MECHANISMS OF ANGIOPLASTY AND ATHERECTOMY OF CORONARY STENOSES

作为开发新的、更有效的血管成形术的努力的一部分， 我们一直在寻求更好地了解局灶性冠状动脉病变的性质， 狭窄及其对干预的急性和慢性反应。 通过 血管内超声（IVUS）临床应用的发展， 我们已经表明，在局灶性慢性的成分和刚度， 狭窄与相邻的血管造影正常的狭窄有显著不同 血管节段，而动脉粥样硬化的总质量是显着的 相似 目前血管成形术治疗的主要病变是 由于纤维化和钙化而僵硬，这阻止了代偿性 在顺应性更强（尽管病变严重）的节段中观察到扩张。 因此，成功的干预措施会破坏/改变僵硬 约束因素，使它们充分和不可逆转地 符合要求，并允许船舶扩张。 成功的治疗需要 刚性瓣环的节段性（有限）破裂和大的， 柔顺弧 由气泡快速膨胀产生的声学瞬变是 激光血管成形术中断的主要原因。 定向 斑块切除术产生深的病灶切除， （约60度）高度柔顺。 旋转器移除管腔 钙化，从而降低壁硬度。 在扩大 “刚性”金属支架在高压下，压缩力 由周围组织产生，引起严重的急性和 慢性反冲 这种急性和慢性压迫性狭窄的治疗 病变可能是再狭窄的主要原因。 一过性，中度 （约60摄氏度）与热相关的热海拔 血管成形术引起了深刻的，剂量依赖性的，增殖反应， 类似于严重机械损伤。

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.