Pathophysiologic Spectrum

Across the spectrum of myocardial ischemia, markers of inflammation, thrombosis, and platelet activation increase in frequency in parallel with the clinical severity of the ACS (Fig. 3). Markers of inflammation, such as C-reative protein (CRP), are found in 13% of patients with stable coronary artery disease vs 65% of patients with UA and 76% of patients with acute MI (43). Similarly, antibodies to C. pneumoniae are found in a higher percentage of patients with ACS than non-ACS patients (84). Activated platelets and markers of ongoing thrombosis, such as fibrinopeptide A, are also found more often in patients with ACS (36,38,70,85-88).

Coronary angiographic and angioscopic findings follow the same pattern across the spectrum of myocardial ischemia (Fig. 4). Angiographic studies have documented

Spectrum Myocardial Ischemia

Fig. 3. The pathophysiology of acute ischemic syndromes. Atherosclerotic plaque rupture leads to coronary artery thrombosis, as indicated by angiographic evidence of thrombus or biochemical markers of increased fibrinopeptide A (FPA), thrombin-antithrombin complexes (TAT), or activated platelets. In acute Q wave MI, which usually presents with STE on the electrocardiogram, complete coronary occlusion is present. In those with unstable angina or non-Q wave MI, a flow-limiting thrombus is usually present, but complete occlusion of the artery is uncommon. In patients with stable angina, thrombus is rarely seen. Mortality increases with the severity of the acute ischemic syndrome. Data from Becker et al. (38,70), Merlini et al. (37), Trip et al. (87), Liuzzo et al. (43), Kruskal et al. (136), and Mazzoli et al. (84).

Fig. 3. The pathophysiology of acute ischemic syndromes. Atherosclerotic plaque rupture leads to coronary artery thrombosis, as indicated by angiographic evidence of thrombus or biochemical markers of increased fibrinopeptide A (FPA), thrombin-antithrombin complexes (TAT), or activated platelets. In acute Q wave MI, which usually presents with STE on the electrocardiogram, complete coronary occlusion is present. In those with unstable angina or non-Q wave MI, a flow-limiting thrombus is usually present, but complete occlusion of the artery is uncommon. In patients with stable angina, thrombus is rarely seen. Mortality increases with the severity of the acute ischemic syndrome. Data from Becker et al. (38,70), Merlini et al. (37), Trip et al. (87), Liuzzo et al. (43), Kruskal et al. (136), and Mazzoli et al. (84).

Stable Unstable Non-Q Q wave Angina Angina Wave Ml M!

Non-ST Elevation ST Elevation ACS Ml

Angiographic Thrombus

Morphology

Acute Coronary Occlusion

Angioscopy

Fig. 4. Angiographic findings across the spectrum of ACS. Data from the TIMI Investigators (12,14), Van Belle et al. (89), DeWood et al. (11,13), Sacks et al. (137), Mizuno et al. (60), and Sherman et al. (57).

"white" thrombi, predominantly platelet-rich thrombi, in patients with UA and non-STEMI, as compared with "red" thrombi in patients with acute STEMI (57,89,90). This distinction was also noted in the landmark study by DeWood, in which coronary thrombi were aspirated with Fogarty catheters from patients with acute STEMI (11). Coronary angiography in patients with STEMI usually documents total occlusion of the infarct-related artery (11,12). In patients with ACS without STE, active lesions are frequently observed, with irregular borders, associated intraluminal lucencies (which may represent thrombus), and ulcerated or eccentrically localized obstructions (14,62,63). Such lesions are more likely to be associated with the pathologic features of plaque rupture, hemorrhage, and superimposed thrombus (5,39). In addition, activated macrophages can frequently be identifed in the hinge-point of the plaques, which may contribute to plaque rupture (40). In patients with stable angina, nonactive lesions (which have symmetric, concentric, and with smooth borders) are usually observed (14,62,63). The typical deformities are smooth with an hourglass configuration and absence of intraluminal lucencies on coronary angiography. The presence of angiographic thrombus thus shows a gradient across the spectrum of ACS.

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