Abstract 1442: Passive Mechanics of Human Ventricular Myocytes from Pressure-loaded, Volume-loaded and Dilated Cardiomyopathy Hearts
Diastolic dysfunction due to altered chamber stiffness is difficult to assess by in vivo methods. Myocardial stiffness of normal hearts at normal sarcomere lengths is due to titin (intrasarco-meric elastic protein) and collagen (~10% of stiffness at small stretches). However the behaviour of myocytes from diseased hearts is unknown. Human ventricular myocyte passive tension and stiffness were measured in vitro by stretching ventricular myocytes from patients having cardiac surgery.
Methods. Ventricular tissue from volume-overloaded (VO: ASD), pressure-overloaded (PO: TOF, conduit change), normal donors and dilated cardiomyopathy (DCM) hearts was used. Skinned myocytes (n=22) were mounted between a force transducer and servomotor. Tension response to passive stretches in relaxing soln, was used to create tension-extension curves and derive stiffness.
Results. Subjects were 1.2– 60 years. Tension-extension curves of PO myocytes were shifted to lower sarcomere lengths (SL) than VO/normals. DCM myocytes were extremely compliant. The rank order of passive tension and stiffness was: PO > normal/VO (p=0.042) and normal/VO > DCM (p=0.036), based on the median SL myocytes were stretched to generate a tension of 0.75 kN/m2.
Conclusion. Loading conditions change myocyte passive mechanics. PO hypertrophied myocardium is stiffer than normal/volume-overloaded myocardium which in turn was stiffer than myocytes from end-stage dilated cardiomyopathy.