title: Doppler myocardial imaging in patients with heart failure receiving biventricular pacing treatment.
abstract: BACKGROUND
  In patients with heart failure, biventricular pacing (BIV) improves left ventricular (LV) performance by counteracting LV unsynchronized contraction caused by the presence of left bundle branch block (LBBB). However, no data are yet available on regional long-axis function in patients with LBBB or on BIV effectiveness in improving such a function in patients with heart failure and LBBB.
  
  
  RESULTS
  We studied with standard 2D echocardiography and tissue Doppler imaging (TDI) 21 nonischemic patients in New York Heart Association (NYHA) class III-IV, with LBBB and QRS >/=120 ms, receiving BIV. To assess long-axis function, TDI qualitative analysis at the basal level of each LV wall was performed in M-mode color and pulsed wave Doppler modalities before and after BIV. By analysis of the interventricular septum, the inferior, posterior, lateral, and anterior walls, of 105 basal segments, the following electromechanical patterns were identified: normal (pattern I), mildly unsynchronized (pattern IIA), severely unsynchronized (pattern IIB), reversed early in systole (pattern IIIA), reversed late in systole (pattern IIIB), and reversed throughout all the systole (pattern IV). After BIV, (1) 49 (46.7%) of 105 segments showed unsynchronized contraction of the same degree as before; (2) 36 (34.3%) of 105 and 20 (19%) of 105 showed unsynchronized contraction of lesser and greater degree, respectively, than before; and (3) a preexcitation pattern was found in 11 (10.5%) of 105, but no segment with pattern IV was observed. According to TDI analysis, patients were divided into group 1 (10 of 21), with less severe LV asynchrony than before BIV, and group 2 (11 of 21), with no change or more severe LV asynchrony than before BIV. In group 1, (1) the LV ejection fraction increased significantly (P =.01); (2) the exercise tolerance, expressed as time and work capacity on the bicycle stress testing, increased significantly (P =.01, P =.003, respectively); (3) the 6-minute walked distance increased significantly (P =.01); and (4) the NYHA class decreased significantly (P =.003). In group 2, no significant differences were found either in LV ejection fraction, in NYHA class, or in exercise tolerance data (P = not significant for all). Conversely, the QRS narrowing was significant in both groups (P =.003 in group 1 and P =.01 in group 2).
  
  
  CONCLUSIONS
  TDI is useful in assessing the severity of LV asynchrony in patients with LBBB with heart failure as well as in evaluating the pacing effects on long-axis function in these patients. BIV reduced unsynchronized and/or dyskinetic contraction in at least one third of the LV basal segments, whereas it induced preexcitation in approximately 10%. Such changes were responsible for better LV synchrony in approximately one half of patients. After BIV, LV performance improved significantly in patients with better LV synchrony evaluated by TDI, whereas the QRS narrowing was not predictive of this functional improvement.
authors.affiliation: Department of Heart Diseases, San Filippo Neri Hospital, Rome, Italy. gansalone@iol.it
authors.forename: G
authors.initials: G
authors.lastname: Ansalone
authors.forename: P
authors.initials: P
authors.lastname: Giannantoni
authors.forename: R
authors.initials: R
authors.lastname: Ricci
authors.forename: P
authors.initials: P
authors.lastname: Trambaiolo
authors.forename: A
authors.initials: A
authors.lastname: Laurenti
authors.forename: F
authors.initials: F
authors.lastname: Fedele
authors.forename: M
authors.initials: M
authors.lastname: Santini
mesh_terms: D002037:Bundle-Branch Block / Q000175:diagnosis / Q000503:physiopathology / Q000628:therapy; D002304:Cardiac Pacing, Artificial / Q000379:methods*; D004452:Echocardiography / Q000706:statistics & numerical data; D015150:Echocardiography, Doppler / Q000706:statistics & numerical data*; D004562:Electrocardiography / Q000706:statistics & numerical data; D005080:Exercise Test / Q000706:statistics & numerical data; D006321:Heart / Q000503:physiopathology; D006333:Heart Failure / Q000175:diagnosis* / Q000503:physiopathology / Q000628:therapy*; D006801:Humans; D009200:Myocardial Contraction / Q000502:physiology; D018754:Ventricular Dysfunction / Q000175:diagnosis / Q000503:physiopathology / Q000628:therapy