Intravascular ultrasound shows that many coronary artery atherosclerotic plaques do not encroach on the lumen and therefore are angiographically invisible.1 ,2 The reason for this phenomenon was first firmly established in human coronary arteries by Glagov and colleagues.3 As a plaque develops the overall cross sectional area of the coronary artery increases to accommodate the plaque without any reduction in the cross sectional area of the lumen. The process was termed compensatory enlargement. The increase in total cross sectional area of the artery is achieved by two mechanisms. One has been recognised by pathologists for many years4and involves the media behind the plaque undergoing atrophy with fracture of the internal elastic lamina. The plaque is extruded outward through the disrupted media leaving the lumen normal in shape and size but giving the artery an external asymmetric bulge. The second mechanism is more common and involves a rearrangement of smooth muscle cells in the media for which the term remodelling can be used. The arterial wall is now recognised as a dynamic structure capable of altering in size. Glagov and colleagues’ work carried out on postmortem samples has been amply confirmed by epicardial echocardiography and intravascular ultrasound.5 ,6

Postmortem specimens of human coronary arteries that have been perfused at systemic pressure during fixation provide excellent illustrations of the process of compensatory enlargement (remodelling). In such preparations the lumen is round and the internal elastic lamina is expanded to its full capacity indicating an arterial state equivalent to maximal vasodilatation. Multiple cross sections of the artery can be made at 2 mm intervals and the area of the lumen and the vessel within the external elastic lamina measured. When these measurements are plotted against distance from the origin of the artery the two lines run parallel …