title: Tissue Doppler echocardiographic evidence of reverse remodeling and improved synchronicity by simultaneously delaying regional contraction after biventricular pacing therapy in heart failure.
abstract: BACKGROUND
  Biventricular pacing has been proposed to improve symptoms and exercise capacity in patients with advanced heart failure and wide electrocardiographic wave complexes. This study investigated the effect of biventricular pacing on reverse remodeling and the underlying mechanisms.
  
  
  RESULTS
  Twenty-five patients with NYHA class III to IV heart failure and electrocardiographic wave complex duration >140 ms receiving biventricular pacing therapy were assessed serially up to 3 months after pacing and when pacing was withheld for 4 weeks. Tissue Doppler echocardiography was performed using a 6-basal, 6-mid segmental model to assess the time to peak sustained systolic contraction (T(S)). There was significant improvement of ejection fraction, dP/dt, and myocardial performance index; decrease in mitral regurgitation, left ventricular (LV) end-diastolic (205+/-68 versus 168+/-67 mL, P<0.01) and end-systolic volume (162+/-54 versus 122+/-42 mL, P<0.01); and improved 6-minute hall-walk distance and quality of life score after pacing for 3 months. The mechanisms of benefits were as follows: (1) improved LV synchrony, as evident by homogeneous delay of T(S) to a timing close to the latest (usually the lateral) segment abolishing the intersegmental difference in T(S) and decreasing the standard deviation of T(S) within the left ventricle (37.7+/-10.9 versus 29.3+/-8.3 ms, P<0.05); (2) improved interventricular synchrony; and (3) shortened isovolumic contraction time (122+/-57 versus 82+/-36 ms, P<0.05) but increased diastolic filling time. These benefits are pacing dependent, because withholding the pacing resulted in varying speeds in the loss of cardiac improvements.
  
  
  CONCLUSIONS
  Biventricular pacing reverses LV remodeling and improves cardiac function. Improvement of LV mechanical synchrony seems to be the predominant mechanism.
authors.affiliation: Division of Cardiology, Department of Medicine, Queen Mary Hospital, The University of Hong Kong. cmyua@hkucc.hku.hk
authors.forename: Cheuk-Man
authors.initials: CM
authors.lastname: Yu
authors.forename: Elaine
authors.initials: E
authors.lastname: Chau
authors.forename: John E
authors.initials: JE
authors.lastname: Sanderson
authors.forename: Katherine
authors.initials: K
authors.lastname: Fan
authors.forename: Man-Oi
authors.initials: MO
authors.lastname: Tang
authors.forename: Wing-Hong
authors.initials: WH
authors.lastname: Fung
authors.forename: Hong
authors.initials: H
authors.lastname: Lin
authors.forename: Shun-Ling
authors.initials: SL
authors.lastname: Kong
authors.forename: Yui-Ming
authors.initials: YM
authors.lastname: Lam
authors.forename: Michael R S
authors.initials: MR
authors.lastname: Hill
authors.forename: Chu-Pak
authors.initials: CP
authors.lastname: Lau
mesh_terms: D000368:Aged; D002304:Cardiac Pacing, Artificial / Q000379:methods*; D015150:Echocardiography, Doppler / Q000379:methods*; D005260:Female; D006333:Heart Failure / Q000000981:diagnostic imaging* / Q000503:physiopathology / Q000628:therapy*; D006352:Heart Ventricles / Q000503:physiopathology; D006439:Hemodynamics; D006801:Humans; D007700:Kinetics; D008297:Male; D008955:Models, Cardiovascular; D009200:Myocardial Contraction; D010507:Periodicity; D018754:Ventricular Dysfunction / Q000000981:diagnostic imaging / Q000503:physiopathology / Q000628:therapy; D018487:Ventricular Dysfunction, Left / Q000000981:diagnostic imaging / Q000503:physiopathology / Q000628:therapy; D020257:Ventricular Remodeling