Acute Coronary Syndrome: Insight From Angioscopy

Abstract

Although the concept of vulnerable plaque has become common, it is still impossible to predict effectively the onset of acute coronary syndrome (ACS). Thin-cap fibroatheroma (TCFA) is regarded as vulnerable from pathological studies and various diagnostic tools have tried to detect TCFA clinically but failed to predict ACS. Because there are so many silent plaque ruptures detected, it is supposed that many vulnerable plaques might have ruptured but not caused ACS. Some factor(s) other than the rupture of vulnerable plaque is required for the onset of ACS. "Vulnerable blood" may be one of them. The thrombogenic potential of blood (ie, vulnerable blood) may play an important and determinant role in the onset of ACS, the process of which will be discussed from the angioscopic point of view. (Circ J 2010; 74: 411 - 417)

The Myth of the “Vulnerable Plaque”

“…While the occurrence of acute coronary events typically requires alterations of coronary atherosclerotic plaques (rupture or erosion), a thrombosis-promoting milieu is necessary to allow a clinically significant decrease in coronary blood flow and associated myocardial ischemia (7,9). Such a setting appears to result from an unfortunate constellation of prothrombotic features, for example, in patients with increased inflammatory activity and systemic or local suppression of fibrinolytic performance, an extraordinarily large stimulus for thrombosis, vasoconstriction, and/or others (7).…”

“…In addition to the presence, extent, and metabolic activity of atherosclerotic disease, individual adaptations and responses to thrombogenic stimulation from altered vascular function are critical for determining the risk of acute coronary events (7, 9). Despite a consensus on the complexity of acute coronary event risk evaluation and the necessity for comprehensive patient assessment (10,11), recent efforts to identify high-risk patients focus on using advanced imaging methods to detect single “vulnerable” atherosclerotic plaques (12).…”

Optical imaging techniques for vulnerable plaque detection

“…This technique can also be used as an adjunctive procedure during the process of bypassing the vascular systems to visualise the valves within the veins system. This technique is widely employed in the detection of unknown conditions in the vascular system through less invasive preparation of the in situ blood vessels grafts [11]. For instance, Ishibashi et al [12] used the angioscopy process to evaluate and study 30 saphenous veins prior to utilising them as bypass conduits.…”

“…The coronary plaques that are characterised by their thin lid with deposition of calcium are the ones that are commonly studied in post-mortem analysis. Furthermore, Ueda et al [11] note that plaques in areas where there is deposition of fats and macrophages are tied together by a small superficial layer and a lipid centre. The oxidised low-density lipoprotein (OX-LDL) has a very critical role in the initiation, progression, and weakening of the atherosclerotic plaque by inducing proliferation as well as elongation of the endurance of the macrophages [12].…”

The role of sphingosine 1 phosphate in coronary artery disease and ischemia reperfusion injury

“…A broad range of microanatomic mechanisms are suggested to be involved in the acute coronary thrombosis. Autopsy studies show that lethal coronary thrombosis most commonly results from a through rupture of the plaque's protective fibrous cap (Ueda et al, ). Intraplaque hemorrhage, superficial erosion, and the erosion of a calcified nodule are among other minor mechanisms responsible for coronary thrombosis (Virmani, Burke, Farb, & Kolodgie, ).…”