Page 14 - Coronary hemodynamics in acute myocardial infarction - Matthijs Bax

Chapter 1
plays an extremely important role in the control process of the vasomotor tone and in influencing the thrombotic risk by, among other things, releasing nitric oxide, endothelin-1, prostacyclin etc. Endothelial dysfunction is part of the increased risk of the reoccurrence of a cardiovascular event.14, 15
The plaque rupture leads to a thrombotic response which is dynamic in nature. Both local thrombosis and thrombolysis and vasospasm can cause intermittent flow obstruction and distal embolization.16 The microvascular obstruction, including distal embolization, can in turn lead to insufficient reperfusion during the treatment of the infarction, resulting in poorer outcomes. It is demonstrated that although the epicardial occlusion is successful treated, the microvascular injury precludes adequate tissue perfusion. This suggests that there is room for improving of our current standard treatment.
Infarct size
The final infarct size is a function of the area-at-risk as result of the location of the epicardial coronary occlusion, ischemic time (time between vessel occlusion and reperfusion) and collateral flow from non-infarct related arteries. The final extend of the infarct might be increased as result of additional damage know as reperfusion injury. The concept of reperfusion injury is believed to be related to tissue damage from oxygen radicals generated at the time of reperfusion.
Cardiac dysfunction due to myocardial reperfusion injury
Timely PCI treatment in ST-elevation myocardial infarction (STEMI) is critical for myocardial reperfusion in order to limit infarct size and to preserve left ventricular function. However, the reperfusion of acutely ischemic myocardium may itself induce cardiomyocyte death. This, so called myocardial reperfusion injury was postulated by Jennings et al. in the sixties of the previous century. 17 It was postulated that reperfusion acutely induced explosive myocardial cell swelling,18 and capillary disruption inducing hemorrhagic necrosis.19
Although the underlying mechanisms leading to reperfusion injury have still not been fully elucidated, potential myocardial reperfusion damage is generally classified into four forms.
Stunned myocardium indicating postischemic (regional) ventricular dysfunction of vital myocytes.20, 21 This phenomenon is probably reversible
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