Why the study?
Does severe ischemic left ventricular failure alter the LV isovolumic relaxation process and diastolic chamber stiffness in a canine model?
Does severe ischemic left ventricular failure alter the LV isovolumic relaxation process and diastolic chamber stiffness in a canine model?
In a canine model, acute ischemic left ventricular failure slows LV relaxation but does not alter diastolic chamber stiffness.
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Slows relaxation without altering stiffness in canine ischemia; leaves open translation to human diastolic assessment.
The significance of severe ischaemic left ventricular (LV) failure on the LV isovolumic relaxation process and diastolic chamber stiffness has been investigated in nine open-chest pentobarbital-anaesthetized dogs. LV failure was induced by bolus injections of 50 micron microspheres into left coronary vascular bed until LV minor axis diameter had increased about 25% and end-diastolic pressure about 20 mmHg. Such ischaemic LV failure did not shift the relation between diastolic LV pressure and minor axis diameter compared with pressure-diameter curves obtained before induction of failure. Neither inotropic nor chronotropic stimulation evoked such shifts. Assuming exponential pressure decline, LV relaxation was significantly slower during failure, but proceeded in all experimental conditions at rates which indicated complete relaxation in late diastole. Analysis of the pressure decline during LV relaxation demonstrated that this process proceeded faster than assumed by an exponential function both before and during LV failure.
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Myhre et al. (1984) studied this question.
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