay; Rakesh Latchamsetty; Francis Marchlinski; John M Miller; Akihiko Nogami; Akash R Patel; Rajeev Kumar Pathak; Luis C Sáenz Morales; Pasquale Santangeli; John L Sapp; Andrea Sarkozy; Kyoko Soejima; William G Stevenson; Usha B Tedrow; Wendy S Tzou; Niraj Varma; Katja Zeppenfeld Journal: Europace Date: 2019-08-01 Impact factor: 5.214