Chest Pain with Normal Coronary Arteries by Juan Carlos Kaski Guy D. Eslick & C. Noel Bairey Merz

Author:Juan Carlos Kaski, Guy D. Eslick & C. Noel Bairey Merz
Language: eng
Format: epub
Publisher: Springer London, London

However, in the setting of acute myocardial infarction, manual thrombus aspiration by nontraumatic aspirations catheters have provided significant improvements in myocardial perfusion which was translated into a reduction in mortality in these patients [25, 26]. This highlights the ­possibility that distal embolization may actually precede the intervention and is also consistent with the possibility that the process of coronary thrombosis is dynamic with thrombosis and also spontaneous lysis. The totality of evidence from multiple sources strongly supports the clinical significance of distal coronary embolization.

In acute myocardial infarction, myocardial and endothelial injury can also be induced by direct ischemic damage (Fig. 17.2). Ischemia- related injury is characterized by endothelial protrusions and membrane-bound bodies leading to luminal obliteration. Furthermore these findings are accompanied by reduction of regional blood flow and myocardial cell swelling is associated with interstitial edema [27–29]. In addition to the damage induced by the limitation of blood flow, indirect biochemical mechanisms may result in incremental damage. Debris material analyzed from embolization protection devices revealed a high concentration of biologically active inflammatory mediators at the site of infarction, which might be released into the coronary microcirculation [30]. In addition, microparticles further impair microvascular endothelial function as a consequence of pro-inflammatory and procoagulant activity [31]. Furthermore vasoactive factors, most notably ­vasoconstrictive endothelin-1 and tissue factor are likely to be involved, as they are expressed in active plaques and in the plasma of these patients [32, 33]. Moreover, slow-flow during PCI is associated with higher fibrofatty plaque volume over the entire lesion length, suggesting that in myocardial infarction, slow flow may be dependent on the tissue characterization of the culprit lesion [34].

In order to restore blood flow, reperfusion technologies are applied as fast as possible. It is well recognized that the successful achievement of flow in the epicardial infarct-related artery might not necessarily be accompanied by myocardial perfusion or infarct size [27]. In the experimental setting the term reperfusion injury was introduced as a description of the aggravation of ischemia-related myocardial injury by the restoration of CBF. Reperfusion injury refers to myocardial stunning, infarction extension, reperfusion arrhythmias and vascular stunning and endothelial function, respectively [35]. The literature about reperfusion injury is abundant but the vast bulk of the data emanate experimental animal studies [36] and a majority of human studies modifying reperfusion injury were not able to show cardioprotective benefit [37]. It is not clear to what extent reperfusion injury is relevant in the clinical setting and whether the process is one of accelerating necrosis in cells already destined to die as opposed to increasing the extent of infarction [38], a long-standing debate which continues.

In the experimental model of ischemia/perfusion, the series of pathophysiologic processes that characterize reperfusion injury have been quite well characterized. As a consequence of the restoration of blood flow to ischemic tissue, oxygen and other reactive molecules interact with hypoxic, abnormal cellular environments, which might produce further damage [29]. At the time of reperfusion of the microcirculation, activation of neutrophils and platelets, representing mainly plaque debris, takes place, thus leading to cell adhesion and migration.

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