title: Chronic kidney disease and cardiac remodelling in patients with mild heart failure: results from the REsynchronization reVErses Remodeling in Systolic Left vEntricular Dysfunction (REVERSE) study.
abstract: OBJECTIVE
  Chronic kidney disease (CKD) is a risk factor for left ventricular hypertrophy (LVH) and heart failure. We evaluated the effect of CKD on left ventricular (LV) remodelling among patients with mild heart failure.
  
  
  RESULTS
  REVERSE was a randomized, controlled trial evaluating cardiac resynchronization therapy (CRT) in patients with New York Heart Association (NYHA) class I/II heart failure. CKD was defined as an estimated glomerular filtration rate (eGFR) <60 mL/min/1.73 m(2). We compared changes in LV function and size over the course of 12 months by CKD status using linear mixed models adjusted for demographics, co-morbidities, medications, cardiomyopathy aetiology, and CRT status. Finally, we evaluated the effect of CKD on cardiac remodelling among patients randomized to CRT on or off. CKD was associated with worsening LV function and dilation compared with the non-CKD group {adjusted, 12-month β coefficients for the CKD group compared with the non-CKD referent group: LV ejection fraction (%) [-1.80, 95% confidence interval (CI) -3.36 to -0.24], LV end-systolic volume (mL) (14.16, 95% CI 3.96-24.36), LV end-diastolic volume (mL) (14.88, 95% CI 2.88-26.76), LV end-systolic diameter (cm) (0.36, 95% CI 0.12-0.48), LV end-diastolic diameter (cm) (0.24, 95% CI 0.012-0.36), mitral regurgitation (%) (3.12, 95% CI 0.48-5.76), and LV shape (0.036, 95% CI 0.012-0.060)}. In participants assigned to CRT, those without CKD had significantly greater improvements in LV structural parameters compared with the CKD group.
  
  
  CONCLUSIONS
  In comparison with participants with normal kidney function, CKD is an independent risk factor for ventricular dysfunction and dilation. CRT improves LV function and structure to a lesser extent in patients with CKD than in those with normal kidney function.
authors.affiliation: Division of Cardiovascular Medicine, University of Pennsylvania, Philadelphia, PA, USA.
authors.forename: Jehu
authors.initials: J
authors.lastname: Mathew
authors.forename: Ronit
authors.initials: R
authors.lastname: Katz
authors.forename: Martin
authors.initials: M
authors.lastname: St John Sutton
authors.forename: Sanjay
authors.initials: S
authors.lastname: Dixit
authors.forename: Edward P
authors.initials: EP
authors.lastname: Gerstenfeld
authors.forename: Stefano
authors.initials: S
authors.lastname: Ghio
authors.forename: Michael R
authors.initials: MR
authors.lastname: Gold
authors.forename: Cecilia
authors.initials: C
authors.lastname: Linde
authors.forename: Michael G
authors.initials: MG
authors.lastname: Shlipak
authors.forename: Rajat
authors.initials: R
authors.lastname: Deo
mesh_terms: D000368:Aged; D015415:Biomarkers / Q000097:blood; D058406:Cardiac Resynchronization Therapy / Q000379:methods*; D016009:Chi-Square Distribution; D004311:Double-Blind Method; D004452:Echocardiography; D005260:Female; D054143:Heart Failure, Systolic / Q000503:physiopathology* / Q000628:therapy*; D006801:Humans; D007676:Kidney Failure, Chronic / Q000503:physiopathology*; D007677:Kidney Function Tests; D016014:Linear Models; D008297:Male; D008875:Middle Aged; D016016:Proportional Hazards Models; D011446:Prospective Studies; D012307:Risk Factors; D018487:Ventricular Dysfunction, Left / Q000503:physiopathology* / Q000628:therapy*; D020257:Ventricular Remodeling
chemical_list: D015415:Biomarkers