Zebrack James S, Anderson Jeffrey L
University of Utah School of Medicine, Department of Internal Medicine, Division of Cardiology, Salt Lake City, UT, USA.
Prog Cardiovasc Nurs. 2002 Fall;17(4):174-85. doi: 10.1111/j.0889-7204.2002.1118.x.
Acute coronary syndromes, stroke, and sudden death are common complications of a disrupted atherosclerotic plaque. Unstable plaque is a result of multiple factors but is commonly characterized by an infiltrate of inflammatory cells. Medical research strongly supports a role for inflammation in the pathogenesis, progression, and disruption of atherosclerotic plaque. Medical science also has improved our understanding of the complex interactions between our environment and our immune, coagulation, and cardiovascular systems. Clinical studies have demonstrated systemic markers of inflammation to be strong predictors of clinical events, and specific treatments of atherosclerosis and its risk factors have been associated with reductions in inflammatory markers. The authors review the current understanding of the role of inflammation in the pathogenesis of atherosclerosis, the common inflammatory markers, and potential anti-inflammatory therapy. Among several potential circulating markers of vascular inflammation, high sensitivity C-reactive protein is best validated and standardized as a marker for cardiovascular risk assessment. Nevertheless, there remain many uncertainties in utilizing C-reactive protein in clinical practice. Here, the authors describe the central role of C-reactive protein in atherosclerosis, review the studies demonstrating predictive value of C-reactive protein, describe the factors requiring consideration when utilizing C-reactive protein, discuss clinical scenarios in which measurement of C-reactive protein may be helpful, and suggest ways to interpret and treat elevated C-reactive protein levels. Finally, the authors summarize future expectations for assessing and modulating the vascular inflammation to inhibit initiation and progression of the atherosclerotic process.
急性冠状动脉综合征、中风和猝死是动脉粥样硬化斑块破裂的常见并发症。不稳定斑块是多种因素导致的结果，但其通常的特征是有炎症细胞浸润。医学研究有力地支持了炎症在动脉粥样硬化斑块的发病机制、进展和破裂过程中所起的作用。医学也增进了我们对环境与我们的免疫、凝血及心血管系统之间复杂相互作用的理解。临床研究已证明，炎症的全身标志物是临床事件的有力预测指标，并且针对动脉粥样硬化及其危险因素的特定治疗已与炎症标志物的降低相关联。作者们综述了目前对炎症在动脉粥样硬化发病机制中的作用、常见炎症标志物以及潜在抗炎治疗的理解。在几种潜在的血管炎症循环标志物中，高敏C反应蛋白作为心血管风险评估的标志物得到了最好的验证和标准化。然而，在临床实践中使用C反应蛋白仍存在许多不确定性。在此，作者们描述了C反应蛋白在动脉粥样硬化中的核心作用，综述了证明C反应蛋白具有预测价值的研究，描述了使用C反应蛋白时需要考虑的因素，讨论了测量C反应蛋白可能有帮助的临床情况，并提出了解释和处理C反应蛋白水平升高的方法。最后，作者们总结了评估和调节血管炎症以抑制动脉粥样硬化进程的起始和进展的未来期望。
