Comparison of the histopathology of culprit lesions in chronic stable angina, unstable angina, and myocardial infarction.

BACKGROUND

The etiology of unstable angina (UA) and myocardial infarction (MI) both involve rupture of an atherosclerotic plaque in a coronary artery. It has been suggested that the two syndromes differ because MI results if a red occlusive permanent thrombus occurs and UA occurs only if a nonocclusive platelet (white) thrombus occurs.

HYPOTHESIS

The purpose of this study was to determine the differences between coronary lesion pathology in MI and UA and compare them with lesions of chronic stable angina (CSA).

METHODS

We reviewed the pathologic specimens of culprit lesions obtained by directional coronary atherectomy in 27 patients with MI, 29 patients with UA, and 16 patients with CSA.

RESULTS

The incidence of ruptured plaque was high and identical in patients with MI (77.8%), and UA (75.8%), and significantly lower in patients with CSA (25.0%) (p < 0.001). Similarly, the incidence of red thrombus was the same in MI (92.6%) and UA (82.7%), and significantly less in CSA (p < 0.001).

CONCLUSIONS

The underlying pathophysiology of both UA and MI appears to be the same, with red thrombus playing an important role in both syndromes. The only difference is in the degree of occlusiveness of the red thrombus on the ruptured plaque and whether the occlusion is transient (UA) or persistent (MI). The balance between thrombosis and endogenous clot lysis determines which syndrome occurs. Lytic therapy is not effective in UA, probably because the clot is not occlusive or because endogenous lysis has already achieved the degree of coronary opening that eventuates from tissue plasminogen activator or streptokinase administration. Prompt catheterization and revascularization may be as indicated in patients with MI if there remains viable myocardium as in patients with UA.