title: Relation of right ventricular peak systolic pressure to major adverse events in patients undergoing cardiac resynchronization therapy.
abstract: The degree to which increased right-sided heart pressures influence outcome in cardiac resynchronization therapy (CRT) is unclear. High right ventricular (RV) pressures may contribute to septal malpositioning, thus hindering effective resynchronization. We hypothesized that patients with high RV systolic pressures before CRT implantation would have poorer outcome. We evaluated echocardiograms, electrocardiograms, and clinical records from 75 consecutive patients with CRT. RV systolic pressure was calculated from the peak tricuspid regurgitant, time-velocity profile. The primary end point was a composite of mortality, cardiac transplantation, or need for a left ventricular assist device. Events were evaluated by Kaplan-Meier curves and Cox proportional hazard ratios. Patients grouped by RV systolic pressure divided at the median of 35 mm Hg were similar except for more renal insufficiency and RV dysfunction when RV systolic pressure was >35 mm Hg. Univariate analysis identified RV systolic pressure >35 mm Hg (hazard ratio [HR] 3.32), diabetes (HR 2.45), renal insufficiency (HR 3.52), atrial fibrillation (HR 3.07), use of nonamiodarone antiarrhythmic medications (HR 2.86), atrial pacing (HR 2.57), and prolonged PR interval (HR 1.009) as associated with poorer outcome. Normal sinus rhythm at implantation (HR 0.34), baseline left bundle branch block (HR 0.44), and beta-blocker use (HR 0.47) were associated with improved outcome. In a multivariable model, high RV systolic pressure (HR 3.71, 95% confidence interval 1.31 to 10.4), renal insufficiency (HR 3.18, 95% confidence interval 1.29 to 7.86), and atrial fibrillation (HR 4.22, 95% confidence interval 1.54 to 11.6) remained significant. In conclusion, despite resynchronization, patients with high RV pressures have significantly decreased survival after adjusting for significant contributing influences.
authors.affiliation: Cardiovascular Division, Brigham and Women's Hospital, Boston, Massachusetts, USA. utedrow@partners.org
authors.forename: Usha B
authors.initials: UB
authors.lastname: Tedrow
authors.forename: Daniel B
authors.initials: DB
authors.lastname: Kramer
authors.forename: Lynne W
authors.initials: LW
authors.lastname: Stevenson
authors.forename: William G
authors.initials: WG
authors.lastname: Stevenson
authors.forename: Kenneth L
authors.initials: KL
authors.lastname: Baughman
authors.forename: Laurence M
authors.initials: LM
authors.lastname: Epstein
authors.forename: Eldrin F
authors.initials: EF
authors.lastname: Lewis
mesh_terms: D000368:Aged; D001281:Atrial Fibrillation / Q000503:physiopathology; D002304:Cardiac Pacing, Artificial; D005260:Female; D006333:Heart Failure / Q000401:mortality / Q000628:therapy*; D016027:Heart Transplantation; D006353:Heart-Assist Devices; D006801:Humans; D008297:Male; D015999:Multivariate Analysis; D016016:Proportional Hazards Models; D051437:Renal Insufficiency / Q000503:physiopathology; D013599:Systole / Q000502:physiology*; D018497:Ventricular Dysfunction, Right / Q000503:physiopathology*; D017725:Ventricular Pressure / Q000502:physiology*