Ellis R W
Department of Clinical Bacteriology, University Hospital NHS Trust, Queen Elizabeth Medical Centre, Edgbaston, Birmingham.
J Med Microbiol. 1997 Jul;46(7):535-9. doi: 10.1099/00222615-46-7-535.
A large body of evidence exists that implicates a number of microbial agents in the pathogenesis of coronary heart disease (CHD). This, if proven, may have far-reaching implications for the prevention and treatment of CHD and other atherosclerotic disease. The histopathology of atherosclerosis and its natural history suggest infectious causation at many points along the progression of disease, particularly with regard to CHD, and a number of pathogens have been the focus of study. Viral agents implicated include Coxsackie B4 virus, for which tenuous sero-epidemiological associations exist, and the Herpesviridae. The animal herpesvirus causing Marek's disease in chickens causes atherosclerotic lesions in these animals. Herpes simplex virus I and II have been found in aortic smooth muscle and produce changes in vitro in smooth muscle that are similar to those seen at the beginning of atherosclerosis and which may also explain some of the features of atherosclerotic complications. Cytomegalovirus is implicated more strongly sero-epidemiologically by in-vivo detection in atherosclerotic lesions and by its links with post-cardiac transplant vasculopathya syndrome similar to atherosclerosis. Bacteria have also been shown to have links with CHD. Chlamydia pneumoniae and Helicobacter pylori have both been associated sero-epidemiologically with CHD, and these findings have been consolidated by recent work showing their presence in atherosclerotic lesions in adults. Bacterial infections in general lead to many changes in lipid, thrombic and other acute-phase protein metabolism, and some of these changes occur with both C. pneumoniae and H. pylori infections. The ubiquity and similar epidemiological features to CHD of all these microbial pathogens make the resolution of the causative issue impossible by retrospective means. All that can be shown at present are a variety of weak and strong links, the significance of which can only be determined by large and perhaps lifetime prospective studies.
大量证据表明,多种微生物因子与冠心病(CHD)的发病机制有关。如果这一点得到证实,可能会对冠心病及其他动脉粥样硬化疾病的预防和治疗产生深远影响。动脉粥样硬化的组织病理学及其自然史表明,在疾病进展的许多阶段都存在感染病因,尤其是对于冠心病而言,许多病原体已成为研究重点。涉及的病毒因子包括柯萨奇B4病毒,其血清流行病学关联较为薄弱,还有疱疹病毒科。导致鸡马立克氏病的动物疱疹病毒会在这些动物身上引发动脉粥样硬化病变。在主动脉平滑肌中发现了单纯疱疹病毒I和II,它们在体外能使平滑肌产生与动脉粥样硬化初期相似的变化,这也可能解释动脉粥样硬化并发症的一些特征。通过在动脉粥样硬化病变中的体内检测以及与心脏移植后血管病变(一种类似于动脉粥样硬化的综合征)的关联,巨细胞病毒在血清流行病学上的关联更为紧密。细菌也已被证明与冠心病有关。肺炎衣原体和幽门螺杆菌在血清流行病学上均与冠心病相关,近期研究表明它们存在于成人的动脉粥样硬化病变中,进一步巩固了这些发现。一般来说,细菌感染会导致脂质、血栓形成及其他急性期蛋白代谢发生许多变化,肺炎衣原体和幽门螺杆菌感染都会出现其中一些变化。所有这些微生物病原体的广泛存在以及与冠心病相似的流行病学特征,使得通过回顾性方法无法解决病因问题。目前所能表明的只是各种强弱不等的关联,其意义只能通过大规模甚至可能是长期的前瞻性研究来确定。