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Target Organ Damage and the Prothrombotic State in Hypertension

机译:高血压的靶器官损害和血栓前状态

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Hypertension causes target organ damage by the direct physical effect of increased blood pressure, as well as the active promotion of atherosclerosis and thrombogenesis. More importantly, the processes of thrombogenesis and atherogenesis are intimately related, and many of the basic concepts of thrombogenesis can be applied to atherogenesis.Over 150 years ago, Virchow1 postulated that a triad of conditions are needed to predispose to thrombus formation, that is, abnormalities in blood flow, blood constituents, and the vessel wall. Although Virchow was referring to venous thrombosis, the same concepts could essentially be applied to arterial thrombosis. A modern viewpoint of Virchow’s triad includes abnormalities of hemorheology and turbulence at bifurcations and stenotic regions (that is, “abnormal blood flow”), abnormalities in platelets and the coagulation and fibrinolytic pathways (“abnormal blood constituents”), and, finally, abnormalities in the endothelium (“abnormal vessel wall”). This may explain an important pathophysiological paradox in hypertension, in which despite the blood vessels being exposed to high pressures, the main complications of hypertension are generally thrombotic in nature rather than hemorrhagic.2 Evidence for the prothrombotic or hypercoagulable state in hypertension has been extensively reviewed.3 4 However, we all recognize that the presence of target organ damage makes a dramatic difference to clinical outcome in hypertension. The “target organ” effects of hypertension are particularly manifest in the heart, brain, kidney, peripheral arteries, and the eye. Indeed, hypertensive patients with evidence of target organ damage are well recognized to be at high risk of cardiovascular and cerebrovascular events, and they should be targeted for aggressive blood pressure and risk factor management.Indeed, one may postulate that the “high-risk” hypertensives with evidence of target organ damage are more likely to exhibit a greater prothrombotic or hypercoagulable state. It is therefore of little surprise that the abnormalities in the prothrombotic or …
机译:高血压通过血压升高的直接物理作用以及积极促进动脉粥样硬化和血栓形成而引起靶器官损伤。更重要的是,血栓形成和动脉粥样硬化的形成过程密切相关,许多血栓形成的基本概念都可以应用于动脉粥样硬化。150多年前,Virchow1认为,需要三重条件来促成血栓形成,也就是说,血流,血液成分和血管壁异常。尽管Virchow指的是静脉血栓形成,但相同的概念实际上可以应用于动脉血栓形成。维尔丘三联征的现代观点包括分叉处和狭窄区域的血液流变学和湍流异常(即“血流异常”),血小板和凝血和纤溶途径异常(“血液成分异常”),以及最后的异常。在内皮中(“异常血管壁”)。这可能解释了高血压的一个重要病理生理悖论,在高血压中,尽管血管处于高压状态,但高血压的主要并发症通常是血栓性的,而不是出血性的。2高血压的前血栓形成或高凝状态的证据已得到广泛审查.3 4但是,我们都认识到靶器官损害的存在对高血压的临床结局有重大影响。高血压的“靶器官”效应尤其表现在心脏,大脑,肾脏,外周动脉和眼睛中。确实,具有目标器官损伤证据的高血压患者被公认为患有心血管和脑血管事件的高风险,因此应该将其作为积极的血压和危险因素管理的目标。事实上,人们可能会假设“高风险”有靶器官损害证据的高血压患者更有可能表现出更大的血栓形成或高凝状态。因此,血栓形成或…的异常并不奇怪。

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