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， 我们一直在寻求对局灶性冠状动脉病变本质的更好理解 狭窄及其对干预的急性和慢性反应。穿过 血管内超声(IVUS)临床应用进展， 我们已经证明了慢性局灶的成分和僵硬 狭窄与邻近的血管造影正常有显著不同。 血管节段，而动脉粥样硬化的总质量显著 很相似。目前血管成形术治疗的主要病变有 由于纤维化和钙化而僵硬，这阻止了代偿性 在较顺应性(尽管病变较重)节段观察到扩张。 因此，成功的干预会扰乱/改变僵化。 约束元素，以使其充分且不可逆转 符合并允许血管扩张。成功的治疗需要 硬环的节段性(局限性)破裂并形成大的、 柔顺圆弧。气泡快速膨胀产生的声学瞬变 这是激光血管成形术中断的主要原因。方向性 动脉粥样硬化切除可形成小弧形的深部局灶性切除 (约60度)高度合规。轮虫去除管腔 钙化，从而降低墙体硬度。在扩展之后 坚硬的金属支架在高压下，压力是 由周围组织产生，引起严重的急性和 慢性后坐力。治疗后的急性和慢性压迫性狭窄 病变可能是再狭窄的主要原因。短暂的，中等的 (约60摄氏度)与热相关的热海拔 血管成形术引起深刻的、剂量依赖的增殖性反应 与严重机械损伤的情况相似。

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.