Coronary artery remodelling in atherosclerosis: unfortunately unpredictable

Coronary heart disease is the main cause of mortality and morbidity worldwide, and occurs because of the growth and complications of coronary atherosclerosis. Therefore, efforts in the understanding of how atherosclerotic plaques grow and undergo complications, and in identifying predictors of such dramatic events are welcome and worthwhile. Atherosclerosis has long been considered a relentless process by which the accumulation of lipids and extracellular matrix leads to progressive lumen encroachment. Two notions in the past 20 years have dramatically altered this conception. One is that most cases of myocardial infarction likely derive from acute plaque complications (plaque fissuring in most instances), and not from progressive lumen stenosis1. The other is that the growth of atherosclerotic plaques is not necessarily towards the lumen, but may also occur towards the outer vessel layers, leading to an actual overall enlargement of the vessel, contrary to the previous tenet that atherosclerosis is similar to the encrustation of metal pipes in a building. This second aspect, although less appreciated in current literature than the burgeoning plethora of investigations on mechanisms of plaque rupture, is also fertile of important clinical consequences.In a series of human histopathological observations, Glagov et al .2 were the first to identify a significant direct correlation between the plaque area—calculated as the area defined externally by the internal elastic lamina (internal elastic membrane, IEM) and internally by the vessel lumen (intimal area) and the potential lumen area—i.e. the area circumscribed by the internal elastic lamina, taken as a measure of the area of the arterial lumen if no plaque had been present and the intima remained a virtual space. This finding indicated that, in general, the larger the plaque, the larger the vessel, and allowed the inference that plaques also grow towards the outside (‘positive remodelling’). These results have … *Corresponding author. Tel: +39 (0) 871 41512; fax: +39 (0) 871 402817. E-mail address : rdecater{at}unich.it