Oral infection-inflammatory pathway, periodontitis, is a risk factor for endothelial dysfunction in patients with coronary artery disease
Oral infection-inflammatory pathway, periodontitis, is a risk factor for endothelial dysfunction in patients with coronary artery disease
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DOI：
10.1016/j.atherosclerosis.2009.03.037
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发表时间：
2009-10-01
期刊：
影响因子：
5.3
通讯作者：
Taguchi, Akira
中科院分区：
文献类型：
--
作者：
Higashi, Yukihito;Goto, Chikara;Taguchi, Akira
目的：牙周炎是心血管疾病的危险因素。炎症和内皮功能障碍之间存在关联。本研究的目的是评估患有牙周炎的冠状动脉疾病（CAD）患者的内皮功能。方法和结果：我们评价了101例冠心病伴牙周炎患者前臂血流（FBF）对乙酰胆碱（ACh）（一种内皮依赖性血管扩张剂）和硝普钠（SNP）（一种内皮非依赖性血管扩张剂）的反应（37名男性和11名女性，63 +/- 12岁）和无牙周炎（36名男性和17名女性，62 +/- 13岁）。采用应变容积描记法测量FBF。牙周炎组血清C-反应蛋白和白细胞介素-6水平显著高于非牙周炎组。牙周炎组FBF对ACh的反应明显小于非牙周炎组。SNP刺激的血管舒张在两组中相似。Periodicals治疗将C-反应蛋白的血清浓度从2.7 +/- 1.9降至1.8 +/- 0.9 mg/L（P < 0.05），白细胞介素-6从2.6 +/- 3.4至1.6 +/- 2.6 ng/L在牙周炎患者中，ACh诱导的血管舒张从14.7 +/- 5.2增加到20.1 +/- 6.1 mL/（min 100 mL）组织（P < 0.05）。SNP刺激的血管舒张作用在治疗前后相似。NG-单甲基-L-精氨酸，一氧化氮合酶抑制剂，FBF反应ACh管理后是类似的治疗前和治疗后。结论：这些研究结果表明，牙周炎与内皮功能障碍的CAD患者通过减少一氧化氮的生物利用度。全身性炎症可能至少部分是内皮功能障碍进展的原因和预测因子。(C)2009爱思唯尔爱尔兰有限公司保留所有权利。
Objective: Several studies have shown that periodontitis is a risk factor for cardiovascular diseases. There is an association between inflammation and endothelial dysfunction. The purpose of this study was to evaluate endothelial function in patients with coronary artery disease (CAD) who had periodontitis.Methods and results: We evaluated forearm blood flow (FBF) responses to acetylcholine (ACh), an endothelium-dependent vasodilator, and to sodium nitroprusside (SNP), an endothelium-independent vasodilator, in 101 CAD patients with periodontitis (37 men and 11 women, 63 +/- 12 yr) and without periodontitis (36 men and 17 women, 62 +/- 13 yr). FBF was measured by using strain-gauge plethysmography. Circulating levels of C-reactive protein and interleukin-6 were significantly higher in the periodontitis group than in the non-periodontitis group. FBF response to ACh was significantly smaller in the periodontitis group than in the non-periodontitis group. SNP-stimulated vasodilation was similar in the two groups. Periodontal therapy reduced serum concentrations of C-reactive protein from 2.7 +/- 1.9 to 1.8 +/- 0.9 mg/L (P < 0.05) and interleukin-6 from 2.6 +/- 3.4 to 1.6 +/- 2.6 ng/L (P < 0.05) and augmented ACh-induced vasodilation from 14.7 +/- 5.2 to 20.1 +/- 6.1 mL/(min 100 mL) tissue (P < 0.05) in patients with periodontitis. The SNP-stimulated vasodilation was similar before and after treatment. After administration of NG-monomethyl-l-arginine, a nitric oxide synthase inhibitor, FBF response to ACh was similar before and after treatment.Conclusion: These findings suggest that periodontitis is associated with endothelial dysfunction in patients with CAD through a decrease in nitric oxide bioavailability. Systemic inflammation may be, at least in part, a cause and predictor of progression of endothelial dysfunction. (C) 2009 Elsevier Ireland Ltd. All rights reserved.