title: Clinical predictors of marked improvement in left ventricular performance after cardiac resynchronization therapy in patients with chronic heart failure.
abstract: BACKGROUND
  Previous studies have shown that cardiac resynchronization therapy (CRT) improves cardiac performance and decreases mortality and hospital admission rates. However, it is not yet clear which patients will benefit from the procedure the most. The purpose of the study was to identify the pre-implant characteristics that better predict which patients will have the best outcome after CRT.
  
  
  METHODS
  In this observational study, 156 patients were studied with echocardiography and a 6-minute walking test at baseline and 12 months after CRT.
  
  
  RESULTS
  After CRT, we observed an increase in left ventricular ejection fraction (+29.6%, P < .0001), a decrease in left ventricular end systolic volume (-26.4%, P < .0001), in the proportion of patients with grade 2-4 mitral regurgitation (from 47.1% to 34.0%, P = .002), and with NYHA functional class III-IV (from 83.2% to 11.6%, P < .0001), an increase in exercise tolerance (+31.1%, P < .0001). Sixty-two patients had a marked increase in left ventricular ejection fraction (> 10 units); the only independent predictor of a marked effect of CRT was the nonischemic etiology of heart failure. In patients with ischemic cardiomyopathy, the benefit on ejection fraction correlates inversely with the extension of the ischemic damage.
  
  
  CONCLUSIONS
  CRT improves left ventricular function and exercise tolerance in the long term. The nonischemic etiology of the cardiomyopathy is the only independent predictor of a marked effect of CRT; this is probably due to the absence of ischemic, nonviable scar tissue in these patients.
authors.affiliation: Department of Cardiology, IRCCS Istituto Clinico Humanitas, Rozzano, Milan, Italy. maurizio.mangiavacchi@humanitas.it
authors.forename: Maurizio
authors.initials: M
authors.lastname: Mangiavacchi
authors.forename: Maurizio
authors.initials: M
authors.lastname: Gasparini
authors.forename: Francesco
authors.initials: F
authors.lastname: Faletra
authors.forename: Catherine
authors.initials: C
authors.lastname: Klersy
authors.forename: Emanuela
authors.initials: E
authors.lastname: Morenghi
authors.forename: Paola
authors.initials: P
authors.lastname: Galimberti
authors.forename: Luca
authors.initials: L
authors.lastname: Genovese
authors.forename: François
authors.initials: F
authors.lastname: Regoli
authors.forename: Francesca
authors.initials: F
authors.lastname: De Chiara
authors.forename: Renato
authors.initials: R
authors.lastname: Bragato
authors.forename: Bruno
authors.initials: B
authors.lastname: Andreuzzi
authors.forename: Daniela
authors.initials: D
authors.lastname: Pini
authors.forename: Edoardo
authors.initials: E
authors.lastname: Gronda
mesh_terms: D000319:Adrenergic beta-Antagonists / Q000627:therapeutic use; D000368:Aged; D057911:Angiotensin Receptor Antagonists; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use; D002304:Cardiac Pacing, Artificial; D017079:Exercise Tolerance; D005260:Female; D006333:Heart Failure / Q000401:mortality / Q000503:physiopathology / Q000628:therapy*; D006801:Humans; D008297:Male; D008944:Mitral Valve Insufficiency / Q000503:physiopathology; D017202:Myocardial Ischemia / Q000503:physiopathology; D010101:Oxygen Consumption; D012189:Retrospective Studies; D013318:Stroke Volume / Q000502:physiology; D013997:Time Factors; D018487:Ventricular Dysfunction, Left / Q000401:mortality / Q000503:physiopathology / Q000628:therapy*; D020257:Ventricular Remodeling
chemical_list: D000319:Adrenergic beta-Antagonists; D057911:Angiotensin Receptor Antagonists; D000806:Angiotensin-Converting Enzyme Inhibitors