title: Left ventricular dyssynchrony predicts right ventricular remodeling after cardiac resynchronization therapy.
abstract: OBJECTIVE
  The purpose of this research was to evaluate right ventricular (RV) remodeling after six months of cardiac resynchronization therapy (CRT).
  
  
  BACKGROUND
  Cardiac resynchronization therapy is beneficial in patients with end-stage heart failure. The effect of CRT on RV size is currently unknown. Accordingly, the effects of CRT on RV size, severity of tricuspid regurgitation, and pulmonary artery pressure were evaluated.
  
  
  METHODS
  Fifty-six consecutive patients with end-stage heart failure (52% ischemic cardiomyopathy), left ventricular (LV) ejection fraction (EF) < or =35%, QRS duration >120 ms, and left bundle branch block were included. Clinical parameters, LV volumes, LVEF, LV dyssynchrony, and RV chamber size were assessed at baseline and after six months of CRT; LV dyssynchrony was assessed using tissue Doppler imaging.
  
  
  RESULTS
  Clinical parameters improved significantly; LV dyssynchrony was acutely reduced after CRT and remained unchanged at six-month follow-up. Left ventricular EF improved significantly from 19 +/- 6% to 26 +/- 8% (p < 0.001), and LV end-diastolic volume decreased from 257 +/- 98 ml to 227 +/- 86 ml (p < 0.001). Right ventricular annulus decreased significantly from 37 +/- 9 mm to 32 +/- 10 mm, RV short-axis from 29 +/- 11 mm to 26 +/- 7 mm, and RV long-axis from 89 +/- 11 mm to 82 +/- 10 mm (all p < 0.001). Left ventricular and RV reverse remodeling were only observed in patients with substantial LV dyssynchrony at baseline. Finally, significant reductions in severity of tricuspid regurgitation and pulmonary artery pressure were observed.
  
  
  CONCLUSIONS
  Cardiac resynchronization therapy results in significant reverse LV and RV remodeling after six months of CRT in patients with LV dyssynchrony. Moreover, CRT leads to a reduction of the severity of tricuspid regurgitation and a decrease in pulmonary artery pressure.
authors.affiliation: Department of Cardiology, Leiden University Medical Center, Leiden, The Netherlands.
authors.forename: Gabe B
authors.initials: GB
authors.lastname: Bleeker
authors.forename: Martin J
authors.initials: MJ
authors.lastname: Schalij
authors.forename: Petros
authors.initials: P
authors.lastname: Nihoyannopoulos
authors.forename: Paul
authors.initials: P
authors.lastname: Steendijk
authors.forename: Sander G
authors.initials: SG
authors.lastname: Molhoek
authors.forename: Lieselot
authors.initials: L
authors.lastname: van Erven
authors.forename: Marianne
authors.initials: M
authors.lastname: Bootsma
authors.forename: Eduard R
authors.initials: ER
authors.lastname: Holman
authors.forename: Ernst E
authors.initials: EE
authors.lastname: van der Wall
authors.forename: Jeroen J
authors.initials: JJ
authors.lastname: Bax
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D001794:Blood Pressure; D002303:Cardiac Output, Low / Q000150:complications* / Q000000981:diagnostic imaging / Q000503:physiopathology / Q000628:therapy*; D002304:Cardiac Pacing, Artificial; D004452:Echocardiography; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D011379:Prognosis; D011651:Pulmonary Artery / Q000503:physiopathology; D013997:Time Factors; D014262:Tricuspid Valve Insufficiency; D018487:Ventricular Dysfunction, Left / Q000209:etiology*; D016278:Ventricular Function, Right; D020257:Ventricular Remodeling