MECHANISMS OF ANGIOPLASTY AND ATHERECTOMY OF CORONARY STENOSES

为了开发新的、更有效的血管成形术，我们 试图更好地了解局灶性冠状动脉狭窄的性质， 他们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 已经表明局灶性慢性狭窄处的成分和硬度 与邻近血管造影正常血管明显不同 节段，而动脉粥样硬化的总质量是非常相似的。 的 目前通过血管成形术治疗的主要病变已经变得僵硬， 纤维化和钙化阻止了代偿性扩张 在更顺从的（尽管病变严重）节段中观察到。 因此，成功的干预会破坏/改变僵硬的 约束元素，使其不可逆转地充分顺应 以允许血管扩张。 成功的治疗需要分段 刚性瓣环（有限）破裂并形成大顺应性 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，可以形成一个小弧（~60~） 高度兼容。 旋转消融仪可去除管腔钙化， 降低壁的刚度。 随着"刚性"金属的膨胀， 支架在高压下，周围组织产生显著的 压缩力，导致急性和慢性压缩性狭窄 可能是再狭窄的主要原因。 短暂的， 与热血管成形术相关的中度（~60 ℃）热升高 引发与上述类似的深度剂量依赖性增殖反应， 有严重的机械损伤。

In an effort to develop new, more effective forms of angioplasty, we have sought to better understand 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 have become rigid due to fibrosis and calcification, which prevent compensatory dilatation observed in more compliant (though heavily diseased) segments. Accordingly, successful interventions disrupt/alter the stiff constraining elements to irreversibly make them sufficiently compliant to 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 that can make a small arc (~60~) highly compliant. Rotablators remove luminal calcification, thereby reducing wall stiffness. Following the expansion of "rigid" metallic stents at high pressures, the surrounding tissues generate significant compressive forces, causing an acute and chronic compressive narrowing of treated lesions that may be the major cause of restenosis. Transient, moderate (~60~C) thermal elevations associated with thermal angioplasty elicit a profound dose-dependent proliferative response similar to that seen with severe mechanical injury.