ABSTRACT
Percutaneous transluminal coronary balloon angio plasty (PTCA) has proven to be an effective treat ment for obstructive coronary artery disease. The mechanism behind luminal enlargement by PTCA was first thought to be compression of the plaque.1 However, in vitro histology examinations after balloon dilatation and, more recently, in vivo intravascular ultrasound imaging have shown that plastic deformation of the obstructive plaque during PTCA with the creation of intimal and medial dissections is the major reason for luminal enlarge ment.2-9 Thereby, no significant change in plaque volume could be detected after PTCA. Postangioplasty intimal and medial dissections were associated with the potential risk of acute vessel closure because of flow limitations and the potential exposure of thrombogenic parts of the disrupted vessel wall.9
