冠心病无症状心肌缺血患者心率变异性分析

目的分析冠心病无症状心肌缺血(SMI)与心率变异性(HRV)的关系。方法选择86例冠心病无症状心肌缺血患者和52例健康人行24h动态心电图心率变异性对比,心率变异性分析包括正常RR间期标准差(SDNN),5min平均RR间期标准差(SDANN)等。结果冠心病无症状心肌缺血各时域指标依次减少与对照组比较,各参数差异有统计学意义(P<0.05)。结论冠心病无症状心肌缺血是冠心病患者心肌缺血最常见的一种表现形式,心肌缺血改变了自主神经调节的均衡性,而冠心病无症状心肌缺血的发生可能与心脏自主神经病变加重有关。     

2型糖尿病合并缺血性心脏病35例心率变异性临床分析

目的探讨2型糖尿病和2型糖尿病合并缺血性心脏病患者对心血管自主神经活动的影响。方法用24h力态心电图检测2型糖尿病患者78例,2型糖尿病合并心肌缺血患者35例及对照组48例健康人的心率变异性(HRV)指示结果2型糖尿病患者心率变异性指标比正常人明显减低,合并心肌缺血比没有合并心肌缺血的2型糖尿病患者,心率变异性指标仅rMSSD、PNN50减低。结论2型糖尿病患者存在植物神经损害,心率变异性减低,心率变异性减低程度亏心脏损害程度有关。合并心肌缺血患者对心血管自主神经损害较没有合并心肌缺血者重。     

老年2型糖尿病合并冠心病患者心率变异性与心脏自主神经病变研究

目的研究老年2型糖尿病合并冠心病患者心率变异性(HRV)与心脏自主神经病变关系。方法单纯2型糖尿病患者31例(Ⅰ组),2型糖尿病合并冠心病患者30例(Ⅱ组),健康对照组31例(Ⅲ组),动态心电图检测每例HRV时域指标,三组对比分析。结果三组HRV降低发生率分别为48.4%、73.3%、3.2%,差异具有统计学意义;三组SDNN、SDANN Index、SDNN Index各组间比较差异均具有统计学意义;rMSSD、PNN50Ⅱ组与Ⅲ组比较差异具有统计学意义,Ⅰ组与Ⅲ组比较差异无统计学意义。结论老年2型糖尿病合并冠心病患者HRV显著降低,较单纯2型糖尿病患者,迷走神经功能损害更重。     

动态心电图评价依帕司他对糖尿病心率变异性影响和疗效分析

目的:应用动态心电图评价依帕司他对糖尿病患者心率变异性的影响,确认依帕司他治疗糖尿病心脏自主神经病变的疗效。方法:收集糖尿病合并心脏自主神经病变患者100例,分为治疗组和对照组,治疗组患者口服依帕司他50 mg,tid,共8周。运用24 h动态心电图检测所有患者在治疗前后心率变异性指标的变化,观察依帕司他治疗糖尿病心脏自主神经病变的疗效。结果:治疗组心率变异性各项指标治疗2个疗程后较治疗前有显著提高,自主神经症状明显好转,与对照组比较有显著意义。结论:依帕司他治疗糖尿病心脏自主神经病变的疗效显著,可改善患者心率变异性。     

2型糖尿病患者心率变异性临床分析

目的探讨2型糖尿病（2-DM）对心血管自主神经活动的影响。方法对65例2型糖尿病患者及50例正常健康人进行24h动态心电图检测，所获资料经过Hotter分析处理系统，由计算机自动进行时域分析。结果2型糖尿病患者心率变异性各项指标比正常健康人明显减低。其中伴有心肌缺血（sT段下移）的糖尿病患者较无心肌缺血的糖尿病患者，心率变异各项性指标更低。结论2型糖尿病患者存在植物神经功能损害，心率变异性减低，心率变异性减低程度和心脏缺血受损程度相关。     

前列地尔治疗2型糖尿病合并颈动脉内膜增厚患者的心率变异性分析及临床意义

目的探讨前列地尔治疗2型糖尿病合并颈动脉内膜增厚患者的心率变异性分析及临床意义。方法选取2型糖尿病合并颈动脉内膜增厚患者121例,分为前列地尔脂微球载体注射液治疗组和丹参针治疗组,并与30例体检正常的正常组进行对照分析。观察治疗前后HolterHRV时域指标,评估心脏自主神经调节的功能。结果 2型糖尿病颈动脉内膜增厚组各HRV指标（SDNN,SDANN,RMSSD,PNN50,SDNN指数）均较正常组低（P均〈0.05）。前列地尔治疗前后各HRV指标有显著差异（P均〈0.05）。结论前列地尔治疗2型糖尿病合并颈动脉内膜增厚患者能改善其的自主神经调节功能。     

高血压合并2型糖尿病患者心率变异与颈动脉内中膜厚度的相关性分析

目的探讨高血压（EH）合并2型糖尿病（T2DM）患者心率变异（HRV）的改变及其与颈动脉内中膜厚度（IMT）的关系。方法选择27例高血压患者、22例高血压合并2型糖尿病患者和25例健康人进行24h动态心电图监测和颈动脉内中膜厚度测量。结果高血压组、高血压合并2型糖尿病组的SDNN、SDANN、RMSSD、SDNNidex较正常对照组均有明显减低（P〈0．01）,高血压合并2型糖尿病组较高血压组也有显著差异（P〈0．05）。高血压或高血压合并2型糖尿病伴颈动脉内中膜增厚者HRV参数较无增厚者有进一步的下降,而且HRV参数与IMT呈负相关。结论心率变异性分析可以作为早期发现高血压和（或）合并2型糖尿病患者心脏自主神经损伤的有价值的指标,HRV也是颈动脉粥样硬化的独立相关因素,可对大血管并发症作出早期的预测．有助于及时治疗,改善预后。     

老年2型糖尿病患者心率变异性与室性心律失常临床分析

自主神经病变是2型糖尿病最常见的并发症之一,目前认为心率变异性(HRV)是评估心脏自主神经活动的无创性指标。本文通过了解老年2型糖尿病、冠心病及糖尿病合并冠心病时的心率变异性改变,并结合室性心律失常的发生率进行临床分析。     

依帕司他对糖尿病患者心率变异性影响的评价

目的:评价依帕司他对糖尿病患者心率变异性的影响。方法:收集患者93例,分为治疗组和对照组,治疗组患者接受依帕司他50mg,每日3次治疗,服用4周,运用24小时动态心电图检测所有患者在治疗前后心率变异性指标的变化,明确依帕司他治疗糖尿病心脏自主神经病变的疗效。结果:治疗组心率变异性各项指标治疗4周后较治疗前有显著提高,自主神经症状明显好转,与对照组比较有显著意义。结论:依帕司他治疗糖尿病心脏自主神经病变的疗效显著,可以改善患者心率变异性。     

原发性高血压患者心率变异性的探讨

目的探讨原发性高血压患者自主神经功能变化。方法随机选择100例原发性高血压患者和97例正常人进行24小时心率变异性分析。结果高血压组患者心率变异性时域指标(SDNN、SDANN、SDNNindex、RMSSD)较对照组明显降低,其差异具有显著性(P<0.01)。结论原发性高血压患者自主神经系统功能存在一定程度损害。     

老年糖尿病患者心电图分析及临床护理

目的探讨心电图在发现老年糖尿病患者无症状心肌缺血中的作用与如何早期开展临床护理工作。方法对60例2型糖尿病患者心电图进行分析,与52例老年非糖尿病患者进行比较。结果糖尿病患者中,无症状心肌缺血发生的比例高于非糖尿病患者（P〈0.01）。结论糖尿病无症状心肌缺血发生率高,心电图对早期诊断有重要意义,早期临床护理工作的开展十分重要。     

动态心电图在老年女性冠心病患者无症状心肌缺血的研究

目的探讨老年女性冠心病患者无症状心肌缺血的发作特点及规律。方法选择老年女性冠心病采用12导联动态心电图记录系统,对109例冠心病患者连续监测24 h,结合患者生活日志分析诊断;109例分成三组：Ⅰ组单纯冠心病组（无高血压糖尿病）、Ⅱ组冠心病合并高血压组、Ⅲ组冠心病合并高血压与2型糖尿病。结果动态心电图检出老年女性冠心病患者心肌缺血主要为无症状心肌缺血（SMI）;SMI发生率Ⅲ组〉Ⅱ组〉Ⅰ组（P〈0.05）,Ⅲ组的SMI总次数与Ⅱ组、Ⅰ组比较有显著差异（P〈0.05）;SMI持续时间Ⅲ组与Ⅱ组比较有显著差异（P〈0.05）;三组的发作高峰均在上午,日间SMI发生次数明显多于夜间,夜间SMI发生比例Ⅲ组与Ⅰ组比较有显著差异（P〈0.05）,Ⅲ组昼夜SMI平均持续时间有显著差异（P〈0.05）。结论二级预防的老年女性冠心病人仍有较高的SMI发生率,应和有症状心肌缺血同样给予足够重视。高血压病、2型糖尿病均可增加老年女性冠心病患者SMI的发生,尤其是夜间的发生。动态心电图是老年女性冠心病,特别是合并高血压、2型糖尿病患者SMI的重要检测手段。     

46例2型糖尿病肾病与糖尿病自主神经病变的关系分析

目的：探讨2型糖尿病肾病与糖尿病自主神经病变的关系。方法：使用NHE－1000高频心电检测仪对46例2型糖尿病肾病患者及30例正常人进行心率变异性（HRV）分析。结果：2型糖尿病病人HRV各时域指标明显低于正常对照人群；临床DN组HRV下降更为显著于早期DN组。结论：两组糖尿病肾病与糖尿病自主神经病变并存，而且两者关系密切。     

急性脑梗死患者动态心电图和肌钙蛋白改变研究

目的探讨肌钙蛋白I（cTnI）改变与脑梗死、心肌缺血的关系;观察急性脑梗死患者心肌缺血（包括无症状心肌缺血）的发生率,为临床治疗提供依据。方法选择156例急性脑梗死患者,其中合并心肌缺血组103例（A组）,无心肌缺血组53例（B组）,患者均行颅脑CT和检测CTNI值并行动态心电图。结果 A组患者中无症状心肌缺血发生率高,尤其是合并糖尿病者（P〈0.05）;糖尿病与高低密度脂蛋白胆固醇（LDL-c）血症为脑梗死患者合并冠心病的独立危险因素。结论脑梗死合并冠心病发生率高,且无症状心肌缺血占比例较大。cTnI做为心肌损伤的特异敏感指标,在脑梗死时出现阳性提示存在心肌损伤。     

动态心电图检出无症状性心肌缺血的临床价值

目的:探讨24小时动态心电图对无症状心肌缺血(SMI)的临床价值.方法:回顾性分析520例患者进行24小时动态心电图检测的资料.结果:心肌缺血患者心律失常发生率明显高于无心肌缺血患者:无症状心肌缺血多发生于日间;心率变异性降低与心肌缺血之间有较好的相关性.结论:动态心电图早期检出SMI具有可靠的诊断价值.     

Regulation of cardiac nerves: a new paradigm in the management of sudden cardiac death?

The heart is extensively innervated, and its performance is tightly regulated by the autonomic nervous system. To maintain cardiac function, innervation density is stringently controlled, being high in the subepicardium and the central conduction system. In diseased hearts, cardiac innervation density varies, which in turn leads to sudden cardiac death. After myocardial infarction, sympathetic denervation is followed by reinnervation within the heart, leading to unbalanced neural activation and lethal arrhythmia. Diabetic sensory neuropathy causes silent myocardial ischemia, characterized by loss of pain perception during myocardial ischemia, which is a major cause of sudden cardiac death in diabetes mellitus (DM). Despite its clinical importance, the molecular mechanism underlying innervation density remains poorly understood. We found that cardiac sympathetic innervation is determined by the balance between neural chemoattraction and chemorepulsion, both of which occur in the heart. Nerve growth factor (NGF), which is a potent chemoattractant, is synthesized abundantly by cardiomyocytes and is induced by endothelin-1 upregulation in the heart. In contrast, Sema3a, which is a neural chemorepellent, is expressed strongly in the trabecular layer in early stage embryos and at a lower level after birth, leading to epicardial-to-endocardial transmural sympathetic innervation patterning. We also found that cardiac NGF downregulation is a cause of diabetic neuropathy, and that NGF supplementation rescues silent myocardial ischemia in DM. Both Sema3a-deficient and Sema3a-overexpressing mice showed sudden death or lethal arrhythmias due to disruption of innervation patterning. The present review focuses on the regulatory mechanisms involved in neural development in the heart and their critical roles in cardiac performance.     

Current concepts of silent myocardial ischemia

The definition, pathogenesis, incidence and characteristics, detection, treatment, and prognosis of silent myocardial ischemia (SMI) are reviewed. SMI is the occurrence of myocardial ischemia for which there is objective evidence (electrophysiological, hemodynamic, and metabolic changes) but no angina. Patients with SMI are classified as type 1 (completely asymptomatic), type 2 (SMI after myocardial infarction), and type 3 (both symptomatic and silent ischemia). Episodes of SMI are true ischemic events. The absence of pain may be due to defects in pain perception, an altered physiological response to ischemia, or a lesser degree of ischemia. The incidence of SMI is 2-5% in totally asymptomatic patients, 20-30% in patients who have suffered myocardial infarction, and 44-84% in patients who have symptomatic ischemia. SMI can be detected by exercise testing, portable electrocardiographic monitoring, or imaging techniques. Patients with SMI have more frequent adverse cardiac events (except death) than patients without SMI. The frequency of adverse cardiac events is similar in patients with angina and patients with SMI. SMI has been treated with nitrates, calcium-channel blockers, and beta blockers. Beta blockers appear to be the most consistent in reducing the number and duration of episodes. Combination therapy with beta blockers and nifedipine may be more effective than therapy with either agent alone. Because of the limited number of studies and the possible contribution to the results of spontaneous variability in the occurrence of SMI, no definite conclusions can be drawn about drug efficacy. There is no evidence that the prognosis of patients with SMI is altered by drug therapy; routine treatment with anti-ischemic drugs cannot be recommended. Patients must be evaluated individually, with aggressive management being reserved for those at high risk for myocardial infarction or other serious cardiac events.     

Optimization of cardiac metabolism in diabetes mellitus

Cardiovascular disease is a major health problem in all over the world. The prevalence of type 2 diabetes mellitus has been rapidly increasing, together with the risk for cardiovascular events. Patients with diabetes, and/or with insulin resistance as well, have an impaired myocardial metabolism of glucose and free fatty acids (FFA) and accelerated and diffuse atherogenesis, with involvement of peripheral coronary segments. Significant metabolic alterations in diabetic patients are the decreased utilization of glucose and the increase in muscular and myocardial FFA uptake and oxidation, occurring as a consequence of the mismatch between blood supply and cardiac metabolic requirements. These metabolic changes are responsible both for the increased susceptibility of the diabetic heart to myocardial ischemia and for a greater decrease of myocardial performance for a given amount of ischemia, compared to non diabetic hearts. A therapeutic approach aimed at an improvement of cardiac metabolism, through manipulations of the utilization of metabolic substrates, may improve myocardial ischemia and left ventricular function. Modulation of myocardial FFA metabolism, in addition to optimal medical therapy, should be the key target for metabolic interventions in patients with coronary artery disease and diabetes. In diabetic patients the effects of modulation of FFA metabolism should be even greater than those observed in patients without diabetes.     

多巴酚丁胺负荷试验结合多普勒评价无症状性心肌缺血左室节段与整体舒张功能

目的 探讨多普勒组织成像(DTI)结合多巴酚丁胺负荷超声心动图(DSE)评价无症状性心肌缺血患者左室局部与整体舒张功能的价值.方法 30例无症状性心肌缺血患者及正常人30例均行DSE,DTI在静息和负荷下于左房室瓣环、左室壁基底段、中间段取样,测量舒张功能参数:舒张早期速度(Ve),舒张晚期速度(Va),E峰减速时问(Te).结果 随着多巴酚丁胺药物剂量的增加,正常组峰值速度均逐渐增加,峰值速度运动时间逐渐缩短,大剂量时Ve/Va比值略有下降,差异无统计学意义;无症状性心肌缺血组峰值速度小剂量负荷时增加,大剂量时则下降,峰值速度运动时间呈逐渐缩短趋势,Ve/Va比值均显著降低,两组间各指标相比差异有统计学意义(P<0.05).结论 DTI技术与DSE结合可定量评价无症状性心肌缺血患者左室局部与整体舒张功能.