The goal is to explore the impact of regional ischemia followed by reperfusion on the long-term changes in ventricular mechanics and diastolic properties, and to relate these changes in diastolic compliance as determinants of ventricular systolic performance. A persistent depression in myocardial performance following transient coronary occlusion has been observed both clinically and in experimental models of myocardial infarction, even after brief periods of ischemia that leave no evidence of histologic necrosis. The reason for this delay in recovery of ventricular performance is unclear and attempts to correlate recovery of systolic function with the recovery of high energy phosphates have been inconsistent. Others have found events surrounding reperfusion of the ischemic myocardium to be significant determinants of recovery of systolic function. As both ischemia and reperfusion of ischemic myocardium have been shown to alter diastolic mechanics acutely, it is our purpose to study the long-term recovery of altered diastolic properties, using the chronically instrumented animal preparation. Ischemic injury will be quantitated in terms of diastolic properties of the left ventricle as measured by alterations in the pressure-strain relatioonship as a reflection of regional myocardial stiffness. A pressure dimension analysis using pulse-transit ultrasound with matched pairs of piezoelectric crystals will be used in the chronically instrumented dog model. Global dimensions will be assessed by ultrasonic crystals in the major and minor axis of the left ventricle, and in the mid-wall thickness. Regional function will be assessed by pairs of smaller crystals placed in the ischemic and non-ischemic zones of myocardium. Pressures will be measured by catheter tip micromanometers, and data will be recorded in the awake, conscious state one week after implantation. Transient LAD coronary occlusion of two hours will be accomplished by a hydraulic occluder, and pressure-dimension data will be measured during ischemia as well as following reperfusion up to a period of four weeks. It is anticipated that quantitation of alterations in diastolic properties over time will improve our understanding of the commonly observed delay in recovery of ventricular performance seen with transient coronary occlusion. Quantitation of this change in diastolic compliance will allow exploration of methods to reduce the amount of reperfusion injury, which has been found by some investigators to be an important determinant of eventual recovery of systolic performance.
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