比索洛尔对心力衰竭患者心功能及血淋巴细胞内游离钙浓度的影响

比索洛尔对心力衰竭患者心功能及血淋巴细胞内游离钙浓度的影响     

比索洛尔、依那普利和螺内酯联合治疗风湿性心脏病慢性心力衰竭的效果

目的:观察比索洛尔、依那普利和螺内酯联合治疗风湿性心脏病（风心病）慢性心力衰竭（心衰,CHF）对心脏重构的影响。方法: 风心病并发心衰患者86例,随机分为比索洛尔、依那普利和螺内酯联合治疗组（试药组）以及常规治疗方案对照组（对照组）。在治疗后1年测定心功能与左室内径等指标。结果: 试药组左室舒张末期内径（LVEDD）、左室收缩末期内径（LVESD）显著下降,左室射血分数（LVEF）增加显著,与对照组比较有显著差异（均P<0．05）。结论: 比索洛尔、依那普利和螺内酯联合治疗治疗风心病心力衰竭较常规治疗方法在改善心衰,阻止心脏重构方面效果更好。     

国产富马比索洛尔耐受量及其对心功能的影响

目的 :观察国人对国产富马比索洛尔的最大耐受剂量 ,及其对心功能的影响。方法 :心力衰竭患者 5 6例 ,在口服地高辛、ACEI制剂、血管扩张剂 （非钙离子拮抗剂 ）和利尿剂等基本抗心力衰竭药物的基础上 ,加服富马比索洛尔。观察患者对此药的耐受性 ,同时在试验初始时和服药 7月后测定患者左室射血分数 （EF）等指标。结果 :心力衰竭患者服用富马比索洛尔的最大耐受剂量各不同 ,主要分布在 5 m g;随访 7月后 ,复查心脏 B超与试验初比较 ,EF值 （30 .5± 2 .3） % vs （42 .3± 3.2 ） % ,有极显著的改善 （P<0 .0 1）。结论 :在心力衰竭治疗用药的基础上 ,加用富马比索洛尔治疗 （按照个体化用药原则 ） ,国人对此药的耐受程度主要分布在 5 m g,治疗 7月后的心力衰竭患者心功能显著改善     

比索洛尔治疗扩张型心肌病心力衰竭的临床疗效及可能机制

为研究比索洛尔治疗扩张型心肌病（ＤＣＭ）心力衰竭的临床疗效及机制，对１９例ＤＣＭ心力衰竭（心衰）患者应用β＿１受体阻滞剂比索洛尔治疗３～１０个月，每日剂量１．２５～５（平均３．２±１．１）ｍｇ。经治疗后心功能改善，运动能力增强，心脏缩小，室性心律失常减轻。运动和异丙肾上腺素激发的心率反应好转。血淋巴细胞β－受体密度增高。结果表明，比索洛尔能有效地治疗ＤＣＭ心衰，其作用可能与抑制过度激活的交感神经系统，减慢心率，及心肌β－受体密度上调有关。     

比索洛尔对老年充血性心力衰竭体液激素的影响

目的　探讨比索洛尔对老年充血性心衰患者循环体液激素的影响。方法　选择在常规强心、利尿及血管紧张素转换酶抑制剂等治疗 2月以上 ,左室射血分数 <0 .49,近二周临床病情相对稳定的慢性充血性心衰患者 2 0例。在原治疗的基础上加用比索洛尔治疗 6月 ,通过放射免疫法测定循环体液激素水平。1 8例心功能正常者作为对照组。结果　心衰患者具有较高的循环体液激素水平 ,与对照组相比 ,Ang 、 RA、 ALD、 ANP、 ET-1、 TNF-α均升高 (均 P<0 .0 1 )。比索洛尔治疗后比治疗前明显降低 (均 P<0 .0 1 ) ,左室射血分数治疗后明显提高 (P<0 .0 1 )。结论　充血性心衰病人即使已使用 ACEI治疗 ,仍然存在着神经体液异常。比索洛尔可有效调节多种体液激素和改善心脏功能。临床上 ,对病情相对稳定的充血性心衰患者应在 ACEI基础上合用 β受体阻滞剂。     

比索洛尔治疗老年高血压及心力衰竭患者的疗效及安全性

目的探讨比索洛尔对70岁以上老年高血压及心力衰竭患者的疗效及安全性。方法观察31例老年高血压(13例伴心力衰竭)患者经用比索洛尔治疗前及治疗后6个月的血压和心功能情况。结果比索洛尔治疗8周后患者收缩压、舒张压均明显下降(P<0.05),6个月后心力衰竭患者左室射血分数(LVEF)明显提高,左室壁厚度以及室间隔厚度均明显下降。心功能改善1级者9例,改善2级者4例。结论比索洛尔治疗老年高血压及伴有心力衰竭患者是安全有效的。     

比索洛尔和卡维地洛治疗慢性心力衰竭的临床疗效观察

目的研究比索洛尔和卡维地洛治疗慢性心力衰竭的临床疗效及安全性。方法选择125例慢性心力衰竭患者,按心功能分级(NYHA)Ⅱ~Ⅳ级,经超声心动图证实左心室射血分数≤40%,将患者随机分配到比索洛尔组(62例)或卡维地洛组(63例),均治疗30周。每次随访评估心功能,记录主要心脏不良事件。结果两组左心室射血分数明显改善,比索洛尔组提高11%,卡维地洛组提高12%,左心室射血分数改善程度组内比较均有显著性意义(P<0.01)。心力衰竭症状两组均较前改善,心功能分级比索洛尔组和卡维地洛组心功能Ⅲ级治疗后减少至5例(8.1%)和6例(9.5%),两组治疗前后组内比较有显著性意义(P<0.01)。比索洛尔组和卡维地洛组主要心脏不良事件发生率分别为32.3%和34.9%,组间比较无显著性意义(P>0.05)。结论慢性心力衰竭患者应用比索洛尔和卡维地洛一样安全有效,比索洛尔可以达到与卡维地洛靶剂量长期治疗相同的疗效。     

卡维地洛与比索洛尔对慢性心力衰竭长期疗效比较

目的 :观察 2种 β受体阻滞剂 [卡维地洛 (carvediol)及比索洛尔 (bisoprolol) ]对慢性心力衰竭 (心衰 )的长期疗效。　　方法 :慢性心衰患者 97例 ,随机分为卡维地洛组 (n =3 2 ) ,比索洛尔组 (n =3 1)及对照组 (n =3 4 ) ,随访 6个月。观察心衰症状及心功能指标。　　结果 :①卡维地洛组及比索洛尔组用药后心衰症状明显改善 (P <0 0 5) ,但两组间无显著差异。②卡维地洛组及比索洛尔组用药后左心室射血分数明显增加 (P <0 0 5) ,左心室舒张末期内径减小 (P <0 0 5) ,但两组间比较无显著差异。③用药后卡维地洛组较对照组血压下降明显 (P <0 0 5) ,而比索洛尔组较对照组心率下降明显 (P <0 0 5)。　　结论 :卡维地洛及比索洛尔均能明显改善心功能 ,提高生活质量 ,但两药之间对慢性心衰的疗效无显著差异     

不同剂量比索洛尔对心力衰竭患者神经内分泌及炎症细胞因子的影响

目的:评价不同剂量比索洛尔对慢性收缩性心力衰竭(心衰)患者神经内分泌活性、细胞因子、心功能和心脏事件的影响.方法:120例慢性心功能不全患者,在常规治疗心衰的前提下,随机分为小剂量比索洛尔组[平均(3.5±1.2)mg]和大剂量比索洛尔组[平均(8.5±1.2)mg],每组60例,观察其对去甲肾上腺素、血浆肾素活性、血管紧张素Ⅱ、醛固酮、内皮素、白细胞介素-6、肿瘤坏死因子-α、心钠素、脑钠素、心功能及心脏事件的影响.结果:两组治疗后与治疗前比心率均有显著下降(P均<0.05).大剂量比索洛尔组左心室射血分数、心排出量、短轴缩短率、左心室舒张末期内径、左心室收缩末期内径、纽约心功能分级及神经内分泌水平治疗后与治疗前相比有显著改善(P均<0.05).而小剂量比索洛尔组治疗前后上述参数均无显著变化(P均<0.05).随访二年,大剂量比索洛尔组1例心源性死亡,因心衰恶化再入院12例,而小剂量比索洛尔组6例心源性死亡,因心衰恶化再入院24例,死亡和再入院复合终点两组间均达极显著差异(P均＜0.001).结论:与小剂量比索洛尔相比,大剂量比索洛尔对神经内分泌及细胞因子抑制更大,心功能改善更好,心脏事件显著减少.     

比索洛尔治疗充血性心力衰竭临床观察

目的　观察比索洛尔对充血性心力衰竭患者心室重塑及心功能的影响。方法　充血性心衰患者 10 4例 ,左室射血分数 <4 0 % ,心功能 (NYHA)Ⅱ～Ⅳ级 ,常规治疗 (强心、利尿、ACEI)基础上随机分为比索洛尔组和对照组。观察心功能、左室舒张末内径 (LVEDD)、左室收缩末内径 (LVESD)、射血分数 (EF)。结果　观察 6个月 ,比索洛尔平均用量 ( 4 35± 1 19)mg/d。比索洛尔组症状和心功能改善 ,与对照组比较 ,临床有效率上升 (P <0 0 5 ) ,LVEDD和LVESD改善 ,EF值升高 (P <0 0 1)。结论　比索洛尔可改善充血性心衰患者的心功能 ,改善心室重塑     

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.     

Athletes' heart and echocardiography: athletes' heart

Sudden death of competitive athletes is rare. However, they continue to have an impact on both the lay and medical communities. These deaths challenge the perception that trained athletes represent the healthiest segment of modern society. There is an increasing frequency of such reported deaths worldwide and the visibility of this issue is underlined by the high-profile nature of each case. Differential diagnosis between pathological and the physiologic (nonpathological) responses to high levels of physical training has become clinically more important. The purpose of this review is to highlight the main echocardiograph characteristics related to different types of training/sports participation and to highlight already recognized and newer concepts in their clinical assessment.