Pathophysiology
Insights from intravascular ultrasound on pathophysiology of acute coronary syndromes

Of the various thrombosis-prone morphologies, thin-capped fibroatheromas account for the majority of events. The rest are comprised of erosions and calcific nodules. Almost all IVUS analyses have either compared stable vs. unstable patients (or ruptured vs. nonruptured plaques) or have reported histopathologic- equivalent findings. While these approaches have limitations, there are important lessons. Greyscale IVUS features of thin-capped fibroatheromas include positive remodeling, hypoechoic plaque, spotty calcification, and attenuated plaque. Plaque rupture, the clinical expression of a vulnerable plaque, is detected in approximately 50-60% of culprit lesions in patients with acute coronary syndrome and in a variable percentage of secondary, non-culprit lesions. A ruptured plaque becomes symptomatic because of thrombus formation and lumen narrowing. Ruptured plaques occur in predictable sites in the coronary tree; however, greyscale IVUS does not have the ability to predict which vulnerable plaques are likely to rupture.