title: Right ventricular pacing improves haemodynamics in right ventricular failure from pressure overload: an open observational proof-of-principle study in patients with chronic thromboembolic pulmonary hypertension.
abstract: OBJECTIVE
  Right ventricular (RV) failure in patients with chronic thromboembolic pulmonary hypertension (CTEPH), and other types of pulmonary arterial hypertension is associated with right-to-left ventricle (LV) delay in peak myocardial shortening and, consequently, the onset of diastolic relaxation. We aimed to establish whether RV pacing may resynchronize the onsets of RV and LV diastolic relaxation, and improve haemodynamics.
  
  
  RESULTS
  Fourteen CTEPH patients (mean age 63.7 ± 12.0 years, 10 women) with large (≥60 ms) RV-to-LV delay in the onset of diastolic relaxation (DIVD, diastolic interventricular delay) were studied. Temporary RV pacing was performed by atrioventricular (A-V) sequential pacing with incremental shortening of A-V delay to advance RV activation. Effects were assessed using tissue Doppler echocardiography and LV pressure-conductance catheter measurements in a subset of patients. Compared with right atrial pacing, RV pacing at optimal A-V delay (average 140 ± 22 ms, range 120-180 ms) resulted in significant DIVD reduction (59 ± 19 to 3 ± 22 ms, P < 0.001), and increase in LV stroke volume as measured by LV outflow tract velocity-time integral (14.9 ± 2.8 to 16.9 ± 3.0 cm, P < 0.001), along with enhanced global RV contractility and LV diastolic filling.
  
  
  CONCLUSIONS
  Right-to-left ventricle resynchronization of the onset of diastolic relaxation results in stroke volume increase in CTEPH patients. Whether RV pacing may be a novel therapeutic target in RV failure following chronic pressure overload remains to be investigated.
authors.affiliation: Heart Failure Research Center , Academic Medical Center, University of Amsterdam, The Netherlands.
authors.forename: Maxim
authors.initials: M
authors.lastname: Hardziyenka
authors.forename: Sulaiman
authors.initials: S
authors.lastname: Surie
authors.forename: Joris R
authors.initials: JR
authors.lastname: de Groot
authors.forename: H A C M Rianne
authors.initials: HA
authors.lastname: de Bruin-Bon
authors.forename: Reinoud E
authors.initials: RE
authors.lastname: Knops
authors.forename: Maurice
authors.initials: M
authors.lastname: Remmelink
authors.forename: Ze-Yie
authors.initials: ZY
authors.lastname: Yong
authors.forename: Jan
authors.initials: J
authors.lastname: Baan
authors.forename: Berto J
authors.initials: BJ
authors.lastname: Bouma
authors.forename: Paul
authors.initials: P
authors.lastname: Bresser
authors.forename: Hanno L
authors.initials: HL
authors.lastname: Tan
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D002302:Cardiac Output / Q000502:physiology; D002304:Cardiac Pacing, Artificial / Q000379:methods*; D002908:Chronic Disease; D003971:Diastole / Q000502:physiology; D004562:Electrocardiography; D005260:Female; D006352:Heart Ventricles / Q000503:physiopathology*; D006439:Hemodynamics / Q000502:physiology*; D006801:Humans; D006976:Hypertension, Pulmonary / Q000150:complications*; D008297:Male; D008875:Middle Aged; D013318:Stroke Volume / Q000502:physiology; D013923:Thromboembolism / Q000150:complications*; D018497:Ventricular Dysfunction, Right / Q000209:etiology / Q000503:physiopathology* / Q000628:therapy*