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 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。 通过血管内注射的临床应用， 超声（IVUS），我们已经表明，成分和刚度在 局灶性慢性狭窄与邻近狭窄明显不同， 血管造影正常的血管节段，而总质量的 动脉粥样化非常相似。 目前的主要病变 通过血管成形术治疗的患者由于纤维化而变得僵硬， 钙化，防止代偿性扩张观察到更多的 （虽然严重患病）的部分。 因此，成功 干涉破坏/改变刚性约束元件， 不可逆转地使其充分顺应， 扩张. 成功的治疗需要节段性（有限）破裂， 刚性环和大的顺应性弧的产生。 声学 气泡快速膨胀产生的瞬态是主要原因 激光血管成形术的破坏。 定向斑块切除 形成深的焦点切除，可以形成小的弧形（大约 60度）高度兼容。 旋转器移除管腔 钙化，从而降低壁硬度。 后 “刚性”金属支架在高压下的扩张， 周围组织产生显著的压缩力， 治疗病变的急性和慢性压迫性狭窄。 的 这些病变的变窄可能是再狭窄的主要原因。

In an effort to develop new, more effective forms of angioplasty, we have sought better 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 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, thus irreversibly making 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 (approximately 60 degrees) 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 that cause an acute and chronic compressive narrowing of treated lesions. The narrowing of these lesions may be the major cause of restenosis.