Abstract

Reperfusion performed too late to salvage myocardium decreases chronic infarct expansion in experimental animals. However, the acute effects of delayed reperfusion are not known. Twenty-two dogs underwent 3 (n = 8), 4 (n = 8) or 6 h (n = 6) of circumflex artery occlusion followed by 3 h of reperfusion. Effects of reperfusion on diastolic expansion were assessed in two ways: 1) change in mean radius of curvature of the infarct segment, and 2) change in the ratio of the length of the diameter from the center of the infarct zone to the opposite wall (septal-lateral diameter) to the length of the diameter perpendicular to this (anteroposterior diameter). Effects on systolic expansion were examined with quantitative two-dimensional echocardiographic systolic thickening analysis.Delayed reperfusion produced an immediate decrease in diastolic infarct expansion. The ratio of septal-lateral/anteroposterior diameters, which had increased with occlusion from a preocclusion baseline of 0.98 ± 0.06 to 1.13 ± 0.08 (p < 0.001), decreased with reperfusion to 1.02 ± 0.07 at 15 min and 1.03 ± 0.08 at 3 h of reperfusion (p = 0.001). This was due solely to a decrease in the septal-lateral diameter. The radius of curvature of the infarcted segment increased from 2.1 ± 0.5 cm before reperfusion to 2.74 ± 0.8 cm at 15 min and 2.6 ± 0.85 cm at 3 h of reperfusion (p = 0.009). This occurred despite a significant (13.6%) decline in end-diastolic cavity area and is compatible with flattening of the reperfused infarct region.Systolic infarct expansion also improved slightly. The length of the abnormally contracting segment decreased by 13 ± 20% (p = 0.02), and systolic thinning was abolished (−5 ± 5%, 1 ± 5% and 1 ± 3% respectively, at the three time points, p = 0.05). Globally, cavity area shrinkage increased from 27 ± 7.5% before reperfusion to 33 ± 7% at 15 min (p = 0.02) and 30 ± 6% (p = NS) at 3 h.In conclusion, late coronary reperfusion leads to an acute reduction in diastolic infarct expansion. Although this reduces end-diastolic cavity area (and thus preload), global systolic function is preserved because systolic infarct expansion is reduced, and the decline in preload is regional, involving primarily the noncontractile infarcted segment. Late reperfusion has potentially important applications to the acute as well as to the chronic stages of myocardial infarction.

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