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MECHANISMS OF ANGIOPLASTY AND ATHERECTOMY OF CORONARY STENOSES

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:
3767462
负责人:
R BONNER
金额:
$0.0万
依托单位国家:
美国
项目类别:
财政年份:
--
资助国家:
美国
项目状态:
未结题
起止时间:
至

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中文摘要
翻译
为了努力开发新的、更有效的血管成形术,我们有 寻求更好地了解局灶性冠状动脉狭窄的性质和 他们对干预的急性和慢性反应。通过 血管内超声(IVUS)临床应用进展 已经表明局灶性慢性狭窄的成分和僵硬 与邻近的血管造影正常的血管有显著的不同 而动脉粥样硬化的总质量非常相似。这个 目前血管成形术治疗的主要病变已经变得僵硬 到纤维化和钙化,这防止了代偿性扩张 在更顺从的(尽管严重患病的)节段中观察到。 因此,成功的干预会扰乱/改变僵化。 约束元素以不可逆转地使其充分符合 以允许血管扩张。成功的治疗需要节段性治疗 (有限)硬环断裂并形成大的顺应性 弧形。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。方向性 动脉粥样硬化切除可形成一条小弧形(~60~) 高度合规。轮虫去除管腔钙化,从而 降低墙体刚度。在“刚性”金属的扩张之后 支架在高压下,周围组织会产生显著的 压缩力,导致急性和慢性压缩狭窄 治疗后的病变可能是导致再狭窄的主要原因。短暂的, 与热血管成形术相关的中等(~60℃)热升高 引起深刻的剂量依赖的增殖反应,类似于 有严重的机械损伤。
英文摘要
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.
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MECHANISMS OF ANGIOPLASTY AND ATHERECTOMY OF CORONARY STENOSES
MECHANISMS OF ANGIOPLASTY AND ATHERECTOMY OF CORONARY STENOSES
MECHANISMS OF ANGIOPLASTY AND ATHERECTOMY OF CORONARY STENOSES
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