Davies M J
Cardiovascular Pathology Unit, St George's Hospital Medical School, University of London, British Heart Foundation, UK.
J Hum Hypertens. 1991 Aug;5 Suppl 1:23-9.
Epidemiological surveys show the clear association of hypertension with an increased risk of developing ischaemic heart disease. One method of quantifying atherosclerosis is to measure, at necropsy, the percentage of the intimal surface of the coronary arteries or aorta which is occupied by raised plaques. When this is done in a large number of subjects the amount of intimal involvement in any particular geographical population correlates directly with the frequency of ischaemic heart disease. In all these populations, whether at a high risk or low risk of developing ischaemic heart disease, hypertensive subjects have a greater intimal involvement by plaques than normotensive subjects. Thus, the increased risk in hypertension is, in part, mediated by possession of more plaques. Plaque growth is due to the accumulation of lipid from the plasma, the ingress of monocytes with their conversion to lipid filled foam cells and the formation of collagen by smooth muscle cells. Hypertension may act by altering endothelial function to potentiate all these processes. Mechanical stress on endothelial cells will evoke the formation of growth factors for smooth muscle cells. Plaque growth in man is also episodic due to the formation of thrombi; a proportion of these episodes are symptomatic producing acute myocardial ischaemia but the majority are silent leading to sudden plaque expansion. Thrombi over plaques are either due to endothelial denudation injury or more commonly due to the tearing of the cap of a plaque leading to deep intimal injury. Necropsy surveys of control populations show that subjects with hypertension have a greater frequency of recent plaque tears compared with normotensive subjects.
流行病学调查显示，高血压与缺血性心脏病发病风险增加之间存在明确关联。量化动脉粥样硬化的一种方法是在尸检时测量冠状动脉或主动脉内膜表面被隆起斑块占据的百分比。当对大量受试者进行此项测量时，任何特定地理区域人群的内膜受累程度与缺血性心脏病的发病率直接相关。在所有这些人群中，无论患缺血性心脏病的风险高或低，高血压患者的斑块内膜受累程度均高于血压正常者。因此，高血压患者风险增加部分是由于有更多的斑块。斑块生长是由于血浆中脂质的积聚、单核细胞的侵入及其转化为充满脂质的泡沫细胞，以及平滑肌细胞形成胶原蛋白所致。高血压可能通过改变内皮功能来增强所有这些过程。内皮细胞上的机械应力会诱发平滑肌细胞生长因子的形成。在人类中，由于血栓形成，斑块生长也是间歇性的；这些血栓形成事件一部分有症状，会导致急性心肌缺血，但大多数是无症状的，会导致斑块突然扩大。斑块上的血栓要么是由于内皮剥脱损伤，要么更常见的是由于斑块帽破裂导致内膜深层损伤。对对照人群的尸检调查显示，与血压正常者相比，高血压患者近期斑块破裂的频率更高。
