LAUSR

Atherosclerosis was thought to be a disease of insidious onset and slow process, secondary to smooth muscle cell proliferation.1 However, this concept was challenged during the past 2 decades by the theory that an alternative mode of rapid step-wise plaque progression might also exist. This sudden change in arterial lumen occurs when mural thrombus is organized after disruption of a plaque or by sudden expansion of a plaque secondary to intraplaque hemorrhage. Because of the sudden change in local geometry, this second mode is significant not only to rapid plaque progression, but also to the development of acute coronary syndromes.2–5 Unlike slow linear progression, which may lead to progressive angina on exertion because of supply–demand imbalance when the luminal narrowing reaches a critical threshold, the second mode, characterized by rapid step-wise progression, does not allow sufficient time for preconditioning or for the development of collaterals, resulting in acute coronary syndrome, including ST-segment–elevation myocardial infarction and sudden cardiac death. Previous angiographic studies showed that the culprit lesion for an acute myocardial infarction often had mild luminal narrowing before the event. However, recent studies …