title: Increased resistance against shortening in myocardium from recipient hearts of 7 patients transplanted for dilated cardiomyopathy.
abstract: The contractile behaviour of demembranized atrial and ventricular myocardium of 7 patients transplanted for end-stage heart failure (ESHF) was analyzed. Atrial muscle specimens of patients undergoing coronary artery bypass surgery (n = 9) and pig papillary muscle were used as reference preparations (n = 9). Extreme care was taken for dissection and mounting the muscle fibres (0.3 x 6 mm) in order to keep the passive series compliance small. Calcium sensitivity, cross-bridge cycling rate (estimated by the force-clamping technique and calculation of the shortening velocity at zero load [Vmax]) and isometric force development were measured. Analysis on light- and electronmicroscopic level was carried out.
  
  
  RESULTS
  1) Calcium sensitivity was not altered in ESHF patients; 2) the velocity of the force generating process (cross-bridge cycling rate) was normal in ventricular and reduced in atrial ESHF myocardium, 3) maximum isometric force development was reduced in ventricular, but not in atrial myocardium of ESHF patients, and 4) Vmax was significantly reduced in ventricular and atrial ESHF myocardium (p < 0.0001). Perimysial and endomysial fibrosis was present in ventricular, not in atrial myocardium of ESHF patients.
  
  
  CONCLUSIONS
  A normal cross-bridge cycling rate in left-ventricular ESHF myocardium combined with a decreased capability of muscle shortening indicates the presence of a resistance against shortening localized either on the cross-bridge level or/and due to intra- and pericellular fibrosis. Left-ventricular contractile dysfunction in patients with end-stage heart failure may be related to a normal contractile apparatus contracting within an abnormal intracellular or interstitial environment.
authors.affiliation: Department of Cardiac Surgery, University of Heidelberg, Germany.
authors.forename: C F
authors.initials: CF
authors.lastname: Vahl
authors.forename: R
authors.initials: R
authors.lastname: Bauernschmitt
authors.forename: A
authors.initials: A
authors.lastname: Bonz
authors.forename: U
authors.initials: U
authors.lastname: Herold
authors.forename: K
authors.initials: K
authors.lastname: Amann
authors.forename: S
authors.initials: S
authors.lastname: Ziegler
authors.forename: S
authors.initials: S
authors.lastname: Hagl
mesh_terms: D000818:Animals; D002118:Calcium / Q000502:physiology; D002311:Cardiomyopathy, Dilated / Q000503:physiopathology*; D016022:Case-Control Studies; D003327:Coronary Disease / Q000503:physiopathology; D005260:Female; D006321:Heart / Q000503:physiopathology*; D006801:Humans; D066298:In Vitro Techniques; D007537:Isometric Contraction / Q000502:physiology; D007551:Isotonic Contraction / Q000502:physiology; D008297:Male; D008854:Microscopy, Electron; D008875:Middle Aged; D009200:Myocardial Contraction / Q000502:physiology*; D009206:Myocardium / Q000648:ultrastructure; D010210:Papillary Muscles / Q000502:physiology / Q000503:physiopathology / Q000648:ultrastructure; D013552:Swine
chemical_list: D002118:Calcium