Cardiovascular Infections

R. Wani, Satya Das
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引用次数: 9

Abstract

Infective endocarditis (IE) is inflammation of the endothelial lining of the heart valves due to infective causes. IE is a rare condition with an incidence rate of three to nine cases per 100,000 population with a male to female ratio of 2:1. The rate is higher in people with unrepaired cyanotic congenital heart disease, prosthetic heart valves and previous endocarditis. Other risk factors for IE include: rheumatic fever (now accounts for < 10% of IE cases in developed countries), degenerative conditions of heart valves, intravenous drug abuse, diabetes, and HIV infection. One third of the cases are now healthcare associated infection (HCAI), particularly with haemodialysis, cardiac surgery, implantable cardiac devices, intravascular lines, and urinary catheters. In the past decade Staphylococcus aureus has replaced viridans streptococci as the leading cause of IE, the rate of enterococcal (mostly E. faecalis) and Bartonella IE has increased, while that of culture negative endocarditis has decreased. Untreated IE is a uniformly fatal condition, but the mortality rate can be reduced to 5–40% with appropriate treatment. There are two important prerequisite steps to the development of IE: 1. A damaged endothelium due to high pressure gradient and turbulent blood flow around a heart valve or septal defect. Fibrin and platelet deposition occur on the roughened endothelium forming a non-infective thrombus or vegetation. 2. Bacteraemia due to endocarditis-prone organisms resulting from trauma to mucous membranes (e.g. oral cavity, urinary, and gastrointestinal tract) or other colonized tissue or foreign body, which is not cleared by host defence mechanisms. Micro-organisms then attach to the damaged endothelium through a specific ligand-receptor interaction (hence the predilection for certain organisms to cause endocarditis, e.g. viridans streptococci from the mouth), colonize the thrombus, and grow and multiply within it to give rise to a mature/infective vegetation, which is the pathological hallmark of IE. Virulent organisms, classically S. aureus, can apparently infect a healthy endocardium. Damage to the endothelium results in valvular incompetence/regurgitation and symptoms and signs of heart failure and when severe, it is a potentially fatal condition that requires urgent valve surgery, even if the infection has fully responded to antimicrobial therapy.
心血管疾病的感染
感染性心内膜炎(IE)是由感染引起的心脏瓣膜内皮层炎症。IE是一种罕见的疾病,发病率为每10万人中3至9例,男女比例为2:1。未修复的青紫型先天性心脏病、人工心脏瓣膜和既往心内膜炎患者的患病率更高。其它诱发IE的危险因素包括:风湿热(目前在发达国家IE病例中占比< 10%)、心脏瓣膜退行性疾病、静脉注射药物滥用、糖尿病和HIV感染。现在,三分之一的病例是医疗保健相关感染(HCAI),特别是血液透析、心脏手术、植入式心脏装置、血管内导管和导尿管。近十年来,金黄色葡萄球菌已取代翠绿链球菌成为IE的主要病因,肠球菌(主要为粪肠球菌)和巴尔通体IE的发生率有所上升,而培养阴性心内膜炎的发生率有所下降。未经治疗的IE是一种普遍致命的疾病,但通过适当的治疗,死亡率可降至5-40%。IE的发展有两个重要的先决条件:1。在心脏瓣膜周围或间隔缺损处,由于高压梯度和湍流血流而造成的内皮受损。纤维蛋白和血小板沉积发生在粗糙的内皮上,形成非感染性血栓或植被。2. 由于粘膜(如口腔、泌尿和胃肠道)或其他定植组织或异物的创伤而引起的心内膜炎易感菌血症,宿主防御机制无法清除。然后,微生物通过特定的配体-受体相互作用附着在受损的内皮上(因此,某些生物倾向于引起心内膜炎,例如来自口腔的翠绿链球菌),定植在血栓上,并在血栓内生长和繁殖,形成成熟/感染性植被,这是IE的病理标志。致命的有机体,典型的金黄色葡萄球菌,显然可以感染健康的心内膜。内皮损伤导致瓣膜功能不全/反流和心衰的症状和体征,严重时,即使感染对抗菌药物治疗完全有效,也可能是一种潜在的致命疾病,需要紧急进行瓣膜手术。
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