Unstable angina

The challenge of understanding the patho-physiology of unstable angina is the wide spectrum of clinical severity.12 Necropsy studies are inevitably biased toward the worst outcome, but within this limitation show unstable angina to be caused by disrupted plaques with exposed mural thrombus and retention of antegrade flow in the artery. This feature of some persistent antegrade flow is all that separates the vascular lesion of unstable angina from that of acute infarction. The persistence of the thrombotic process so that it neither progresses to occlude nor resolves to heal represents a balance between prothrombotic and antithrombotic factors. Confirmation of plaque disruption and thrombosis as the basis for severe unstable angina has come from angio-graphy in vivo where type II lesions with irregular overhanging edges and intraluminal filling defects (fig 1.6) representing thrombus are found.13 These angiographic appearances are rare in stable angina. Type II lesions have been shown to be disrupted plaques by pathology studies. Angioscopy has directly observed torn plaque caps in vivo and intravascular ultrasound has also identified disrupted plaques in vivo. Atherectomy studies comparing tissue from plaques thought to be responsible for stable and unstable angina have shown very consistent results. A significant proportion, but not all, of samples from unstable

Figure 1.6. Angiogram of plaque disruption. In this postmortem angiogram there is a typical type II eccentric ragged stenosis with an overlying intraluminal filling defect indicating thrombus over the plaque.

angina contain thrombus, while most samples from stable angina, but not all, do not contain thrombus. The absence of thrombus in unstable angina is in part related to the time delay between acute symptoms and atherectomy.14

Samples taken some weeks after the last episode of rest pain often show accelerated smooth muscle proliferation—that is, the healing process rather than the acute thrombotic process. The presence of thrombus in plaque causing stable angina highlights the role of subclinical disruption or erosion in plaque growth. The pathological changes in plaques causing unstable angina expose thrombus in an artery in which antegrade flow continues. Platelet emboli into the myocardium cause microscopic foci ofnecrosis which are the basis of the increased concentrations of troponin T found in the blood in a proportion of cases of unstable angina.

The problem of the pathophysiology of unstable angina lies in patients who have milder and persistent rest pain over months or even years. The perception is that these cases are related to vasomotor tonal abnormalities often occurring at specific sites in the coronary artery tree. Why one such plaque should lead to local spasm is unclear—one suggestion is that there is local endothelial damage and repetitive ultramicroscopic thrombosis. The preponderance of literature reports of such vasospastic angina from Japan suggests there may be racial or geographic differences in the pathogenesis of this form of unstable angina.

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