Abstract 3755: Passive Mechanics of Human Ventricular Strips from Volume-loaded or Pressure-loaded Hearts
Diastolic dysfunction due to altered chamber stiffness is difficult to assess by in vivo methods. Myocardial stiffness at normal sarcomere lengths is due to titin (intrasarcomeric elastic protein) and collagen (~10% of stiffness at small stretches). Human myocardial stiffness was measured in vitro by stretching ventricular muscle strips from patients having cardiac surgery.
Methods. Tissue from volume-overloaded (VO: ASD, pulmonary valve replacement, aortic regurgitation) and pressure-overloaded (PO: TOF, DCRV, conduit change, AS) hearts was used. Skinned muscle strips 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. Mechanics were repeated after removal of actomyosin and titin (KCL, KI) to evaluate the titin contribution. Collagen content was measured by HPLC.
Results. Subjects were 0.4 – 66 years. Muscle strips (n=91) had a biphasic tension-extension response, titin and collagen responsible for tension at short and long stretches respectively. PO muscle strips generated more tension (p <<178> 0.01) and were stiffer (p <<178> 0.01) than VO strips at short stretches and also large stretches (tension, p <0.01; stiffness, p < 0.01). In VO strips collagen contributed ~ 40% of tension at small stretches (5% muscle length). The collagen content did not vary significantly with disease.
Conclusion. Loading conditions alter myocardial stiffness. PO myocardium is stiffer than VO myocardium at several levels (extracellular matrix, myocytes).