title: High-risk percutaneous coronary intervention is associated with reverse left ventricular remodeling and improved outcomes in patients with coronary artery disease and reduced ejection fraction.
abstract: BACKGROUND
  Therapies that reverse pathologic left ventricular (LV) remodeling are often associated with improved outcomes. The incidence and impact of reverse LV remodeling after high-risk percutaneous coronary intervention (PCI) are unknown.
  
  
  METHODS
  The PROTECT II study was a multicenter trial in patients with complex, multivessel coronary artery disease and reduced ejection fraction (EF) that revealed an increase in visual EF after high-risk PCI. Among patients with quantitative echocardiography (LV volumes and biplane EF), we assessed the extent and predictors of reverse LV remodeling, defined as improved systolic function with an absolute increase in EF ≥5% and correlated these findings with clinical events.
  
  
  RESULTS
  Quantitative echocardiography was performed in 184 patients at baseline and longest follow-up. Mean EF at baseline was 27.1%. Ninety-three patients (51%) demonstrated reverse LV remodeling with an absolute increase in EF of 13.2% (P < .001). End-systolic volume decreased from 137.7 to 106.6 mL (P = .002). No significant change in EF or end-systolic volume was seen among non-remodelers. Reverse LV remodeling occurred more frequently in patients with more extensive revascularization (odds ratio, 7.52; 95% CI [1.31-43.25]) and was associated with significantly fewer major adverse events (composite of death/myocardial infarction/stroke/transient ischemic attack): 9.7% versus 24.2% (P = .009). There was also a greater reduction in New York Heart Association class III/IV heart failure among reverse LV remodelers (66.7% to 24.0%) than non-remodelers (56.3% to 34.4%), P = .045.
  
  
  CONCLUSIONS
  Reverse LV remodeling can occur after high-risk PCI in patients with complex coronary artery disease and reduced EF and is associated with improved clinical outcomes.
authors.affiliation: Duke Clinical Research Institute, Duke University Medical Center, Durham, NC. Electronic address: melissa.daubert@duke.edu.
authors.forename: Melissa A
authors.initials: MA
authors.lastname: Daubert
authors.affiliation: Harvard Clinical Research Institute, Boston, MA; Boston University, Boston, MA.
authors.forename: Joseph
authors.initials: J
authors.lastname: Massaro
authors.affiliation: Duke Clinical Research Institute, Duke University Medical Center, Durham, NC.
authors.forename: Lawrence
authors.initials: L
authors.lastname: Liao
authors.affiliation: Banner Good Samaritan Hospital, Phoenix, AZ.
authors.forename: Ashish
authors.initials: A
authors.lastname: Pershad
authors.affiliation: University of Pittsburgh Medical Center, Pittsburgh, PA.
authors.forename: Suresh
authors.initials: S
authors.lastname: Mulukutla
authors.affiliation: Duke Clinical Research Institute, Duke University Medical Center, Durham, NC.
authors.forename: Erik
authors.initials: E
authors.lastname: Magnus Ohman
authors.affiliation: Harvard Clinical Research Institute, Boston, MA; Beth Israel Deaconess Hospital, Boston, MA.
authors.forename: Jeffrey
authors.initials: J
authors.lastname: Popma
authors.affiliation: Henry Ford Hospital, Detroit, MI.
authors.forename: William W
authors.initials: WW
authors.lastname: O'Neill
authors.affiliation: Duke Clinical Research Institute, Duke University Medical Center, Durham, NC.
authors.forename: Pamela S
authors.initials: PS
authors.lastname: Douglas
mesh_terms: D000368:Aged; D003324:Coronary Artery Disease / Q000175:diagnosis / Q000503:physiopathology* / Q000601:surgery; D004452:Echocardiography; D004562:Electrocardiography; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D008297:Male; D062645:Percutaneous Coronary Intervention; D011446:Prospective Studies; D012307:Risk Factors; D013318:Stroke Volume; D016896:Treatment Outcome; D016277:Ventricular Function, Left / Q000502:physiology*; D020257:Ventricular Remodeling