周口地区感染性心内膜炎患者的致病菌与临床特征研究

目的:探讨感染性心内膜炎患者的致病菌与临床特征,以期为感染性心内膜炎患者的诊治和改善患者预后提供理论依据。方法:选择2016年5月至2018年6月在我院心内科接受治疗的感染性心内膜炎患者94例,详细记录患者的临床资料,对导致患者发生感染性心内膜炎的基础病因进行统计和分析。利用血培养方式鉴别感染性心内膜炎患者的致病菌类型,对94例患者入院后的临床表现和超声心动图结果进行统计分析,记录所有患者的治疗方式和不同治疗方式下的临床疗效。结果:94例患者经过血培养发现感染阳性患者75例,以革兰阳性菌为主,占比58.4%;分离出革兰阴性菌共33株;分离出真菌共9株,占比8.9%。导致感染性心内膜炎的基础病因中以先天性心脏病和风湿性心脏病为主。通过对患者的临床表现进行分析发现,有88例患者出现不同程度的发热。通过超声心动图检测,70例患者有赘生物。94例患者中有28例进行了外科手术治疗,另外66例患者选择内科治疗。手术治疗患者治疗总有效率为71.4%,内科治疗患者治疗总有效率为53.0%。外科手术治疗的效果要优于内科治疗。结论:感染性心内膜炎患者的致病菌主要以草绿色链球菌、铜绿假单胞菌、大肠埃希菌为主。患者的临床表现以发热为主,超声心动图中有赘生物是主要表现;外科手术治疗效果好。     

感染性心内膜炎的预后与相关因素分析

目的 分析感染性心内膜炎的预后与相关因素的分析。方法 对４１例感染性心内膜炎的诊治过程、临床表现以及出院时的状况进行综合分析。结果 ４１例中２７例有不同程度的并发症，其中１４例死亡、心功能状况、抗生素开始使用时间及疗程及并发症有关，而性别、病变部位、原来是否有器质性心脏病变无明显关系。结论 及是诊断、早期、足量、长疗程使用抗生素是改善感染性心内膜炎预后的关键。     

感染性心内膜炎患者临床特征与预后影响因素分析

目的 对我院收治的感染性心内膜炎患者的临床特征进行观察分析,了解分析各类对于患者预后的影响因素,为今后感染性心内膜炎患者的治疗及术后恢复提供参考。方法 2016年6月~2017年6月黑龙江省佳木斯市中心医院共收治符合本次研究要求的感染性心内膜炎患者80例,回顾性分析患者的临床资料及病例特征,应用多因素Logistic回归的方法对影响患者预后的因素进行总结分析。结果 统计学结果显示,80例患有感染性心内膜炎患者当中,75例存在基础性心脏疾病（93.75%）,患者具体临床特征如下,发热温度≥39 ℃,患病时间范围77 d~89 d,血清白蛋白≤30 g/l,血红蛋白含量≤90 g/L,患者不同程度存在胸痛或者胸闷的症状。心脏功能,病原菌类型以及患者术后营养水平均是术后影响患者预后的独立影响因素。结论 感染性心内膜炎患者多伴随患有基础性心脏疾病,心脏功能,病原菌类型以及患者术后营养水平均是术后影响患者预后的独立影响因素。     

感染性心内膜炎合并急性肾损伤的临床特点和手术预后分析

目的分析感染性心内膜炎(IE)合并急性肾损伤(AKI)的诊治和预后情况,评判手术治疗对预后的影响。方法回顾性分析北京协和医院2010年1月至2016年5月45例IE合并AKI患者的临床资料,其中包括8例肾脏病理组织学改变;将患者分为手术(22例)和非手术组(23例),比较两组的临床资料和预后。结果本组资料男女比2.46∶1,发病年龄(48.3±16.6)岁。35.6%有基础瓣膜疾病,先天性瓣膜疾病最常见。好发感染瓣膜依次为二尖瓣(46.7%)、主动脉瓣(28.9%)和人工瓣膜(8.9%)。常见的感染病原为链球菌(46.7%)和葡萄球菌(35.6%),感染病原中也可见部分少见及特殊类型。肾脏表现中,尿潜血和尿蛋白的比例分别为82.2%和64.4%;8例肾活检病理中,新月体肾炎3例,局灶增生性肾炎和系膜增生性肾炎各2例,急性间质性肾炎1例;免疫荧光最常见的形式是C3沉积。手术和非手术患者基线资料、手术存活率无显著差别,但手术组肾功能恢复显著优于非手术组(P0.05),血清肌酐在术后7 d和30 d即较术前显著下降(P0.05和P0.01)。结论 IE的基础疾病和感染病原学较传统记载存在变化,IE导致肾实质损害时,新月体肾炎并非少见;适时手术有利于改善IE合并AKI患者的肾脏预后。     

18例感染性心内膜炎尸检资料临床病理分析

感染性心内膜炎(IE)是较常见的心脏疾患,由于抗生素的广泛使用及其他原因,不典型病例增多,加之原有心脏病及并发症,更使临床表现复杂因而诊断困难,为探讨IE临床与病理的联系,提高对本病的认识水平,现将我院1965～1 987年18例尸检资料作一对照分析。 1 对象与方法 18例均为住院死亡病例,死后24 h内进行尸检,其中5例仅进行心、肺局部剖检。各     

感染性心内膜炎48例分析

目的分析感染性心内膜炎临床特点的变化。方法回顾性分析近年来我院收治的48例感染性心内膜炎患者的临床资料。结果 48例患者中,〈40岁28例,〉40岁20例;21例患先天性心脏病,23例患风湿性心脏病,6例老年性瓣膜退行性改变;23例血培养阳性,其中金黄色葡萄球菌11例,链球菌9例。结论随着抗生素的广泛使用,感染性心内膜炎致病菌发生了变化,先天性心脏病、风湿性心脏病为常见基础疾病,老年性疾病也逐渐增加,超声心动图及血培养有助于疾病诊断。     

感染性心内膜炎48例分析

目的 分析感染性心内膜炎临床特点的变化.方法 回顾性分析近年来我院收治的48例感染性心内膜炎患者的临床资料.结果 48例患者中,＜40岁28例,＞40岁20例;21例患先天性心脏病,23例患风湿性心脏病,6例老年性瓣膜退行性改变;23例血培养阳性,其中金黄色葡萄球菌11例,链球菌9例.结论 随着抗生素的广泛使用,感染性心内膜炎致病菌发生了变化,先天性心脏病、风湿性心脏病为常见基础疾病,老年性疾病也逐渐增加,超声心动图及血培养有助于疾病诊断.     

超声在诊断感染性心内膜炎的临床价值

目的 探讨临床上应用超声心动图的特点来诊断感染性心内膜炎的诊断价值.方法 回顾80例均已确诊为感染性心内膜炎患者的临床资料,并且结合诊断时超声心动图的检查进行综合分析.结果 80例患者中其中72例患者有基础心脏病,临床特征表现占比为:脾肿大患者50例,占比为62.5%、发热患者76例,占比为95%、栓塞患者16例,占比为20%.80例患者都作了血培养,培养结果阳性患者43例,占53.75%.超声心动图检查,发现赘生物67例,占83.75%.死亡3例,占3.75%.结论 虽然感染性心内膜炎具有典型的临床表现,大部分患者血培养检测为阴性,但是在早期诊断上还是存在一定困难,通过超声心动图检查可以看到患者的病理特点赘生物,不但为该病的诊断和病因提供了依据,     

22例先天性心脏病的临床分析

目的：为减少先心病的发生,需了解先心病的发病率、病因及其死亡率。方法：总结分析因围产儿出生缺陷监测资料。结果：先心病的发病率为0.60‰,其病因复杂,死亡率为77.2%,结论：父母的职业与疾病对先心病的发生,可能有影响;患儿的死亡取决于心脏畸形的严重程度和是否伴有并发症,也与早产有关。     

新生儿先天性心脏病的临床分析

本文对1978年以来在我院就诊的22例新生儿先天性心脏病进行临床分析，其中足月儿18例，早产儿4例，3例于新生儿期死亡均做了尸检，证实青紫型先心病2例，及晚期青紫型1例。对存活的19例患儿，经临床随诊心脏手术证实青紫型4例，晚期青紫型15例，非青紫型3例。先心病主要临床表现是：苍白、脉弱、肢体软、青紫和心力衰竭，此外为呼吸快及心源性休克的表现。对一部分无心杂音的患儿，应及时做辅助检查以防漏诊。     

Chromosome abnormalities in congenital heart disease

Refinements in cytogenetic techniques have promoted progress in understanding the role that chromosome abnormalities play in the cause of congenital heart disease. To determine if mutations at specific loci cause congenital heart disease, irrespective of the presence of other defects, and to estimate the prevalence of chromosome abnormalities in selected conotruncal cardiac defects, we reviewed retrospectively cytogenetic and clinical databases at St. Louis Children's Hospital. Patients with known 7q11.23 deletion (Williams syndrome), Ullrich-Turner syndrome (UTS), and most autosomal trisomies were excluded from this analysis. Two groups of patients were studied. Over a 6.5-year period, 57 patients with chromosomal abnormalities and congenital heart disease were identified. Of these, 37 had 22q11 deletions; 5 had abnormalities of 8p; and 15 had several other chromosome abnormalities. The prevalence of chromosome abnormalities in selected conotruncal or aortic arch defects was estimated by analysis of a subgroup of patients from a recent 22-month period. Chromosome abnormalities were present in 12% of patients with tetralogy of Fallot, 26% in tetralogy of Fallot/pulmonary atresia, 44% in interrupted aortic arch, 12% in truncus arteriosus, 5% in double outlet right ventricle, and 60% in absent pulmonary valve. We conclude that chromosome analysis should be considered in patients with certain cardiac defects. Specifically, fluorescent in situ hybridization (FISH) analysis of 22q11 is indicated in patients with conotruncal defects or interrupted aortic arch. High resolution analysis should include careful evaluation of the 8p region in patients with either conotruncal or endocardial cushion defects. Am. J. Med. Genet. 70:292–298, 1997. © 1997 Wiley-Liss, Inc.     

Sir A.E. Garrod,congenital heart disease in Down syndrome,and the doctrine of fetal endocarditis

Archibald Garrod was apparently the first to document congenital heart disease as a component of Down syndrome. This arose from his interest in fetal endocarditis, a theoretical cause of cardiac malformations, in vogue roughly from 1840–1940, that drew its strength from analogies with rheumatic heart disease in adults. Garrod's discovery sheds light not only on nineteenth century ideas about teratology, but also on his methodology, genius, and approaches that, in many ways, foreshadowed the techniques that guided his later work on inborn errors.     

Recent progress in the molecular genetics of congenital heart defects

Congenital heart defects (CHD) constitute the single most common anatomic class of birth defects and are a major cause of infant mortality. Correlation of normal and pathological embryology/anatomy has led to the formulation of mechanistic models, but there is limited understanding of the genetic basis for the inferred embryological processes. Most evidence points to extensive etiologic heterogeneity and a re-evaluation of simple multifactorial models is required. The recent identification of several genes responsible for congenital heart defects in the context of more complex clinical disorders provides significant entry points for the genetic analysis of human heart development. The association of aneusomies (particularly microdeletion syndromes) with specific cardiac lesions provides further strong support for mechanistic classification. Studies in the mouse are laying the groundwork for a comprehensive genetic model of cardiac organogenesis. Nevertheless, the basis for the large majority of CHD, especially isolated defects, remains obscure. Dissection of the genetic components of CHD is one of the greatest challenges in medical genetics for the coming decades.     

Adults with congenital heart disease: patients' knowledge and concerns about inheritance

With recent advances in medical and surgical management, most patients with congenital heart disease (CHD) survive to reproductive age. Current guidelines recommend counseling about inheritance and transmission of CHD to offspring. We evaluated whether adult CHD patients recalled having received information about the inheritance of their CHD, patients' knowledge about inheritance and their concerns in this regard. A questionnaire was sent to 486 non-syndromic CHD patients aged 20-45 years. We received 332 useful questionnaires (response rate 68%). One-third (33%) of patients recalled receiving information about inheritance of CHD from their cardiologist, and 13% had consulted a clinical geneticist. Eight percent of patients who were considering having children estimated the recurrence risk for their own offspring to be 1% or lower, whereas one-fourth (25%) estimated it to be higher than 10%. According to our classification, 44% estimated the recurrence risk in a correct range of magnitude. Additional information about inheritance of CHD was desired by 41% of patients. Forty-two percent of patients considering having children reported concerns about transmitting CHD to offspring. We conclude that a substantial proportion of adult CHD patients lacks knowledge and desires more information about inheritance, indicating a need for better patient education. Current guidelines and/or their implementation do not seem to meet the needs of these patients. A dedicated program of counseling for adults with CHD has to be developed to optimize knowledge and satisfaction with information provision and to reduce or manage concerns regarding inheritance of CHD.     

Maternal age and prevalence of isolated congenital heart defects in an urban area of the United States

Although maternal age has been associated with a number of birth defects in several reports, the literature on the association of maternal age with isolated congenital heart defect (CHD) phenotypes has been limited. We evaluated CHD prevalence based on a cohort of 5,289 infants and fetuses with isolated CHDs born during the period 1968–2005 and ascertained by the Metropolitan Atlanta Congenital Defects Program (MACDP) among residents of five central counties in Atlanta. For our denominator, we obtained information on births to residents of the same counties from vital records (n = 1,301,143). We calculated prevalence ratios for 23 CHD phenotypes by several maternal age categories, using the group 25–29 years of age as a reference group. We used Poisson regression models to estimate adjusted prevalence ratios (aPRs) and 95% confidence intervals (CIs), controlling for maternal race, infant sex, and birth cohort. A maternal age of 35 years or older was associated with an increased prevalence for several CHD phenotypes: laterality defects (aPR = 2.06; CI 1.22–3.48), all conotruncal defects (aPR = 1.30; CI 1.03–1.65), and specifically for dextro‐transposition of the great arteries (aPR = 1.65; CI 1.10–2.48), coarctation of the aorta (aPR = 1.54; CI 1.10–2.16), ventricular septal defects (aPR = 1.20; CI 1.06–1.36), and atrial septal defects (aPR = 1.36; CI 1.05–1.77). Our findings suggest that the birth prevalence of specific isolated CHDs varies with maternal age. Further studies are warranted to corroborate these observations, taking into account potential confounding by known modifiable risk factors. Published 2011 Wiley‐Liss, Inc.     

Clinical manifestations of device-related infective endocarditis in cardiac resynchronization therapy recipients

IntroductionThe aim of the study was to analyse microbiological characteristics and clinical manifestations of cardiac device-related infective endocarditis (CDRIE) in cardiac resynchronization therapy (CRT) recipients, and to compare the diagnostic value of modified Duke (MDC) versus modified Duke lead criteria (MDLC; including to MDC local infection and pulmonary infection or embolism as major criteria).Material and methodsThe study population comprised 765 consecutive CRT patients from a high-volume, tertiary care centre from 2002 to 2015. All patients were screened for CDRIE.ResultsDuring a median follow-up of 1692 days (range: 457–3067) 5.36% of patients (n = 41) developed CDRIE, which was accompanied by CRT pocket infection in 17.1% (n = 7) and recurrent pulmonary infection or pulmonary embolism in 29.3% (n = 12). Fever was present in 95.1% of patients (n = 39), whereas blood cultures were positive in 65.9% (n = 27). Staphylococcus was the most prevalent pathogen in 59.3% (n = 16), Gram-negative bacteria in 25.9% (n = 7). Transoesophageal echocardiography showed intracardiac vegetations in 73.2% of patients (n = 30). Non-different pathogen types with the most common methicillin-sensitive Staphylococcus aureus were observed for early versus late CDRIE (endocarditis ≤ 6 vs. > 6 months from CRT or other device-related procedure). All 3 inflammatory markers (C-reactive protein, white blood cells, procalcitonin) were normal in 4.9% of patients (n = 2). MDC versus MDLC indicated definite CDRIE in 48.8% versus 80.5%, respectively (p = 0.003).ConclusionsFever is the most common symptom of CRT-related CDRIE, and transoesophageal echocardiography allows vegetations to be visualised in nearly 3/4 of patients with CDRIE. Although the most common pathogens were Staphylococci, Gram-negative bacteria accounted for a quarter of CDRIE. Modified Duke lead criteria proved superior to MDC.     

The genetics of isolated congenital heart disease

The genetic mechanisms underlying congenital heart disease (CHD) are complex and remain incompletely understood. The majority of patients with CHD have an isolated heart defect without other organ system involvement, but the genetic basis of isolated CHD has been even more difficult to elucidate compared to syndromic CHD. Our understanding of the genetics of isolated CHD is advancing in large part due to advances in next generation sequencing, and the list of genes associated with CHD is rapidly expanding. Variants in hundreds of genes have been identified that may cause or contribute to CHD, but a genetic cause can still only be identified in about 20–30% of patients. Identifying a genetic cause for CHD can have an impact on clinical outcomes and prognosis and thus it is important for clinicians to understand when and what to test in patients with isolated CHD. This chapter reviews some of the known genetic mechanisms that contribute to isolated inherited and sporadic CHD as well as recommendations for evaluation and genetic testing in patients with isolated CHD.     

22q11.2 deletion syndrome and congenital heart disease

The 22q11.2 deletion syndrome has an estimated prevalence of 1 in 4–6,000 livebirths. The phenotype varies widely; the most common features include: facial dysmorphia, hypocalcemia, palate and speech disorders, feeding and gastrointestinal disorders, immunodeficiency, recurrent infections, neurodevelopmental and psychiatric disorders, and congenital heart disease. Approximately 60–80% of patients have a cardiac malformation most commonly including a subset of conotruncal defects (tetralogy of Fallot, truncus arteriosus, interrupted aortic arch type B), conoventricular and/or atrial septal defects, and aortic arch anomalies. Cardiac patients with a 22q11.2 deletion do not generally experience higher mortality upon surgical intervention but suffer more peri‐operative complications than their non‐syndromic counterparts. New guidelines suggest screening for a 22q11.2 deletion in the patient with tetralogy of Fallot, truncus arteriosus, interrupted aortic arch type B, conoventricular septal defects as well as those with an isolated aortic arch anomaly. Early identification of a 22q11.2 deletion in the neonate or infant when other syndromic features may not be apparent allows for timely parental screening for reproductive counseling and anticipatory evaluation of cardiac and noncardiac features. Screening the at‐risk child or adult allows for important age‐specific clinical, neurodevelopmental, psychiatric, and reproductive issues to be addressed.