Prasad Kailash
Department of Physiology, College of Medicine, University of Saskatchewan, Saskatoon, Saskatchewan, Canada.
Cardiovasc Drug Rev. 2006 Spring;24(1):33-50. doi: 10.1111/j.1527-3466.2006.00033.x.
C-reactive protein (CRP) plays a role in the pathogenesis of cardiovascular disease. It is a marker and predictor of cardiovascular disease. CRP possesses numerous cardiovascular effects (clotting, generation of oxygen radicals, increase in the expression of adhesion molecules and plasminogen activator inhibitor-1, plaque destabilization) that could result in cardiovascular disease. This review describes the effects of various cardiovascular drugs on the levels of CRP in health and disease. Cyclooxygenase inhibitors (aspirin, rofecoxib, celecoxib), platelet aggregation inhibitors (clopidogrel, abciximab), lipid lowering agents (statins, ezetimibe, fenofibrate, niacin, diets), beta-adrenoreceptor antagonists and antioxidants (vitamin E), as well as angiotensin converting enzyme (ACE) inhibitors (ramipril, captopril, fosinopril), reduce serum levels of CRP; while enalapril and trandolapril have not been shown to have the same effect. Angiotensin receptor blockers (ARBs) (valsartan, irbesartan, olmesartan, telmisartan) markedly reduce serum levels of CRP. The findings with other ARBs (losartan and candesartan) were inconsistent. Antidiabetic agents (rosiglitazone and pioglitazone) reduce CRP levels, while insulin is ineffective. Calcium channel antagonists have variable effects on CRP levels. Hydrochlorothiazide and oral estrogen do not affect CRP. The CRP-lowering effect of statins is more pronounced than their lipid lowering effect and is not dependent on their hypolipemic activity. The effect of atorvastatin on CRP seems to be dose-dependent. CRP-lowering effect of statins is likely to contribute to the favorable outcome of statin therapy. The data suggest that lipid lowering agents, ACE inhibitors, ARBs, antidiabetic agents, antiinflammatory and antiplatelet agents, vitamin E, and beta-adrenoreceptor antagonists lower serum or plasma levels of CRP, while vitamin C, oral estrogen and hydrochlorothiazide do not affect CRP levels.
C反应蛋白（CRP）在心血管疾病的发病机制中起作用。它是心血管疾病的一个标志物和预测指标。CRP具有多种心血管效应（凝血、氧自由基生成、黏附分子和纤溶酶原激活物抑制剂-1表达增加、斑块不稳定），这些效应可能导致心血管疾病。本综述描述了各种心血管药物对健康和疾病状态下CRP水平的影响。环氧化酶抑制剂（阿司匹林、罗非昔布、塞来昔布）、血小板聚集抑制剂（氯吡格雷、阿昔单抗）、降脂药物（他汀类、依折麦布、非诺贝特、烟酸、饮食）、β肾上腺素能受体拮抗剂和抗氧化剂（维生素E），以及血管紧张素转换酶（ACE）抑制剂（雷米普利、卡托普利、福辛普利）可降低血清CRP水平；而依那普利和trandolapril尚未显示有相同效果。血管紧张素受体阻滞剂（ARBs）（缬沙坦、厄贝沙坦、奥美沙坦、替米沙坦）可显著降低血清CRP水平。其他ARBs（氯沙坦和坎地沙坦）的研究结果不一致。抗糖尿病药物（罗格列酮和吡格列酮）可降低CRP水平，而胰岛素无效。钙通道拮抗剂对CRP水平有不同影响。氢氯噻嗪和口服雌激素不影响CRP。他汀类药物降低CRP的作用比其降脂作用更明显，且不依赖于其降血脂活性。阿托伐他汀对CRP的作用似乎呈剂量依赖性。他汀类药物降低CRP的作用可能有助于他汀类治疗取得良好效果。数据表明，降脂药物、ACE抑制剂、ARBs、抗糖尿病药物、抗炎和抗血小板药物、维生素E以及β肾上腺素能受体拮抗剂可降低血清或血浆CRP水平，而维生素C、口服雌激素和氢氯噻嗪不影响CRP水平。
