流行性腮腺炎并发心脏损害临床分析（附596例报告）

目的探讨流行性腮腺炎并发心脏损害的临床特点，提高对本病的认识。方法回顾分析596例流行性腮腺炎，其中并发35例心脏损害的临床资料，对其发生率、临床表现、辅助检查及治疗进行分析。结果流行性腮腺炎心脏损害发生率为5．87％，临床症状特异性差，主要表现心电图和心肌酶谱异常，治疗后心电图和心肌酶谱均恢复正常。结论流行性腮腺炎并发心脏损害，临床表现不典型，容易漏诊，需常规做心电图和心肌酶检查，一旦发现心脏损害，积极治疗，减少不良后果。     

急性酒精中毒对心脏损害98例临床分析

目的：探讨急性酒精中毒对心脏损害的程度。方法：回顾性分析162例急性酒精中毒病例0098例出现心脏损害的临床资料。结果：治疗后所有患者心电图均恢复正常,心肌酶除1例仍偏高外其余均正常,总有效率达98．9％。酒精中毒对心脏损害程度与中毒的时间和中毒的程度成正比。结论：急性酒精中毒尽早给予正确治疗是减少心肌损害的有效方法。     

肺炎支原体肺炎合并心肌损害30例分析

目的探讨肺炎支原体(MP)肺炎支原体肺炎合并心肌损害的临床特点及治疗措施。方法对517例MP肺炎支原体肺炎合并心肌损害的30例(5.80%)病历,进行回顾性分析。结果 30例心肌损害患儿中,5例(16.67%),临床症状稍重,心电图为多导联ST-T改变,房室传导阻滞等,心肌酶显著升高,特别是CK-MB最明显,符合心肌炎诊断;其余25例(83.33%),临床症状轻微,心电图正常或轻度异常,心肌酶不同程度升高。阿奇霉素及足量维生素C等治疗,27例(90%)心肌酶及心电图1~3周内恢复正常。结论肺炎支原体肺炎合并心肌损害,大部分患儿临床症状不典型,及时进行心肌酶谱和心电图检查,对早期诊断非常必要;阿奇霉素和足量维生素C治疗尚好。     

磷酸肌酸钠治疗婴幼儿轮状病毒肠炎并心肌损害疗效观察

目的：观察磷酸肌酸钠治疗婴幼儿轮状病毒肠炎并心肌损害的疗效。方法：将120例轮状病毒肠炎并心肌损害的患儿,随机分为对照组60例与治疗组60例,两组均给予补液、抗感染、纠正水电解质紊乱、酸中毒及对症治疗,在此基础上对照组加用大剂量维生素C、能量合剂等常规治疗。治疗组加用磷酸肌酸钠治疗,疗程均为7d。结果：治疗组患儿的心肌酶、心肌肌钙蛋白I（cTnI）下降快于对照组,心电图恢复正常率、总有效率高于对照组,两组差异均有统计学意义（P〈0.05）。结论：磷酸肌酸钠治疗婴幼儿轮状病毒性肠炎并心肌损害安全有效,值得临床推广应用。     

过敏性紫癜患儿并心脏损害的观察及护理

目的：观察和探讨过敏性紫癜患儿合并心脏损害的临床症状及治疗护理措施。方法：分析本科2005年5月～2008年12月收治的112例过敏性紫癜患儿中25例合并心脏损害的临床资料。结果：合并心脏损害的25例患儿中,表现为心前区不适、胸闷或心律失常。心电图示：频发室性早搏6例,Q—T间期延长4例,I°房室传导阻滞3例．窦性心动过速8例,窦性心动过缓2例,心肌劳损2例。有15例乳酸脱氢酶增高;11例血清肌酸磷酸激酶升高．且CK～MB明显增高,超声心动图未发现异常。经过治疗和周到的护理,1～3周后临床症状消失,心电图、心肌酶恢复正常。结论：过敏性紫癜合并心脏损害并不少见,但临床症状不典型．心电图、心肌酶有显著改变．遇到该类患儿要全面检查,以及时发现和诊治。     

36例儿童过敏性紫癜并发心肌损害的临床观察

目的 探讨儿童过敏性紫癜并发心肌损害的临床特点.方法 回顾分析我院36例过敏性紫癜并发心肌损害的患儿的病例特点和治疗过程.结果 36例患儿出院时心肌酶谱、心电图异常消失,2例左心室轻度扩大者及轻度1例,心包积液患儿复查心脏超声恢复正常.随访1～6个月,无并发症发生.结论 对过敏性紫癜的患儿临床应进行常规的心肌酶学、ECG检查,及早发现并治疗心肌损害,可避免严重并发症的发生.     

磷酸肌酸钠联合大剂量维生素C治疗轮状病毒肠炎并心肌损害疗效观察

目的：观察磷酸肌酸钠联合大剂量维生素C治疗轮状病毒肠炎并心肌损害的疗效。方法将180例轮状病毒肠炎并心肌损害的患儿,随机分为三组,分为对照组、治疗1组、治疗2组,分别60例。对照组给予大剂量维生素C治疗心肌损害,治疗1组及2组分别加用果糖二磷酸钠注射液及磷酸肌酸治疗,疗程均为7d。结果治疗2组患儿的心肌酶、心肌肌钙蛋白、B型钠尿肽下降均快于对照组,差异均有统计学意义（P〈0.05）。结论磷酸肌酸联合大剂量维生素C治疗婴幼儿轮状病毒肠炎并心肌损害临床效果好,值得广泛推广。     

儿童过敏性紫癜心肌损害时心肌酶谱、心肌肌钙蛋白检测的临床意义

目的：探讨过敏性紫癜（HSP）并发心肌损害时心肌酶谱、肌钙蛋白的变化及临床意义。方法：对2003年12月～2008年11月收治的28例过敏性紫癜并发心肌损害住院患儿的临床资料进行回顾性分析。入院24h内、入院后1周及恢复期分别测定心肌酶、心肌肌钙蛋白（cTnI）,同时做心电图。结果：发病初期AST、CK、CK—MB、HBDH、LDH、cTnI明显增高,尤以混合型增高更明显,在病情稳定后降至正常。结论：过敏性紫癜可造成心肌损伤,心肌酶谱、心肌肌钙蛋白的变化,能较好地反映心肌受损情况,及时发现心脏损害,为尽早治疗、减轻心肌损害提供实验室依据。     

轮状病毒肠炎患儿血清心肌酶谱检测及其临床意义

目的探讨轮状病毒（RV）肠炎惠儿的心肌酶谱变化及其对心脏的影响,为RV肠炎并发心肌损害提供客观依据,指导临床治疗。方法对确诊RV肠炎的85例患儿做心肌酶谱检测。结果24例血清心肌酶谱及各项均高于正常,其中5例CK—MB》75U／L,此5例心电图均提示QRS波低电压,ST段偏移,T波低平,24例患儿给予干扰素并辅以能量、维生素C、微生态等治疗。腹泻治愈一周后门诊复查心肌酶谱22例恢复正常,2例明显好转,5例心电图异常均恢复正常。结论RV肠炎可致部分忠儿心肌酶谱改变及心肌损害,应引起注意。     

儿童过敏性紫癜合并心脏损害的临床分析

目的：探讨过敏性紫癜（HSP）患儿心脏损害的发生率及其临床特点。方法：对2002年12月-2006年2月525例HSP住院患儿的临床资料进行回顾性分析，按有无心脏受损分为心脏受累组和无心脏受累组，分析两组患儿的临床表现及心脏损害的临床特点及HSP患儿合并心脏损害可能的高危因素。结果：HSP患儿心脏损害最常见的改变为心肌酶的升高，其次为心电图的改变；心肌受累组患儿与无心脏受累组相比，多脏器损害及肾脏受累的比例明显增高（P〈0．05）。结论：HSP心脏损害临床表现多数较轻，HSP多脏器损害症状多．脏器损害症状越重，心脏受累的概率越高，重症HSP患儿宜行心肌酶谱和心电图检查。     

冠心病患者血浆同型半胱氨酸与叶酸维生素B_(12)水平的相关性研究

目的　探讨冠心病 (CHD)患者血浆同型半胱氨酸 (Hcy)与叶酸、维生素 B1 2 浓度的变化及其相关性。方法　选择 76例经冠状动脉造影术证实为冠心病的患者 ,应用荧光偏振免疫分析法 (FPIA)测定血浆 Hcy浓度 ,离子捕获免疫分析法 (ICIA)测定血清叶酸浓度 ,非均相微粒子酶免疫分析法 (MEIA)测定血清维生素 B1 2 浓度。结果　冠心病患者血浆 Hcy浓度与正常对照组比较显著增高 (P<0 .0 0 1) ,而叶酸、维生素 B1 2 浓度则显著降低 (P<0 .0 0 1) ,以上两种变化呈负相关 (P<0 .0 0 1)。结论　高同型半胱氨酸血症是冠心病的新的独立危险因素 ,叶酸、维生素 B1 2 缺乏可能是诱发高 Hcy的重要因素。     

心肌致密化不全的超声诊断

目的通过对心肌致密化不全（NVM）的超声影像特征分析,探讨彩色多普勒超声心动图对该病的诊断及鉴别诊断。方法采用彩色多普勒超声心动图对临床心功能不全及心脏扩大的患者进行多切面扫查,以获取心脏形态、结构及血流信号,重点观察近心尖1/3的心肌与心内膜。结果 18例超声诊断为NVM,其中16例为左心室受累,2例右心室受累。超声心动图主要表现为：（1）左室或右室中、下1/3至心尖的心腔内可见异常粗大的肌小梁和其间深陷的隐窝;受累室壁增厚分为两层,致密层较薄而非致密层较厚,收缩末期非致密化层与致密化层之比〉2;（2）受累腔室扩大,室壁变薄,运动减弱,收缩增厚率减低;（3）彩色多普勒显示隐窝内的低速血流与心腔内高速血流相通。结论彩色多普勒超声心动图是诊断及鉴别诊断NVM的首选方法。     

Long-term coenzyme Q10 therapy: a major advance in the management of resistant myocardial failure

Coenzyme Q10 (CoQ10) treatment, orally administered as 100 mg daily dose, was initiated in a series of patients with advanced heart failure in an open, controlled design. They were all showing an insufficient response to classical therapy with diuretics and digitalis. Twelve patients with various causes of heart failure, classified clinically by echocardiography (ECHO), (12/12), and heart catheterization with endomyocardial biopsy, (10/12), were followed prospectively for a mean period of seven months. Serial assessments: Clinical examination (with questionnaire), ECG, chest X-ray, ECHO, systolic time intervals (STI) and blood levels of CoQ10 were performed. With a mean latency period of 30 days, eight out of 12 patients (67%) showed definite clinical improvement. Subjectively, the patients felt less tired, their general activity tolerance increased and dyspnoea at rest disappeared. There were obvious signs of decreased right-sided stasis (hepatic congestion). The heart rate fell significantly, and the heart volume (chest X-ray) decreased in the eight responders (although n.s.). A significant reduction in the left atrial size (ECHO) was registered, suggesting a reduced preload of the left ventricle, Furthermore, a significant decline in the PEP/LVET ratio (STI) was indicative of an improved myocardial performance. Preliminary CoQ10 withdrawal results showed severe clinical relapse with subsequent improvement on CoQ10 reinstatement, supporting the interpretation that treatment of these patients corrected a myocardial deficiency of CoQ10 and increased contractility. Hence CoQ10 appears to be an effective therapeutic agent in advanced cases of heart failure. This is an attractive circumvention of the traditional principles of therapy: supporting the myocardium directly by ameliorating a supposed underlying mitochondrial dysfunction (exhausted bioenergetics).     

轮状病毒肠炎合并病毒性心肌炎临床特点及治疗分析

目的：探讨轮状病毒肠炎合并病毒性心肌炎的临床特点。方法：随机抽取我院2003年7月-2004年7月轮状病毒性肠炎242例。对其临床特点及治疗进行回顾性分析。结果：242例中合并病毒性心肌炎者133例;心肌酶阳性率高达97．93％,特异性仅为56．12％．心电图特异性76．88％。结论：轮状病毒肠炎易伴发病毒性心肌炎,心肌酶和心电图结合分析对轮状病毒肠炎合并病毒性心肌炎有重要的诊断价值。     

补救性冠脉支架置入患者血C-反应蛋白水平变化

目的观察补救性冠脉支架置入对急性心肌梗死(AMI)患者C-反应蛋白(CRP)水平的影响。方法52例AMI静脉溶栓失败患者分为两组。A组32例,静脉溶栓失败2周后行冠状动脉造影并对病变血管置入冠脉支架;B组20例,溶栓失败90min内急诊对"罪犯血管"补救性置入冠脉支架。全部患者分别于溶栓前、后或补救性冠脉支架置入术后1、2、3、7d采集静脉血测定CRP水平。结果A组溶栓前CRP为(9.26±5.21)mg/L,支架置入后1、2、3d血清CRP水平和溶栓前比较无显著性差异(P>0.05),支架置入后7dCRP水平较溶栓前明显降低(≤3mg/L,P<0.01)。B组溶栓前CRP为(8.79±4.85)mg/L,溶栓及补救性冠脉支架术后1、2、3dCRP水平高于溶栓前(P<0.01);支架置入后第7d两组CRP水平比较无显著性差异(P>0.05)。结论AMI静脉溶栓失败行补救性冠脉支架置入术后血CRP水平升高明显,可能与局部炎症反应或局部血管内膜撕裂有关。     

斑蝥酸钠维生素B6注射液联合化疗治疗晚期肺癌

目的:评价斑蝥酸钠维生素B₆注射液联合化疗治疗晚期非小细胞肺癌的临床疗效及不良反应。方法:将68例晚期非小细胞肺癌患者随机分为两组,治疗组（35例）给予斑蝥酸钠维生素B₆注射液25 ml,同时进行多西紫杉醇联合奈达铂化疗,对照组（33例）予单纯联合化疗。治疗2周期后评价两组的疗效、毒副反应及生活质量改变。结果:治疗组、对照组的有效率分别为54.29%和24.27%（P<0.05）。治疗组患者生活质量提高率高于对照组（P<0.05）,毒性反应小于对照组（P<0.05）。结论:斑蝥酸钠维生素B₆注射液联合化疗治疗晚期非小细胞肺癌可提高临床疗效,改善患者的生活质量,同时可减少化疗毒副反应。     

Effects of selenium deficiency on the response of cardiac tissue to ischemia and reperfusion

Over a 10-week period, female Wistar rats received a diet containing a low level of selenium, cofactor of the antioxidant enzyme glutathione peroxidase (GPx) in order to examine the influence of deficiency of this trace element (i) on tissue antioxidant enzyme defence systems, and (ii) on the susceptibility of the myocardium to ischemia-reperfusion injury. At the end of the dietary treatment, hearts were perfused at constant flow (11 ml/min) before being subjected to 15 min of global normothermic ischemia, followed by 30 min of reperfusion. The effects of selenium deficiency were estimated by studying functional recovery of various cardiac parameters (left ventricular developed pressure LVDevP, heart rate HR, and the product HR x LVDevP), as well as ultrastructural tissue characteristics. Furthermore, superoxide dismutase (SOD) and glutathione peroxidase (GPx) activities were measured at the end of the reperfusion period. Results suggest that: (a) the activity of GPx is decreased by selenium deficiency while SOD activity remains unchanged, (b) the recovery of cardiac function and myocardial ventricular ultrastructure during reperfusion are altered in the selenium-deficient group compared to controls. These results illustrate the crucial role that selenium, the co-factor of one of the major antioxidant enzymes of the myocardium, plays in determining the vulnerability of the heart to ischemia and reperfusion.     

1,6-二磷酸果糖治疗急性一氧化碳中毒性心肌损伤

目的观察1,6-二磷酸果糖在急性一氧化碳中毒所致心肌损伤患者的治疗作用。方法一氧化碳中毒心肌损伤患者98例,随机分为观察组与对照组各49例。两组均给予常规治疗,观察组在此基础加用1,6-二磷酸果糖治疗,为期10d。比较两组治疗前后心肌酶学、心电图的变化。结果两组患者均可见到明显的心肌酶学下降,心电图的改善,自觉症状的好转。但实验组心肌酶学下降速度更快,心电图好转率明显高于对照组,未见明显毒副作用。结论早期使用1,6-二磷酸果糖可有效保护心脏,缩短心肌损伤恢复时间。     

冠状动脉造影诊断冠心病的价值探讨

目的：研究冠状动脉造影在冠心病诊断中的临床应用价值。方法选取临床拟诊的冠心病患者108例为研究对象,所有患者均经静息心电图、动态心电图、超声心动图及冠状动脉造影检查,并结合相关文献,研究冠心病诊断“金标准”-冠状动脉造影的应用价值。结果108例受检者,冠状动脉造影诊断冠心病74例,阳性检出率68．5％;静息心电图、动态心电图及超声心动图与冠状动脉造影检查结果差异均有统计学意义（χ2＝84．43、6．37、163．55,均P＜0．05）。单支病变中19例冠状动脉造影未见明显狭窄（狭窄＜50％）或正常,而根据超声心动图、心电图表现及家族史或高血压等高危因素,临床作出了冠心病的诊断。结论冠状动脉造影作为冠心病诊断最重要的微创手段,与其他无创检查方法相比,对冠心病的检出率及准确性高,并可明确冠状动脉病变位置、范围,宜作为冠心病诊断的常规方法。     

BCNU-induced gR2 DEFECT mediates S-glutathionylation of Complex I and respiratory uncoupling in myocardium

A deficiency of mitochondrial glutathione reductase (or GR2) is capable of adversely affecting the reduction of GSSG and increasing mitochondrial oxidative stress. BCNU [1,3-bis (2-chloroethyl)-1-nitrosourea] is an anticancer agent and known inhibitor of cytosolic GR ex vivo and in vivo. Here we tested the hypothesis that a BCNU-induced GR2 defect contributes to mitochondrial dysfunction and subsequent impairment of heart function. Intraperitoneal administration of BCNU (40 mg/kg) specifically inhibited GR2 activity by 79.8 ± 2.7% in the mitochondria of rat heart. However, BCNU treatment modestly enhanced the activities of mitochondrial Complex I and other ETC components. The cardiac function of BCNU-treated rats was analyzed by echocardiography, revealing a systolic dysfunction associated with decreased ejection fraction, decreased cardiac output, and an increase in left ventricular internal dimension and left ventricular volume in systole. The respiratory control index of isolated mitochondria from the myocardium was moderately decreased after BCNU treatment, whereas NADH-linked uncoupling of oxygen consumption was significantly enhanced. Extracellular flux analysis to measure the fatty acid oxidation of myocytes indicated a 20% enhancement after BCNU treatment. When the mitochondria were immunoblotted with antibodies against GSH and UCP3, both protein S-glutathionylation of Complex I and expression of UCP3 were significantly up-regulated. Overexpression of SOD2 in the myocardium significantly reversed BCNU-induced GR2 inhibition and mitochondrial impairment. In conclusion, BCNU-mediated cardiotoxicity is characterized by the GR2 deficiency that negatively regulates heart function by impairing mitochondrial integrity, increasing oxidative stress with Complex I S-glutathionylation, and enhancing uncoupling of mitochondrial respiration.