title: Pulmonary endarterectomy normalizes interventricular dyssynchrony and right ventricular systolic wall stress.
abstract: BACKGROUND
  Interventricular mechanical dyssynchrony is a characteristic of pulmonary hypertension. We studied the role of right ventricular (RV) wall stress in the recovery of interventricular dyssynchrony, after pulmonary endarterectomy (PEA) in chronic thromboembolic pulmonary hypertension (CTEPH).
  
  
  METHODS
  In 13 consecutive patients with CTEPH, before and 6 months after pulmonary endarterectomy, cardiovascular magnetic resonance myocardial tagging was applied. For the left ventricular (LV) and RV free walls, the time to peak (Tpeak) of circumferential shortening (strain) was calculated. Pulmonary Artery Pressure (PAP) was measured by right heart catheterization within 48 hours of PEA. Then the RV free wall systolic wall stress was calculated by the Laplace law.
  
  
  RESULTS
  After PEA, the left to right free wall delay (L-R delay) in Tpeak strain decreased from 97 ± 49 ms to -4 ± 51 ms (P < 0.001), which was not different from normal reference values of -35 ± 10 ms (P = 0.18). The RV wall stress decreased significantly from 15.2 ± 6.4 kPa to 5.7 ± 3.4 kPa (P < 0.001), which was not different from normal reference values of 5.3 ± 1.39 kPa (P = 0.78). The reduction of L-R delay in Tpeak was more strongly associated with the reduction in RV wall stress (r = 0.69,P = 0.007) than with the reduction in systolic PAP (r = 0.53, P = 0.07). The reduction of L-R delay in Tpeak was not associated with estimates of the reduction in RV radius (r = 0.37,P = 0.21) or increase in RV systolic wall thickness (r = 0.19,P = 0.53).
  
  
  CONCLUSIONS
  After PEA for CTEPH, the RV and LV peak strains are resynchronized. The reduction in systolic RV wall stress plays a key role in this resynchronization.
authors.affiliation: Department of Pulmonary Diseases, University of Amsterdam, Amsterdam, The Netherlands.
authors.forename: Gert-Jan
authors.initials: GJ
authors.lastname: Mauritz
authors.forename: Anton
authors.initials: A
authors.lastname: Vonk-Noordegraaf
authors.forename: Taco
authors.initials: T
authors.lastname: Kind
authors.forename: Sulaiman
authors.initials: S
authors.lastname: Surie
authors.forename: Jaap J
authors.initials: JJ
authors.lastname: Kloek
authors.forename: Paul
authors.initials: P
authors.lastname: Bresser
authors.forename: Nabil
authors.initials: N
authors.lastname: Saouti
authors.forename: Joachim
authors.initials: J
authors.lastname: Bosboom
authors.forename: Nico
authors.initials: N
authors.lastname: Westerhof
authors.forename: J Tim
authors.initials: JT
authors.lastname: Marcus
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D001696:Biomechanical Phenomena; D001794:Blood Pressure; D006328:Cardiac Catheterization; D002908:Chronic Disease; D004691:Endarterectomy; D005260:Female; D006801:Humans; D006976:Hypertension, Pulmonary / Q000209:etiology / Q000503:physiopathology / Q000601:surgery*; D016014:Linear Models; D019028:Magnetic Resonance Imaging, Cine; D008297:Male; D008875:Middle Aged; D008955:Models, Cardiovascular; D009426:Netherlands; D011651:Pulmonary Artery / Q000503:physiopathology / Q000601:surgery*; D011655:Pulmonary Embolism / Q000150:complications / Q000503:physiopathology; D020127:Recovery of Function; D013314:Stress, Mechanical; D013318:Stroke Volume; D013599:Systole; D013997:Time Factors; D016896:Treatment Outcome; D018487:Ventricular Dysfunction, Left / Q000209:etiology / Q000503:physiopathology*; D018497:Ventricular Dysfunction, Right / Q000209:etiology / Q000503:physiopathology*; D016277:Ventricular Function, Left; D016278:Ventricular Function, Right