Sattar Naveed, McCarey David W, Capell Hilary, McInnes Iain B
Department of Pathological Biochemistry and Centre for Rheumatic Diseases, North Glasgow Hospitals University NHS Trust, Glasgow Royal Infirmary, Glasgow, Scotland, UK.
Circulation. 2003 Dec 16;108(24):2957-63. doi: 10.1161/01.CIR.0000099844.31524.05.
There is intense interest in mechanisms whereby low-grade inflammation could interact with conventional and novel vascular risk factors to promote the atheromatous lesion. Patients with rheumatoid arthritis (RA), who by definition manifest persistent high levels of inflammation, are at greater risk of developing cardiovascular disease. Mechanisms mediating this enhanced risk are ill defined. On the basis of available evidence, we argue here that the systemic inflammatory response in RA is critical to accelerated atherogenesis operating via accentuation of established and novel risk factor pathways. By implication, long-term suppression of the systemic inflammatory response in RA should be effective in reducing risk of coronary heart disease. Early epidemiological observational and clinical studies are commensurate with this hypothesis. By contrast, risk factor modulation with conventional agents, such as statins, may provide unpredictable clinical benefit in the context of uncontrolled systemic inflammatory parameters. Unraveling such complex relationships in which exaggerated inflammation-risk factor interactions are prevalent may elicit novel insights to effector mechanisms in vascular disease generally.
人们对低度炎症与传统及新型血管危险因素相互作用以促进动脉粥样硬化病变的机制有着浓厚兴趣。类风湿性关节炎（RA）患者，根据定义表现出持续的高水平炎症，患心血管疾病的风险更高。介导这种风险增加的机制尚不清楚。基于现有证据，我们在此认为，RA中的全身炎症反应对于通过强化既定和新型危险因素途径加速动脉粥样硬化形成至关重要。这意味着，长期抑制RA中的全身炎症反应应能有效降低冠心病风险。早期的流行病学观察和临床研究与这一假设相符。相比之下，在全身炎症参数未得到控制的情况下，使用他汀类等传统药物进行危险因素调节可能带来不可预测的临床益处。揭示这种普遍存在过度炎症与危险因素相互作用的复杂关系，可能会对一般血管疾病的效应机制产生新的见解。
