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SUMMARY. In studies utilizing the isolated isovolumic blood-perfused canine heart, left ventricular pressure was measured following a sudden expansion of ventricular volume. An increase in performance occurred in two phases: first, there was an instantaneous rise of developed pressure simultaneous with ventricular distension; in the second phase, developed pressure continued to increase for several minutes until a final steady state was reached. The immediate increase in developed pressure occurred with a prolongation of the time-to-peak pressure, and there was no further change of time-to-peak pressure during the time-dependent increase of developed pressure. In another series of experiments, systolic pressure was elevated without changing resting volume, and mechanical performance changed in a different manner: after an increase in systolic load, there was a modest and transient decrease of developed pressure; thereafter, ventricular pressure recovered only to original values. The influence of different degrees of ventricular expansion, calcium, and verapamil were studied. Under higher ventricular dilations the immediate as well as the slow increase of contraction were heightened and the time to reach half of the slow increase was shortened. When ventricular dilation was induced during an infusion of calcium chloride, higher values for the immediate pressure increase were observed, whereas the timedependent increase and the time to reach half of the slow increase did not change in comparison with control studies. Verapamil decreased the immediate and the time-dependent enhancement of contraction. The time-dependent increase in developed pressure occurs more slowly with verapamil. These findings in the intact heart are in accord with the hypothesis that myocardial stretch is followed by an increase in intracellular calcium stores, and with the concept that the Frank-Starling mechanism involves an activation of the contractile state. (Circ Res 55: 59-66, 1984)

No abstract

Remodeling process after acute myocardial infarction (AMI) is clinically characterized by ventricular cavity increase. In the acute phase, ventricular dilation is a result of infarction expansion process, whereas late cavity dilation is the result of the eccentric hypertrophy process.Ventricular remodeling plays a key role in the pathology of post-infarction ventricular dysfunction. When reacting to aggression, the genetic, structural, and biochemical changes arising from that process will result in the deterioration of the functional ability of the heart in the long run. Signs and symptoms of the onset of heart failure and/or sudden death will result. The mechanisms that have been proposed for the onset of ventricular dysfunction are complex, but the ones to be pointed out are changes in: calcium transit; betaadrenergic pathway; contractile proteins; increased cell death; collagen accumulation; methaloproteases; higher oxidative stress; energy deficit; cytoskeletal, membrane and matrix proteins; and ventricular geometry. Additionally, remodeling is associated to higher prevalence of cardiac rupture, arrhythmia, and aneurysm formation after infarction.Remodeling is therefore associated to impaired postinfarction prognosis. As a result, a better understanding of such process is critical since remodeling course can be modified through a number of therapeutic interventions.