title: Remission of left ventricular systolic dysfunction and of heart failure symptoms after cardiac resynchronization therapy: temporal pattern and clinical predictors.
abstract: BACKGROUND
  The aim of the study was to determine whether cardiac resynchronization therapy (CRT) may induce a heart failure (HF) remission phase (recovery to New York Heart Association functional class I-II and regression of left ventricular [LV] dysfunction: LV ejection fraction [EF] > or = 50%) and to define the incidence and predictors of such a process.
  
  
  METHODS
  Cardiac resynchronization therapy devices were successfully implanted in 520 consecutive HF patients from 1999 to 2006 (mean age 66 years, 82% male sex, New York Heart Association class > or = II, LVEF 28%, QRS 164 milliseconds, 6-minute hall walk distance 302 m) at our institution. Follow-up data were prospectively collected every 3 to 6 months. Continuous variables were stratified in tertiles.
  
  
  RESULTS
  Over a median follow-up of 28 months, 26% of patients achieved LV remission (rate: 16 per 100 person-years). At univariate analysis, female sex (P = .032), non-coronary artery disease (CAD) etiology (P < .001), mitral regurgitation < 2/4 (P = .022), higher EF tertile (P < .001), lower diameter and volume tertiles (both P < .001), previous conventional right ventricle pacing (P = .029), and post-CRT-paced QRS (P = .008) predicted remission. At multivariate analysis, non-CAD etiology, LVEF 30% to 35%, and LV end-diastolic volume < 180 mL were strongly associated with HF remission phase (all P < .001). Concomitance of these 3 factors yielded a significantly higher remission rate compared with either no or only 1 factor (respectively, 60 vs 7 and 11 per 100 person-years, P < .001).
  
  
  CONCLUSIONS
  Cardiac resynchronization therapy induces HF remission phase in 26% of patients, even after 3 years. Non-CAD etiology and moderately compromised LV function at baseline may easily predict this process.
authors.affiliation: Department of Cardiology IRCCS Istituto Clinico Humanitas Rozzano-Milano, Italy. maurizio.gasparini@humanitas.it
authors.forename: Maurizio
authors.initials: M
authors.lastname: Gasparini
authors.forename: François
authors.initials: F
authors.lastname: Regoli
authors.forename: Carlo
authors.initials: C
authors.lastname: Ceriotti
authors.forename: Paola
authors.initials: P
authors.lastname: Galimberti
authors.forename: Renato
authors.initials: R
authors.lastname: Bragato
authors.forename: Stefano
authors.initials: S
authors.lastname: De Vita
authors.forename: Daniela
authors.initials: D
authors.lastname: Pini
authors.forename: Bruno
authors.initials: B
authors.lastname: Andreuzzi
authors.forename: Maurizio
authors.initials: M
authors.lastname: Mangiavacchi
authors.forename: Catherine
authors.initials: C
authors.lastname: Klersy
mesh_terms: D000368:Aged; D017147:Defibrillators, Implantable; D004554:Electric Countershock / Q000295:instrumentation*; D005260:Female; D005500:Follow-Up Studies; D006333:Heart Failure / Q000209:etiology / Q000503:physiopathology / Q000628:therapy*; D006801:Humans; D008297:Male; D009200:Myocardial Contraction / Q000502:physiology*; D016016:Proportional Hazards Models; D012074:Remission Induction / Q000379:methods; D012189:Retrospective Studies; D012720:Severity of Illness Index; D013599:Systole; D016896:Treatment Outcome; D018487:Ventricular Dysfunction, Left / Q000150:complications / Q000503:physiopathology / Q000628:therapy*