Department of Cardiology, The He Xian Memorial Hospital of Panyu District, Guangzhou, People's Republic of China.
Dig Dis Sci. 2011 Jan;56(1):109-14. doi: 10.1007/s10620-010-1274-6. Epub 2010 May 26.
The role of infection in the pathogenesis of atherosclerosis is still a matter of debate.
This study aimed to investigate the effect of CagA-positive Helicobacter pylori (H. pylori) strains infection on coronary atherosclerosis in patients with coronary heart disease and to elucidate how cytotoxin-associated gene A (CagA)-positive H. pylori strains infections were involved in coronary heart disease by examining the levels of serum lipid, high-sensitivity C-reactive protein (hsCRP) and oxidized low-density protein (oxLDL).
Recruited for this study were 159 patients with coronary heart disease. The severity of coronary heart disease was estimated by calculating the Gensini score. Serum oxLDL and hsCRP were examined in all subjects. Current H. pylori infection was determined in all participants by means of a modified (13C) urea breath test (>200 dpm classified as positive). IgG antibodies against CagA protein were analyzed by enzyme immunoassays. Antibody titers against CagA (≥8 U/ml) were classified as positive. All subjects were divided into three groups, including an uninfected group (n=30), an H. pylori +CagA- group (n=69), and an H. pylori +CagA+ group (n=60).
Significant differences were found among the three groups in levels of total cholesterol, low-density lipoprotein cholesterol, apolipoprotein B, serum hsCRP, oxLDL, and severity of coronary atherosclerosis (p<0.05). The levels of total cholesterol, LDL, apolipoprotein B, serum hsCRP, oxLDL were significantly elevated and the severity of coronary atherosclerosis was significantly increased in H. pylori +CagA+ group (p<0.05).
More serious coronary atherosclerosis was observed in CHD patients with H. pylori +CagA+ infection. H. pylori +CagA+ infection might be involved in coronary atherosclerosis by modifying serum lipids, enhancing LDL oxidation, and activating the inflammatory responses.
感染在动脉粥样硬化发病机制中的作用仍存在争议。
本研究旨在探讨 CagA 阳性幽门螺杆菌（H. pylori）菌株感染对冠心病患者冠状动脉粥样硬化的影响，并通过检测血清脂质、高敏 C 反应蛋白（hsCRP）和氧化型低密度脂蛋白（oxLDL）水平，阐明 CagA 阳性 H. pylori 菌株感染如何参与冠心病。
本研究纳入了 159 例冠心病患者。通过计算 Gensini 评分来评估冠心病的严重程度。所有受试者均检测血清 oxLDL 和 hsCRP。所有参与者均通过改良（13C）尿素呼气试验（>200 dpm 为阳性）确定当前 H. pylori 感染。采用酶联免疫吸附试验分析 CagA 蛋白的 IgG 抗体。CagA 抗体滴度（≥8 U/ml）为阳性。所有患者均分为三组，即未感染组（n=30）、H. pylori+CagA-组（n=69）和 H. pylori+CagA+组（n=60）。
三组间总胆固醇、低密度脂蛋白胆固醇、载脂蛋白 B、血清 hsCRP、oxLDL 水平及冠状动脉粥样硬化严重程度差异有统计学意义（p<0.05）。H. pylori+CagA+组总胆固醇、LDL、载脂蛋白 B、血清 hsCRP、oxLDL 水平显著升高，冠状动脉粥样硬化严重程度显著增加（p<0.05）。
H. pylori+CagA+感染的冠心病患者冠状动脉粥样硬化更严重。H. pylori+CagA+感染可能通过改变血清脂质、增强 LDL 氧化和激活炎症反应参与冠状动脉粥样硬化的发生。
