title: Right ventricular failure following chronic pressure overload is associated with reduction in left ventricular mass: evidence for atrophic remodeling.
abstract: OBJECTIVE
  We sought to study whether patients with right ventricular failure (RVF) secondary to chronic thromboembolic pulmonary hypertension (CTEPH) have reduced left ventricular (LV) mass, and whether LV mass reduction is caused by atrophy.
  
  
  BACKGROUND
  The LV in patients with CTEPH is underfilled (unloaded). LV unloading may cause atrophic remodeling that is associated with diastolic and systolic dysfunction.
  
  
  METHODS
  We studied LV mass using cardiac magnetic resonance imaging (MRI) in 36 consecutive CTEPH patients (before/after pulmonary endarterectomy [PEA]) and 11 healthy volunteers selected to match age and sex of patients. We studied whether LV atrophy is present in monocrotaline (MCT)-injected rats with RVF or controls by measuring myocyte dimensions and performing in situ hybridization.
  
  
  RESULTS
  At baseline, CTEPH patients with RVF had significantly lower LV free wall mass indexes than patients without RVF (35 ± 6 g/m(2) vs. 44 ± 7 g/m(2), p = 0.007) or volunteers (42 ± 6 g/m(2), p = 0.006). After PEA, LV free wall mass index increased (from 38 ± 6 g/m(2) to 44 ± 9 g/m(2), p = 0.001), as right ventricular (RV) ejection fraction improved (from 31 ± 8% to 56 ± 12%, p < 0.001). Compared with controls, rats with RVF had reduced LV free wall mass and smaller LV free wall myocytes. Expression of atrial natriuretic peptide was higher, whereas that of α-myosin heavy chain and sarcoplasmic reticulum calcium ATPase-2 were lower in RVF than in controls, both in RV and LV.
  
  
  CONCLUSIONS
  RVF in patients with CTEPH is associated with reversible reduction in LV free wall mass. In a rat model of RVF, myocyte shrinkage due to atrophic remodeling contributed to reduction in LV free wall mass.
authors.affiliation: Heart Failure Research Center, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands.
authors.forename: Maxim
authors.initials: M
authors.lastname: Hardziyenka
authors.forename: Maria E
authors.initials: ME
authors.lastname: Campian
authors.forename: Herre J
authors.initials: HJ
authors.lastname: Reesink
authors.forename: Sulaiman
authors.initials: S
authors.lastname: Surie
authors.forename: Berto J
authors.initials: BJ
authors.lastname: Bouma
authors.forename: Maarten
authors.initials: M
authors.lastname: Groenink
authors.forename: Christine A
authors.initials: CA
authors.lastname: Klemens
authors.forename: Leander
authors.initials: L
authors.lastname: Beekman
authors.forename: Carol A
authors.initials: CA
authors.lastname: Remme
authors.forename: Paul
authors.initials: P
authors.lastname: Bresser
authors.forename: Hanno L
authors.initials: HL
authors.lastname: Tan
mesh_terms: D000328:Adult; D000368:Aged; D000818:Animals; D001284:Atrophy / Q000473:pathology; D016022:Case-Control Studies; D004195:Disease Models, Animal; D004691:Endarterectomy / Q000379:methods; D005260:Female; D006333:Heart Failure / Q000175:diagnosis* / Q000209:etiology; D006801:Humans; D006976:Hypertension, Pulmonary / Q000150:complications* / Q000175:diagnosis; D008279:Magnetic Resonance Imaging / Q000379:methods; D008297:Male; D008875:Middle Aged; D009206:Myocardium / Q000473:pathology*; D011379:Prognosis; D011655:Pulmonary Embolism / Q000150:complications / Q000175:diagnosis / Q000601:surgery; D051381:Rats; D012016:Reference Values; D012189:Retrospective Studies; D013318:Stroke Volume / Q000502:physiology*; D018497:Ventricular Dysfunction, Right / Q000150:complications* / Q000175:diagnosis; D020257:Ventricular Remodeling / Q000502:physiology*