The course of passive elasticity of myocardial tissue following experimental infarction in rabbits and its relation to mechanical dysfunction.

Given the substantial reserve of normal myocardium, its inability to sustain life in the presence of 30-50% necrosis of the left ventricle (LV) seems a paradox. It is known that dyskinesia of the infarcted area probably plays a dominant role in initiating failure after an infarction. To study this problem, a well defined experimental infarction was produced by cryogenic means in 58 rabbits, and the animals were allowed to recover. Groups of rabbits were killed 4 hours and 1,2,5, or 10 days following infarction. As quickly as possible (within 4 minutes) a sample specimen from the infarcted area was removed from the LV and subjected to a force-elongation test while being bathed in Ringer solution at 37 degrees C equilibrated with 95% O2-5% CO2. The data were interpreted assuming an exponential stress-strain law with constants K and C. Mean values of K of 10.6 +/- 0.94 (SEM) were found for the noninfarcted control group, whereas, rather surprisingly, no significant trend in K over 10 days was found in the infarcted group. Mean values of K +/- SEM for the postinfarction groups were as follows: 4 hours, 9.51 +/- 0.63; 1 day 10.54 +/- 1.13; 2 days, 13.15 +/- 2.28; 5 days, 11.59 +/- 1.36; and over 10 days, 12.93 +/-1.02. The functional implications were estimated with a simple model of the shortening required of the viable muscle during the isovolumic phase. It was found that contractile reserve fell rapidly with increasing infarct size, reaching zero for a 60% infarct when K = 10. With K greater than 100, there was no appreciable reduction in reserve. With a constant infarct size, variation in reserve with the afterload-preload ration was found to be logarithmic.