MECHANISMS OF ANGIOPLASTY AND ATHERECTOMY OF CORONARY STENOSES

冠状动脉狭窄的血管成形术和斑块切除术的机制

• 批准号: 3852976
• 负责人: R BONNER
• 金额: --
• 依托单位: NATIONAL CENTER FOR RESEARCH RESOURCES
• 依托单位国家: 美国
• 资助国家: 美国
• 起止时间: 至
• 项目状态: 未结题
• 来源: https://reporter.nih.gov/project-details/3852976
• 关键词: artery stenosis; coronary artery; elasticity; human therapy evaluation; method development; ultrasound

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.

作为开发新的、更有效的血管成形术形式的努力的一部分， 我们寻求更好地了解局灶性冠状动脉的性质 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，局灶性慢性病灶的成分和硬度 狭窄与邻近的、血管造影正常的狭窄明显不同 血管段，而粥样斑块的总质量则显着 相似的。 目前血管成形术治疗的主要病变是 由于纤维化和钙化而变得僵硬，阻碍了代偿性 在更顺应的（尽管患病严重）节段观察到扩张。 因此，成功的干预措施会破坏/改变僵化的状态 约束要素，使其充分且不可逆转 合规并允许船舶扩张。 成功的治疗需要 刚性环带的节段（有限）破裂并产生大的、 顺应弧。 气泡快速膨胀产生的声瞬变是 这是激光血管成形术中断的主要原因。 定向 斑块旋切术可进行深部病灶切除，形成小弧形 （约 60 度）高度合​​规。 旋转器移除管腔 钙化，从而降低壁硬度。 扩展后 高压下的“刚性”金属支架，压缩力是 由周围组织产生，导致严重的急性和 慢性反冲。 这种急性和慢性压缩性狭窄的治疗 病变可能是再狭窄的主要原因。 短暂、中等 （约 60 摄氏度）与热相关的热升高 血管成形术引起深刻的、剂量依赖性的增殖反应 与严重机械损伤相似。