As part of an effort to develop new, more effective forms of angioplasty, we have sought improved understanding of the nature of focal coronary stenoses and their acute and chronic responses to intervention. Through the development of the clinical use of intravascular ultrasound (IVUS), we have shown that the composition and stiffness at focal chronic stenoses is remarkably different from adjacent, angiographically normal vessel segments, whereas the total mass of atheroma is remarkably similar. The principal lesions currently treated by angioplasty are rigid due to fibrosis and calcification, which prevents compensatory dilatation observed in more compliant (though heavily diseased) segments. Accordingly, successful interventions disrupt/alter the stiff constraining elements so as to make them sufficiently and irreversibly compliant and permit vessel expansion. Successful therapy requires segmental (limited) rupture of the stiff annulus and creation of a large, compliant arc. Acoustic transients created by rapid bubble expansion are the principal cause of this disruption in laser angioplasty. Directional atherectomy creates deep focal excisions which can make a small arc (approximately 60 degrees) highly compliant. Rotablators remove luminal calcification, thereby reducing wall stiffness. Following expansion of """"""""rigid"""""""" metallic stents at high pressures, compressive forces are generated by the surrounding tissues which cause significant acute and chronic recoil. Such acute and chronic compressive narrowing of treated lesions may be the major cause of restenosis. Transient, moderate (approximately 60 degrees C) thermal elevations associated with thermal angioplasty elicit a profound, dose-dependent, proliferative response similar to that seen with severe mechanical injury.
