Page 16 - Coronary hemodynamics in acute myocardial infarction - Matthijs Bax

Chapter 1
microvascular changes in the infarcted area might influence reflow. Red blood cell packing in the capillary lumens indicate downstream obstruction to flow. These localized areas of increased hematocrit can increase blood viscosity and stimulate hemostasis and flow obstruction.
Furthermore, hemorrhages are not-uncommon in infarcted areas, and are determined as a potential consequence of microvascular injury.32 In cardiovascular magnetic resonance (CMR) studies, infarcts of substantial size show core necrosis and erythrocyte extravasation without intact vasculature and hence, no microvascular obstruction.33
In some studies platelet and fibrin thrombi were infrequently seen by electron microscopy in areas of no reflow, making it questionable that capillary thrombosis is the primary cause of no reflow. Peripheral embolization of thrombus caused by mechanical actions of PCI equipment might play a role in suboptimal reperfusion. In patients treated with primary PCI (PPCI) in whom angiographically blood flow in the infarct related artery appears to be normal, 30-40% of them have evidence of microvascular obstruction as detected by contrast echocardiography34, 35 or CMR36
Severe downstream localized microvascular obstruction after PPCI is related to the duration of myocardial ischemia, 37 the extent of transmural necrosis and age.38, 39 It is striking that the maximum extent of the microvascular obstruction does not occur immediately during ischemia but after reperfusion. In a rat model, Hollander et al. showed that ischemia for 90 minutes effected limited morphological changes to the coronary microcirculation, but that 30 minutes of ischemia followed by 60 minutes of reperfusion caused massive microvascular injury.40 This illustrates the potentially adverse effect of reperfusion on the integrity of the microvasculature.
Interventions in reperfusion injury
Despite many attempts to improve the reperfusion injury, such as targeting coagulation with IIb/IIIa receptor blockers or targeting metabolic modulation via glucose-insulin-potassium (GIK) infusion, no adequate additional treatments have been successfully implemented to date in clinical practice.41, 42 In some countries intracoronary infused Nicorandil, a potassium channel opener, is
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