Felmeden Dirk C, Spencer Charles G C, Chung Natali A Y, Belgore Funmi M, Blann Andrew D, Beevers D Gareth, Lip Gregory Y H
Haemostasis, Thrombosis, and Vascular Biology Unit, University Department of Medicine, City Hospital, Birmingham, United Kingdom.
Am J Cardiol. 2003 Aug 15;92(4):400-5. doi: 10.1016/s0002-9149(03)00657-x.
Increasing evidence points toward a prothrombotic state in hypertension and atherosclerosis, conditions associated with thrombosis-related complications, such as myocardial infarction and stroke. We hypothesized that this increased risk of thrombogenesis may be related to endothelial damage/dysfunction and abnormal angiogenesis, and thus, an increased risk of future cardiovascular disease. Thrombogenesis, endothelial damage/dysfunction, and angiogenesis can be assessed by measurement of tissue factor (TF), von Willebrand Factor (vWF), flow-mediated dilatation (FMD), and vascular endothelial growth factor (VEGF), respectively. To test this hypothesis, we measured TF, vWF, FMD, and VEGF in 76 patients with systemic hypertension (71 men; mean age 64; mean blood pressure 167/72 mm Hg), considered additional risk factors such as diabetes, and related them to the patient's 10-year cardiovascular and cerebrovascular risk score using the Framingham equation. Patients were compared with 48 healthy normotensive controls. In these patients, the effects of 6 months of intensified blood pressure and (where appropriate) lipid-lowering treatment were investigated. In our patients, TF, VEGF, and vWF levels were higher, but FMD was lower (all p <0.001) compared with the controls. All markers correlated with each other and with both cardiovascular and cerebrovascular risk scores (all p <0.001). After intensified blood pressure and hypercholesterolemia treatment, total cholesterol, blood pressure, TF, VEGF, and vWF levels all decreased, whereas FMD increased (all p <0.001). Thus, in subjects with hypertension and other risk factors, endothelial damage/dysfunction (and thus, atherogenesis), thrombogenesis, and angiogenesis are abnormal, correlate with overall cardiovascular risk, and importantly, can be related to each other in a "Birmingham Vascular Triangle." Furthermore, these processes are beneficially affected by intensive blood pressure and lipid treatment.
越来越多的证据表明，高血压和动脉粥样硬化存在促血栓形成状态，这些疾病与血栓形成相关并发症有关，如心肌梗死和中风。我们推测，这种血栓形成风险增加可能与内皮损伤/功能障碍及异常血管生成有关，进而导致未来心血管疾病风险增加。血栓形成、内皮损伤/功能障碍和血管生成可分别通过测量组织因子（TF）、血管性血友病因子（vWF）、血流介导的血管舒张功能（FMD）和血管内皮生长因子（VEGF）来评估。为验证这一假设，我们对76例系统性高血压患者（71例男性；平均年龄64岁；平均血压167/72 mmHg）进行了TF、vWF、FMD和VEGF测量，考虑了糖尿病等其他风险因素，并使用弗雷明汉方程将其与患者的10年心血管和脑血管风险评分相关联。将患者与48例健康血压正常的对照者进行比较。在这些患者中，研究了6个月强化血压及（酌情）降脂治疗的效果。与对照组相比，我们的患者TF、VEGF和vWF水平较高，但FMD较低（均p<0.001）。所有标志物相互之间以及与心血管和脑血管风险评分均相关（均p<0.001）。强化血压和高胆固醇血症治疗后，总胆固醇、血压、TF、VEGF和vWF水平均降低，而FMD升高（均p<0.001）。因此，在患有高血压和其他风险因素的受试者中，内皮损伤/功能障碍（进而动脉粥样硬化形成）、血栓形成和血管生成均异常，与总体心血管风险相关，重要的是，它们在“伯明翰血管三角”中可能相互关联。此外，这些过程受到强化血压和血脂治疗的有益影响。
