title: Left Ventricular Myocardial Fibrosis, Atrophy, and Impaired Contractility in Patients With Pulmonary Arterial Hypertension and a Preserved Left Ventricular Function: A Cardiac Magnetic Resonance Study.
abstract: OBJECTIVE
  Using a cardiac magnetic resonance (CMR) approach we investigated left ventricular (LV) myocardial changes associated with pulmonary arterial hypertension (PAH) by strain analysis and mapping techniques.
  
  
  METHODS
  Seventeen patients with PAH (9 men; mean age, 64.2±13.6 y) and 20 controls (10 men, 63.2±10.5 y) were examined using CMR at 1.5 T. Native LV T1-relaxation times (T1) and extracellular volume fraction (ECV) were assessed using a MOLLI sequence, T2-relaxation times (T2) by means of a gradient spin-echo sequence, and LV longitudinal strain (LVS) and right ventricular (RV) longitudinal strain (RVS) by means of CMR feature tracking. The hematocrit and serum levels of pro-Brain Natriuretic Peptide were determined on the day of the CMR examination. Pulmonary arterial pressure and 6-minute walking distance were assessed as part of the clinical evaluation.
  
  
  RESULTS
  T1 and ECV were higher (1048.5±46.6 vs. 968.3±22.9 ms and 32.4%±5.7% vs. 28.4%±3.8%; P<0.05) and LVS was lower in patients with PAH (-18.0±5.6 vs. -23.0±2.9; P<0.01) compared with controls. LV mass and interventricular septal thickness were lower in PAH patients (65.7±18.0 vs. 86.7±26.9 g and 7.6±1.9 vs. 10±2.4 mm; P<0.05); there were no differences in LV ejection fraction (61.2%±6.9% vs. 61.9%±6.7%; P=0.86). T1-derived parameters correlated significantly with RVS, LVS, the 6-minute walking distance, RV ejection fraction, pro-Brain Natriuretic Peptide, and baseline mean pulmonary arterial pressure. There were no significant differences in T2.
  
  
  CONCLUSIONS
  In patients with PAH, changes in T1 and ECV support the hypothesis of LV myocardial fibrosis and atrophy with a consecutively impaired contractility despite a preserved LV function, possibly due to longstanding PAH-associated LV underfilling.
authors.affiliation: *Department of Radiology, University of Bonn, Germany †Department of Internal Medicine, Cardiology, Pneumology and Angiology, Heart Centre Bonn, University of Bonn, Germany ‡Philips Healthcare Germany, Lübeckertordamm, Hamburg, Germany.
authors.forename: Rami
authors.initials: R
authors.lastname: Homsi
authors.forename: Julian A
authors.initials: JA
authors.lastname: Luetkens
authors.forename: Dirk
authors.initials: D
authors.lastname: Skowasch
authors.forename: Carmen
authors.initials: C
authors.lastname: Pizarro
authors.forename: Alois M
authors.initials: AM
authors.lastname: Sprinkart
authors.forename: Juergen
authors.initials: J
authors.lastname: Gieseke
authors.forename: Julia
authors.initials: J
authors.lastname: Meyer Zur Heide Gen Meyer-Arend
authors.forename: Hans H
authors.initials: HH
authors.lastname: Schild
authors.forename: Claas P
authors.initials: CP
authors.lastname: Naehle
mesh_terms: D001284:Atrophy; D005260:Female; D005355:Fibrosis; D006352:Heart Ventricles / Q000000981:diagnostic imaging / Q000473:pathology* / Q000503:physiopathology*; D006801:Humans; D006976:Hypertension, Pulmonary / Q000473:pathology / Q000503:physiopathology*; D008279:Magnetic Resonance Imaging / Q000379:methods*; D008297:Male; D008875:Middle Aged; D009206:Myocardium / Q000473:pathology*; D011446:Prospective Studies; D016277:Ventricular Function, Left / Q000502:physiology*