β受体阻滞剂对慢性充血性心力衰竭患者心动周期信号混沌特征的影响

目的　探讨 β受体阻滞剂对慢性充血性心力衰竭患者心动周期信号混沌特征的影响。　 方法　将用 β受体阻滞剂治疗的 2 3例慢性充血性心力衰竭患者的心动周期信号混沌特征参数与常规治疗组的心动周期信号混沌特征参数进行比较分析。　结果　β受体阻滞剂治疗组的心动周期信号混沌度参数 (Hrd、Hle、Hfd、Hcc)和总功率Tfp与常规治疗组相比显著增加 (P <0 0 5或P <0 0 1 ) ,功率谱参数Pvv、Pvr和Rvh较常规治疗组显著降低(P <0 0 5或P <0 0 1 ) ,但两组Phv和Phr相比差异无显著性 (P>0 0 5 )。　结论　β受体阻滞剂能显著提高慢性充血性心力衰竭患者心动周期信号的混沌度 ,降低交感神经活性 ,改善交感神经和迷走神经的平衡和心功能状态。     

心动周期信号混沌特征分析对慢性充血性心力衰竭患者预后的评价

目的 探讨心动周期信号混沌特征分析在判断慢性充血性心力衰竭患者预后中的临床应用价值。方法 对40例慢性充血性心力衰竭患者进行心动周期信号混沌特征分析,然后对其进行跟踪随访,了解其预后和转归。结果 随访12～36个月,平均(28±10)个月,12例死亡。死亡组与存活组比较,死亡组的混沌度参数(Hrd、Hle、Hfd、Hcc)显著降低(P<0.01);在功率频谱指标中,Pvv、Pvr、Pvh显著升高(P<0.01),Phv、Phr和Tfp显著降低(P<0.01)。结论 心动周期信号混沌特征分析是判断慢性充血性心力衰竭患者预后的一项有用指标,有助于对慢性充血性心力衰竭患者进行危险分层。     

β-阻断剂对慢性充血性心力衰竭患者心动周期信号混沌特征的影响

为探讨 β 阻断剂对慢性充血性心力衰竭 (简称心衰 )患者心动周期信号混沌特征的影响 ,将 4 6例慢性心衰患者治疗前与 30例正常健康对照组的心动周期信号混沌特征参数进行比较 ;再将 4 6例慢性心衰患者随机分为 β 阻断剂治疗组和常规治疗组 ,并将两组的心动周期信号混沌特征参数进行比较。结果 :4 6例慢性心衰患者治疗前的心动周期信号混沌度参数相对分散度 (Hrd)、李雅普诺夫指数 (Hle)、分维数 (Hfd)、混沌度 (Hcc)均较正常健康对照组显著降低 (P <0 .0 5或P <0 .0 1 ) ;功率频谱指标中 ,超低频段功率 (Pw)、超低频段相对功率 (Pvr)和超低频段与高频段功率 (Rvh)之比均较正常健康对照组显著升高 (P <0 .0 1 ) ,高频段功率 (Phv)、高频段相对功率 (Phr)和总功率(Tfp)均较正常对照组显著降低 (P <0 .0 1 )。β 阻断剂治疗组的心动周期信号混沌度参数Hrd、Hle、Hfd、Hcc和Tfp与常规治疗组相比显著增加 (P <0 .0 5或P <0 .0 1 ) ;功率谱参数中 ,Pw、Pvr和Pvh之比较常规治疗组显著降低 (P <0 .0 5或P <0 .0 1 ) ,但Phv和Phr两组相比差异无显著性 (P >0 .0 5 )。结论 :β 阻断剂能显著提高慢性充血性心衰患者心动周期信号的Hcc ,降低交感神经活性 ,改善交感神经和迷走神经的平衡状态     

老年充血性心力衰竭QT离散度与室性心律失常

观察了46例老年充血性心力衰竭患者QT离散度的变化及其与室性心动过速(PVT)和心室颤动(VF)发生之间的关系。结果表明,心衰患者的QT离散度和校正QT离散度显著增加,伴有PVT或VF发作的患者增加更为明显。QT离散度可以作为老年充血性心力衰竭患者发生恶性心律失常的预测指标之一。     

心血管系统疾病

心血管系统疾病１３０重症慢性充血性心力衰竭患者血清镁浓度的临床和预后意义［英］ＥｉｃｈｈｏｒｎＥＪ…ＪＡｍＣｏｌｌＣａｒｄｉｏｌ．－１９９３，２１．－６３４～６４０以前的资料提示低镁在室性心律失常发生方面起重要作用，并可能是充血性心力衰竭（ＣＨＦ）病...     

动态心电图监测分析心衰患者室性心律失常

目的分析充血性心力衰竭患者室性心律失常发生率及动态心电图监测的意义。方法应用24h动态心电图记录分析119例充血性心力衰竭患者,并按NYHA分级标准将其分为4组,比较各组间室性心律失常的发生率,及比较分析心功能分级与心律失常程度,并对其中54例心衰患者进行了为期3年的随访,以比较各组生存情况。结果室性心律失常的发生率随心衰级别的加重而升高。结论动态心电图24 h监测室性心律失常发生情况,对病情估计及预后判断极具临床价值。     

严重充血性心力衰竭患者中非持续性室性心动过速的高发生率

近来发现伴有室性心动过速的充血性心力衰竭患者猝死的危险性很大。但是在各种原因引起的严重心力衰竭病人中室性心动过速的发生率尚无所知。本文目的在于估价室性心律失常的发生率以及其对严重慢性充血性心力衰竭病人预后的潜在影响。方法:35名心功能为Ⅲ～Ⅳ级的充血性心力衰竭患者(6名女性,29名男性,年龄17～80岁),均未接受过抗心律失常的治疗,但使用了狄戈辛、利尿剂和硝酸酯等药物治疗。血清狄戈辛浓度和血钾均在正常范围。所有病员在室喷血分数<20％,出现心力衰竭已有6～94个月。其中31例为窦性心律,4例为心房颤动。18例患有缺血性心脏病,17例患有非缺血性心肌病。使用三腔漂浮气球囊热稀     

充血性心力衰竭 （9）心力衰竭伴发室性心律失常的处理和预后

充血性心力衰竭（９）心力衰竭伴发室性心律失常的处理和预后浙江医科大学附属第二医院吕俊陞１充血性心力衰竭并发室性心律失常的临床意义无血性心力衰竭（ＣＨＦ）并发室性心律失常，是指ＣＨＦ发生室性早搏、非持续性室性心动过速（ＮＳＶＴ）及持续性室性心动过速（Ｓ...     

硫酸镁治疗伴低钾、心律失常的慢性充血性心力衰竭的效果

本文报告用硫酸镁治疗21例慢性充血性心力衰竭、伴低钾和心律失常的患者,在常规抗心衰治疗下,补镁、补钾后,15例室性心律失常均消失。19例心功能在1周内改进一级（其中10例改进二级）,2例无效。提示低钾、心律失常的慢性充血性心力衰竭患者常合并机体缺镁,在常规治疗的同时注意补镁,可取得较好的疗效。     

老年慢性充血性心力衰竭患者血清内源性洋地黄样因子的初步研究

30例老年慢性充血性心力衰竭患者和20例正常人用放射免疫法测定血清内源性洋地黄样因子(EDF)浓度。结果显示:老年慢性充血性心力衰竭患者血清EDF浓度明显低于正常;心力衰竭纠正后,血清EDF浓度明显升高;心力衰竭程度、心律失常有无、原发病因、心力衰竭类型对血清EDF浓度无明显影响。     

A heart within a heart

A 44‐year‐old man with a history of end‐stage dilated cardiomyopathy status‐post orthotopic cardiac transplant 14 years ago presented for coronary angiography in preparation for re‐operative tricuspid valve replacement. Coronary angiography revealed an anomalous origin of the left coronary artery, with a common coronary trunk arising from the right coronary cusp and bifurcating into right and left main coronary arteries. Interestingly, the right and left coronary arteries coursed to form the shape of a heart, hence, a heart within a heart! © 2017 Wiley Periodicals, Inc.     

冠心病和心力衰竭

冠心病心力衰竭（简称冠心病心衰）顾名思义是指由于冠心病引起的心力衰竭,据统计大约65％的心力衰竭由冠状动脉疾病引发的。冠心病心衰在临床上分急性和慢性两种,急性心衰主要由急性心肌梗死和急性冠脉缺血诱发的心肌收缩或舒张功能异常所致,慢性心衰主要是心肌梗死后心肌重塑和心肌的血供长期不足,心肌组织发生营养障碍和萎缩,以致纤维组织增生所致。由于冠心病导致心衰的成因不同,因此治疗上的侧重点就会有所不同,下面就对冠心病心衰发病机制及诊治作一浅谈。     

Congenital heart disease and heart failure

The syndrome of heart failure in adult non-congenital heart disease patients includes myocardial disease and ventricular dysfunction. In the presence of congenital abnormalities the cause of heart failure is often multi-factorial and can be a result of the underlying anomaly, surgical intervention, or ventricular dysfunction. Despite the possible clinical similarities, the two conditions are fundamentally different. In congenital heart disease the neurohormonal system is already abnormal even in the absence of clinical manifestations of heart failure and, in many cases, exercise intolerance is related to cyanosis. The approach to heart failure management in the two etiologies might be similar. Preventative attempts to preserve ventricular function in coronary or valve disease parallels early reparative therapy in congenital heart disease Pharmacological therapy is common for the two conditions, despite the limited number of evidence-based recommendations for congenital diseases. In drug-resistant patients, cardiac electrical resynchronization is an established therapy for treating ventricular asynchrony in non-congenital heart failure sufferers, but has only recently been adopted in selected congenital cases. Due to this, congenital heart disease patients are managed in highly specialized unites in close cooperation with cardiologists and surgeons. The ideal follow-up protocol for such patients remains to be determined, particularly in those individuals with subclinical signs of residual cardiac dysfunction. Heart Fail Monit 2008;6(1):2-8.     

Ischemic heart disease and heart weight

Separate weights for heart ventricle walls and interventricular septa were analyzed in 110 hearts with autopsy findings of ischemic heart disease (coronary atherosclerosis, recent or old myocardial infarcts) and with no other cardiac or systemic causes of cardiac enlargement. In hearts with coronary atherosclerosis alone (without old or recent myocardial infarcts) no weight increase was observed in the left ventricle when compared to 29 controls. Patients having infarcts associated with nonstenosing atherosclerosis (less than 50% of the luminal diameter narrowed) of the coronaries had normal heart weights as well. On the contrary, infarcts associated with stenosing coronary sclerosis (narrowing more than 50%) showed significant signs of left ventricular weight increase, which is interpreted as compensatory heart hypertrophy. The greatest degree of hypertrophy was observed in hearts with left ventricular aneurysms.