从病毒性心肌炎到扩张型心肌病

病毒性心肌炎是目前各种原因引起的心肌炎中发病率最高的疾患之一。病毒性心肌炎病因为病毒感染。与其有关的病毒主要是柯萨奇病毒、埃可病毒、脊髓灰质炎病毒、粘病毒、腺病毒等。病毒性心肌炎的发病机制为病毒直接侵袭心肌和免疫反应。病毒性心肌炎大多数预后良好 ,但也有一部分转变为扩张型心肌病 ,是继发性心肌病的重要原因之一。本文对病毒性心肌炎时免疫系统与心肌病理变化的关系、病毒性心肌炎转变为扩张型心肌病的决定因素等作一综述。1　病毒性心肌炎的病理变化引起病毒性心肌炎的病毒 ,感染机体以后 ,患者是否即患病毒性心肌炎以…     

柯萨奇B组病毒与病毒性心肌炎和扩张型心肌病关系的研究

病毒性心肌炎和扩张型心肌病是心血管疾病中的常见病和多发病。许多学者的研究证实病毒性心肌炎的发病大部分与肠道病毒感染有关,尤其以柯萨奇病毒最为多见[1～4],占心肌炎的40%～50%。关于扩张型心肌病的病因很复杂,可能与病毒感染、免疫障碍、神经体液因素、小血管病变?..     

应用聚合酶链式反应探讨肠道病毒感染与病毒性心肌炎及扩张型心肌病的关系

一般认为,肠道柯萨奇B(Coxsackie B,COXB)病毒引起的心肌炎是青少年猝死的重要原因,亦是扩张型心肌病(Dilatecl Cardiomoputhy,DCM)的重要发病基础.我们应用聚合酶链式反应(PCR)方法对72例患者进行血中白细胞和心肌组织肠道病毒的检测,探讨该方法,对病毒性心肌炎(Virus myocarditir,VMC)诊断的价值,以及在心肌炎病毒感染持续存在时向扩张型心肌病发展中的作用.     

多因子联合调控致病毒性心肌炎炎症通路研究进展

病毒性心肌炎（viralmyocarditis）是儿科心血管系统常见的疾病之一,近年来在我国的发病率逐渐上升。超过20％的患儿最终发展为扩张型心肌病,心脏移植是惟一的治疗方法。病毒性心肌炎是指嗜心肌病毒感染引起的心肌特异性间质性炎症,最常见的病原是柯萨奇病毒B组（coxsackievirus,CVB）。其发病机制尚未完全阐明,目前认为初期病毒的直接损害作用及继发的自身免疫损伤是该病主要的发病机制。     

应用聚合酶链式反应探讨肠道病毒感染与病毒性心肌炎及扩张型心？…

一般认为 ,肠道柯萨奇 B(Coxsackie B,COXB)病毒引起的心肌炎是青少年猝死的重要原因 ,亦是扩张型心肌病 (DilateclCardiomoputhy,DCM)的重要发病基础。我们应用聚合酶链式反应 (PCR)方法对 72例患者进行血中白细胞和心肌组织肠道病毒的检测 ,探讨该方法 ,对病毒性心肌炎 (Virus myocarditir,VMC)诊断的价值 ,以及在心肌炎病毒感染持续存在时向扩张型心肌病发展中的作用。1　材料与方法1.1　实验对象及分组1.1.1　心肌炎组 34例 ,年龄 2 1～ 45岁 ,男 14例 ,女 2 0例 ,汉族 2 4例 ,维族 10例。诊断符合 1995年全国心肌炎心肌病专题…     

小儿病毒性心肌炎50例分析

病毒性心肌炎是一种小儿常见的后天性心脏病,部分患儿起病隐匿,长年不愈,可演变为扩张型心肌病,预后不良,而急重症病毒性心肌炎则常危及患儿的生命,故及时、准确地诊断病毒性心肌炎对治疗该病显得尤为重要。     

肥厚型心肌病与扩张型心肌病分子机制研究进展

分子遗传学研究表明,肥厚型心肌病和扩张型心肌病的发病机制主要是心肌细胞肌小节的基因突变,但扩张型心肌病突变区域及种类具有多样性和严重性,同时扩张型心肌病也发生在除肌小节外的其他区域。本文比较肥厚型心肌病和扩张型心肌病分子机制的异同性以及二者研究的最新进展。     

急性心肌炎和扩张型心肌病患儿血清TNF—α测定及意义

测定２６例急性心肌为和２３例扩张型心肌病患儿血清ＴＮＦ－α水平，并以３０例正常儿童对照。结果发现急性心肌炎和扩张型心肌病患儿血清ＴＮＦ－α水平较对照组明显升高。表明ＴＮＦ－α在急性心肌炎和扩张型心肌病心肌损伤的发病机理方面可能起着重要作用。     

多肽抗原检测心肌肌球蛋白重链抗体方法研究

目的建立抗肌球蛋白重链(AMHC)自身抗体的间接酶联免疫吸附法(ELISA),并探讨此抗体与病毒性心脏病的关系。方法以合成肽作为抗原,建立ELISA方法,检测心肌炎40例,扩张型心肌病48例和30名正常人血清中AMHC自身抗体。结果阳性血清批内和批间变异系数分别为0.086与0.127,用抗原吸收后,吸光度(A)值下降了62.9%,慢性病毒性心肌炎,扩张型心肌病患者AMHC自身抗体阳性率分别为42.1%和47.9%,显著高于急性病毒性心肌炎组(9.5%)和正常对照组(3.3%)。结论用多肽抗原代替天然肌球蛋白检测AMHC自身抗体,特异性和敏感性高,操作简便,为临床开展心肌炎、心肌病的免疫学监测提供了新的检测方法。     

超声心动图对病毒性心肌炎发展为扩张型心肌病的动态观察

本文对36例病毒性心肌炎患者(均经1987年我国心肌炎心肌病座谈会订出的成人急性病毒性心肌炎诊断参考标准而确诊)进行了为期4年的追踪观察,发现其中11例有左心室扩大伴左心舒缩功能欠佳的患者最终演变为扩张型心肌病.     

Role of toll-like receptors in cardiovascular diseases

The discovery and characterization of the TLR (Toll-like receptor) family has led to a better understanding of the innate immune system. The strategy of innate immune recognition is based on the detection of constitutive and conserved products of micro-organisms. However, host molecules that are released during injury can also activate TLRs. Engagement of TLRs by microbial or host-derived molecules induces the expression of pro-inflammatory cytokines, which may have both beneficial and detrimental effects on the host. In addition to being expressed in immune cells, TLRs are expressed in other tissues such as those of the cardiovascular system. In the present review, the role of TLRs in septic cardiomyopathy, viral myocarditis, atherosclerosis, ischaemia/reperfusion injury and cardiac remodelling after myocardial infarction are outlined, with attention paid to genetically modified murine models. Although much has been learned about stress-induced TLR activation in the tissues of the cardiovascular system, the role of individual TLRs in initiating and integrating homoeostatic responses within the heart remains to be defined. Accumulating evidence indicates that TLRs may play an important role in the pathogenesis of atherosclerosis, viral myocarditis, dilated cardiomyopathy, cardiac allograft rejection and sepsis-induced left ventricular dysfunction. Moreover, heart failure of diverse aetiology is also now recognized to have an important immune component, with TLR signalling influencing the process of cardiac remodelling and prognosis. In the present review, we outline the biology of TLRs as well as the current experimental and clinical evidence for the role of TLRs in cardiovascular diseases.     

Diagnosis and Treatment of Viral Myocarditis

Myocarditis, an inflammatory disease of heart muscle, is an important cause of dilated cardiomyopathy worldwide. Viral infection is also an important cause of myocarditis, and the spectrum of viruses known to cause myocarditis has changed in the past 2 decades. Several new diagnostic methods, such as cardiac magnetic resonance imaging, are useful for diagnosing myocarditis. Endomyocardial biopsy may be used for patients with acute dilated cardiomyopathy associated with hemodynamic compromise, those with life-threatening arrhythmia, and those whose condition does not respond to conventional supportive therapy. Important prognostic variables include the degree of left and right ventricular dysfunction, heart block, and specific histopathological forms of myocarditis. We review diagnostic and therapeutic strategies for the treatment of viral myocarditis. English-language publications in PubMed and references from relevant articles published between January 1, 1985, and August 5, 2008, were analyzed. Main keywords searched were myocarditis, dilated cardiomyopathy, endomyocardial biopsy, cardiac magnetic resonance imaging, and immunotherapy.ACCF/AHA/ESC = American College of Cardiology Foundation/American Heart Association/European Society of Cardiology; CK-MB = creatine kinase—MB isoenzyme; DCM = dilated cardiomyopathy; ECMO = extracorporeal membrane oxygenation; EF = ejection fraction; LV = left ventricular; LVEF = left ventricular ejection fraction; MRI = magnetic resonance imaging; PCR = polymerase chain reactionMyocarditis is an important and often unrecognized cause of dilated cardiomyopathy (DCM). It is defined as inflammation of the heart muscle that may be identified by clinical or histopathologic criteria. Recent developments in the diagnosis and treatment of patients with suspected myocarditis include improved histologic criteria and use of cardiac magnetic resonance imaging (MRI). The aim of this review is to provide a contemporary evidence-based approach to evaluation and treatment of patients with suspected myocarditis. Main keywords searched are as follows: myocarditis, dilated cardiomyopathy, endomyocardial biopsy, cardiac magnetic resonance imaging, and immunotherapy. Articles were screened on the premise of importance, quality, and relevance.     

Viral myocarditis--new aspects of pathomechanisms, diagnosis and therapy

The diagnosis of "viral myocarditis" remains uncertain in most cases, despite varied efforts to obtain diagnostic criteria and techniques. The combination of virological, histological and immunohistological data may offer an opportunity to improve diagnosis. The pathophysiological processes which are involved in the transition from myocarditis into dilated cardiomyopathy are still unclear. A variety of new data point out that viral infection induces a loss of self-tolerance and subsequent autoaggression towards myocardial structures. The management of viral myocarditis remains problematic and a specific form of therapy still does not exist. Studies on immune suppressive therapy are contradictory. Moreover, in these studies the diagnostic criteria were non-uniform and the number of patients was low. Nevertheless, immune suppressive therapy can be very effective in individual cases. But until now, a clear decision cannot be made on the selection of those patients who would respond favourably to immune suppressive therapy. Only controlled studies which consider the aetiology, the grade of clinical severity, the duration of clinical symptoms, the degree of cellular infiltration, and the histological alterations may answer the questions concerning the benefit of immune suppressive therapy for viral myocarditis and its sequelae. Until these studies are available, the general implementation of immune suppressive therapy in viral heart disease should not be recommended, especially in view of the incidence of side effects.     

Virus infection of the heart--unmet therapeutic needs

For over 50 years, viral infection has been recognized as an important trigger of acute myocarditis, inflammatory dilated cardiomyopathy (DCM) and congestive heart failure. Nevertheless, viral heart disease remains challenging to diagnose and treat. Improved diagnostic methods for myocarditis have led to a better understanding of its pathophysiology. The recognition of virus-mediated damage, inflammation and autoimmune dysregulation in these patients highlights the importance of differentiating between virus-positive and virus-negative inflammatory DCM. These insights have led to the development of novel treatment strategies, including intravenous immunoglobulin and interferon therapy for virus-positive patients. This article will focus on the pathogenesis of viral myocarditis, especially parvovirus B19-induced, its progression to inflammatory DCM and future treatment strategies.     

The efficacy of taktivin in patients with viral myocarditis and dilated cardiomyopathy

The aim of the present research was to study the efficacy of the immunomodulating agent T-activin in patients with viral myocarditis and dilated cardiomyopathy (DCMP). The data obtained indicate that under the influence of the general therapy with T-activin cellular immunity manifested positive changes and the patients with viral myocarditis and DCMP felt better.     

病毒性心肌炎向扩张型心肌病转变进展的诊断学特征

目的探讨病毒性心肌炎向扩张型心肌病转变进展的临床诊断学特征。 方法回顾性分析2021年9月3日山东省千佛山医院心内科收治的1例由病毒性心肌炎向扩张型心肌病转变患者9年来的临床资料。 结果患者自2012年3月,9年来5次因感冒后出现胸闷、心悸,服用药物控制不佳入院。9年来患者左室射血分数及室间隔厚度随时间显著上下波动,自2018年持续降低。2017年6月心脏MRI显示心室壁广泛变薄,左室舒张末期最大径60.15 mm。基因检测报告提示患者有扩张型心肌病,桥粒斑蛋白(DSP)基因C.2794-2 A>G位点突变,与临床表型相关。患者9年来规律服药且尽量规避疾病相关诱因,心脏的生理结构仍然出现了难以逆转的改变。 结论对于携带有致病基因的扩张型心肌病患者,其发生相关疾病的可能性更大,产生的损害更为严重。因此,推进个体化精准治疗,早期发现相关致病基因,对于早期发现病因、控制疾病进展具有非常重要的意义。     

A morphological analysis of the specimens obtained during endomyocardial biopsies in patients with a clinical diagnosis of dilated cardiomyopathy]

The authors summarize experience gained with a study of biopsy specimens obtained on endomyocardial biopsies from 88 patients with a clinical diagnosis of dilated cardiomyopathy. The diagnostic value of the study was equal to 70%. Dilated cardiomyopathy largely masked myocarditis and alcoholic cardiomyopathy which were diagnosed morphologically in 30 and 13% of the patients, respectively. No morphological alterations which would allow one to change the clinical diagnosis of dilated cardiomyopathy were discovered in 26% of cases. It has been shown that endomyocardial biopsy is an important tool of diagnosis. In order to introduce it on a broader scale, it is necessary that quantitative uniform criteria for the diagnosis of endomyocardial diseases, primarily myocarditis, be elaborated.