Plaque rupture with subsequent thrombus formation is the central mechanism behind acute coronary syndromes. Clinical manifestations depend mainly on the extent of thrombosis and degree of coronary flow obstruction. In unstable angina, only minor plaque ulceration and transient thrombus formation occur, while more extensive thrombosis happens in non-ST-elevation MI and sudden death. Despite initial promising results, a large randomized trial showed that thrombolytic therapy is not beneficial, and may even be harmful in unstable angina and non-ST-elevation MI. Possible explanations include the predominance of platelet-rich rather than fibrin-rich thrombi, and paradoxical activation of platelet by thrombolytics. Initial trials comparing early invasive and conservative strategies in the management of acute coronary syndromes yielded conflicting
results. In the modern era of stenting and glycoprotein IIb/IIIa receptor blockers, an early invasive strategy seems to be more effective, especially in high-risk patients. Low risk patients may benefit more from a conservative strategy.
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