Relationship between aortic stiffening and microvascular disease in brain and kidney - Cause and logic of therapy
Relationship between aortic stiffening and microvascular disease in brain and kidney - Cause and logic of therapy
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DOI：
10.1161/01.hyp.0000168052.00426.65
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发表时间：
2005-07-01
期刊：
影响因子：
8.3
通讯作者：
Safar, ME
中科院分区：
文献类型：
--
作者：
O'Rourke, MF;Safar, ME
大脑和肾脏的微血管损伤与年龄和高血压指数（脉压、主动脉脉搏波速度和增强指数）之间存在密切关系。这种关联的机制尚未确定，预防和治疗微血管损伤的原理也尚未确定。与其他全身血管床相比，可以根据大脑和肾脏的差分输入阻抗提供逻辑病理生理学解释。这些器官中的湍流和低流动阻力使小动脉暴露于颈动脉、椎动脉和肾动脉中存在的高压波动中。这种波动（可以通过中心脉压来测量）会随着年龄的增长而增加 3 至 4 倍。根据 Byrom 50 多年前建立的机制，小血管暴露于高脉动压力和流量可以解释微血管损伤以及由此导致的肾功能不全和智力衰退。预防和治疗的合理方法需要降低中心脉压。由于主动脉和大动脉不会直接受到药物的影响，因此需要通过扩张身体其他部位的导管动脉来减少波反射。这可以通过定期锻炼和硝酸盐、钙通道阻滞剂、血管紧张素转换酶抑制剂和血管紧张素受体阻滞剂等药物来实现。这里给出的解释解释了糖尿病中更大和更早的血管损伤（相对微血管脆性），并且与室间隔缺损和其他先天性血管分流引起的肺动脉高压的血管变化的解释相似。
A close relationship has been established between microvascular damage in brain and kidney and indices of age and hypertension ( pulse pressure, aortic pulse wave velocity, and augmentation index). The mechanism of such association has not been established, nor has rationale for prevention and treatment of microvascular damage. A logical pathophysiological explanation can be offered on the basis of differential input impedance in the brain and kidney compared with other systemic vascular beds. Torrential flow and low resistance to flow in these organs exposes small arterial vessels to the high-pressure fluctuations that exist in the carotid, vertebral, and renal arteries. Such fluctuations, measurable as central pulse pressure, increase 3- to 4-fold with age. Exposure of small vessels to highly pulsatile pressure and flow explains microvascular damage and resulting renal insufficiency and intellectual deterioration, according to the mechanism established by Byrom > 50 years ago. The logical approach to prevention and treatment requires reduction of central pulse pressure. Because the aorta and large arteries are not directly affected by drugs, this entails reduction of wave reflection by dilation of conduit arteries elsewhere in the body. This can be accomplished by regular exercise and by drugs such as nitrates, calcium channel blockers, angiotensin-converting enzyme inhibitors, and angiotensin receptor blockers. The explanation given here accounts for greater and earlier vascular damage in diabetes mellitus ( relative microvascular fragility) and is similar to that given for vascular changes of pulmonary hypertension caused by ventricular septal defects and other congenital vascular shunts.