Abstract

Next to plaque formation, arterial geometric remodelling is an important determinant of luminal narrowing in atherosclerotic disease. Expansive remodelling retards, whereas constrictive remodelling accelerates lumen loss by plaque formation. Expansive arterial remodelling is a double edged sword, however. While luminal area is preserved, the plaque beneath the surface of the lumen often reveals large atheroma with heavy inflammation in expansive remodelling. These characteristics have been associated with plaque rupture and subsequent myocardial infarction. Thus, in the long term expansive remodelling may lead to thrombosis of angiographically silent lesions while constrictive remodelling is often associated with stable coronary syndromes. The mechanisms of arterial remodelling are poorly understood. This is mainly due to lack of good in vitro and animal models which makes mechanistic studies difficult.

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