Myocardial protection by collateral vessels during experimental coronary ligation: a prospective study in a canine two-infarction model.

Previous work of this laboratory has shown that collateral flow can be increased over six weeks by a subcritical external constriction of the circumflex artery causing a 50 +/- 10% reduction of postocclusive reactive hyperemia. To investigate collateral function in acute myocardial infarction, the model was used to ligate two distant coronary branches on the ventricle simultaneously in order to compare in 8 dogs infarct size and perfusion area of the ligated vessels in control and collateralized sections. The acute collateral flow measured 7.2 +/- 2.5 ml/100 g/min-1 and increased to 17.3 +/- 6.7 (p less than 0.001) over 6 weeks. Separate analysis revealed a predominant increase of collateral flow in the epicardial layers 23.1 +/- 7.5 (p less than 0.01) versus 6.9 +/- 2.8 (p less than 0.01) in the subendocardium. Infarct size in the control area was 52.0 +/- 14.7% of the perfusion area, in the collateralized zone 19.0 +/- 14.2% (p less than 0.001). Infarct size expressed as per cent of perfusion area and collateral flow in the area at risk expressed as per cent of flow of normal sections correlated: (r = 0.76; p less than 0.05). Therefore, infarct size after a 6 hour coronary occlusion can be considered a function of the collateral flow over normal perfusion ratio. Localized induction of collaterals in this model caused a significant reduction of infarct size in relation to the perfusion area at risk.