An Etiologic Approach to Management
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Nonocclusive Thrombus on Preexisting Plaques
Unstable angina results from an imbalance between myocardial oxygen supply and demand. Probably the most common cause is reduced myocardial perfusion resulting from a nonocclusive thrombus on a fissured or eroded atherosclerotic plaque that often had caused only mild to moderate obstruction previously.3 Nonocclusive thrombi in patients with unstable angina have been demonstrated by coronary angioscopy and arteriography.4 They occur most commonly on complex, irregular lesions.5 Plaques that have undergone disruption often have a core that is rich in cholesteryl esters and tissue factor. They have a thin fibrous cap; disruption is caused by shear forces acting on the shoulder of the plaque. In patients with unstable angina, products of aggregating platelets are released into the coronary circulation,6 and there appears to be continued thrombus formation, often for months, after the index event.7 Nonocclusive coronary thrombi often become organized and incorporated into the growing plaque.
Treatment with antithrombotic agents (unfractionated heparin8 and low-molecular-weight heparin9 ) and antiplatelet agents (aspirin,8 ticlopidine,10 and glycoprotein IIb/IIIa inhibitors2 ) is beneficial in this form of angina. Perhaps tissue factor inhibitors will prove useful as well.
A second form of unstable angina is caused by dynamic obstruction, ie, coronary vasoconstriction. Four subgroups are recognized. (1) The first is Prinzmetal’s variant angina, with intense focal spasm of a segment of an epicardial coronary artery not involved by coronary atherosclerosis. (2) In the second, also called Prinzmetal’s angina, the spasm occurs adjacent to a nonobstructive atheromatous plaque. Both of these forms of vasospastic angina appear to be due to hypercontractility of vascular smooth muscle and endothelial dysfunction occurring in the region of spasm. They are characterized by ST-segment elevation accompanying rest pain and …