Chronic Changes in the Canine Myocardium After Coronary Microembolization

Abstract

Recently, there has been interest in acute microcirculatory abnormalities of the coronary arteries, particularly microembolism, as a primary cause of or secondary outcome of the no-reflow phenomenon following recanalization of occluded coronary arteries [1, 2]. It is reported that interruption of the coronary blood flow for more than 30 min produces an incomplete return of blood flow after reperfusion [1], and the area of no-reflow increases with the duration of ischemia [3]. Recanalization of occluded arteries is often observed in the clinical setting either spontaneously or after coronary thrombolytic therapy (PTCR) in patients with acute myocardial infarction. The heart reperfused after a certain time-lag may have regional impairment of coronary perfusion, presumably’ at the level of the capillaries or feeding arterioles. Several mechanisms for the noreflow phenomenon have been suggested. Capillary compression by parenchymal cell swelling [2] or interstitial edema [4], obstruction by endothelial cell swelling [5], thrombosis [6], erythrocyte impaction [7], leukocyte plugging [8], and platelet aggregates [9] have been reported as a cause of the perfusion impedance after reperfusion. Although it has been claimed in several studies that plugging of the blood cells in the microvasculature may not be a primary cause of noreflow [10, 11], entrapment of blood cells secondary to the microcirculatory disturbance could further impede the flow and delay the recovery of ischemia. Prolonged myocardial stunning often observed following reperfusion might be attributed in part to this microcirculatory abnormality. We have previously demonstrated a characteristic hyperemic flow response of coronary blood flow after coronary embolization of microspheres, which mimic blood cell plugging [12]. In this chapter, we shall discuss the chronic changes in coronary blood flow and functional and histological changes in the embolized myocardium.

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