关注高血压患者残余风险提高临床治疗获益 .pptxVIP

关注高血压患者残余风险，提高临床治疗获益;早期研究提示 高血压患者降压治疗后死亡风险仍高于正常人群;血压控制不佳 可能是早期研究中高血压患者心血管风险高的原因;;高血压患者经包括降压的多重危险干预及生活方式改变后仍具有较高的心血管风险;;高血压时血浆中过氧化氢、超氧阴离子和羟自由基（活性氧簇）增高，内皮细胞生成一氧化氮（NO）减少，增加白细胞粘附 和外周阻力，促进炎症反应。文献报道，炎症可诱导LDL的氧化修饰。而修饰的LDL可进一步导致动脉内膜的炎症过程。氧化型低密度脂蛋白（oxLDL）上调内皮细胞产生单核细胞趋化因子，使单核巨噬细胞聚集增殖，并使巨噬细胞分化成泡沫细 胞。此外还可使一些细胞成分活化，分泌化学因子、细胞因子以及一些至炎症因子，参与动脉粥样硬化的形成和发展。;在血压升高的状态下，NO活性降低，ETA介导的血管收缩性内皮素-1活性增强，结果导致血管张力增加，管壁增生，随后全 身血管阻力增加，在传导血管水平，相似的内皮释放因子活性不平衡导致预动脉硬化环境，从而有利于LDL氧化，单核细胞迁移和粘附，并形成泡沫细胞，这些最终导致动脉硬化斑块的形成。;Med Hypotheses. 2005;64(5):925-9. Inflammation may be a bridge connecting hypertension and atherosclerosis. Li JJ, Chen JL. Author information Abstract Pathogenesis of the atherosclerotic process is deemed as multi-factorial, and characterized by chronic inflammatory response. Althoughhypertension is known to be one of the most important risk factors for atherosclerosis in causasians, its relative contribution to early atherosclerosisare still unknown. Increased evidence has indicated that hypertension, through the vasoactive peptides, such as angiotensin and endothelin-1, promotes and accelerates the atherosclerotic process via inflammatory mechanisms. In animal and human studies pro- inflammatory properties of angiotensin II has been demonstrated in large conduit and small arteries, in the kidney as well as in the heart. Activation of oxidative stress by angiotensin II is a key component of this process. Angiotensin II stimulates nicotinamide adenine dinucleotide phosphate/nicotinamide adenine dinucleotide oxidase in endothelium, smooth muscle cells, and the adventitia of blood vessel to generate reactive oxygen species, leading to endothelial dysfunction, growth, and inflammation, upregulation of endothelin-1, adhesion molecules, nuclear factor- kappa B, and other inflammatory mediators, as well as increased breakdown of nitric oxide and uncoupling of nitric oxide synthase, contribute to the progression of vascular disease and atherogenesis. In addition, recent advances concerning role o