卡维地洛治疗慢性心力衰竭40例疗效观察

目的评估卡维地洛治疗慢性心力衰竭的临床疗效及安全性。方法80例慢性心力衰竭患者随机分为治疗组和对照组各40例。对照组采用慢性心力衰竭的标准治疗;治疗组在此标准治疗的基础上,卡维地洛从小剂量2．5mg／次、2次／d开始,每2周增加1倍剂量,直至最大剂量（靶剂量）25mg,2次／d。治疗前后分别对两组患者行血常规、心电图、心功能、肝肾功能、心脏B超等检查。结果治疗6个月后,治疗组左室收缩末径、左室舒张末径减小,左室射血分数增加,且血压、心率均明显改善,与治疗前比较差异有统计学意义（P〈0．05或〈0．01）;而对照组治疗前后以上指标比较差异无统计学意义。两组治疗后肝肾功能、血常规均无异常改变。结论卡维地洛治疗慢性心力衰竭安全、有效。     

国产卡维地洛治疗心力衰竭的临床观察

目的观察国产卡维地洛治疗心力衰竭（CHF）的临床疗效及不良反应。方法将118例住院CHF患者随机分为对照组40例，给予常规治疗。治疗组78例，在常规治疗基础加用国产卡维地洛起始剂量2．5mg／次；2次／d，若耐受，每2周剂量加倍，直至20．0mg／次，2次／d，共8周，观察治疗前、后各组及组间的心功能分级，血压、心率及超声心动图变化。结果两组患者疗效间差异有显著性意义（P〈0．05）；治疗组治疗后2、4、6、8周与治疗前比较血压、心率均有明显改善（P〈0．01）；治疗组除个别患者出现心动过缓外，无一例发生严重低血压及严重房室传导阻滞。结论国产卡维地洛对心力衰竭患者有明显疗效，且副作用少。     

安体舒通在治疗67例慢性充血性心力衰竭中的作用

目的观察安体舒通在治疗慢性充血性心力衰竭（CHF）中的临床疗效。方法CHF病人132例,对照组65例,治疗组67例,对照组应用常规心力衰竭治疗,治疗组在常规心力衰竭治疗的基础上,加用安体舒通片20mg,1次／d,治疗4周,治疗前后评价左心功能,利用动态心电图监测心律失常情况。结果与对照组比较,治疗组心功能改善明显（P〈0．05）;治疗组室性心律失常发生率减少（P〈0．01）。结论安体舒通能够改善CHF患者心功能,减少室性心律失常发生。     

比索洛尔对慢性心力衰竭室性心律失常和心率变异性的影响

目的 :观察比索洛尔对慢性心力衰竭患者的室性心律失常和心率变异性的影响。方法 :86例慢性心力衰竭 (CHF)患者在常规抗心衰药物治疗的基础上 ,随机分成两组 ,比索洛尔组每日口服比索洛尔 1.2 5～ 10mg ,对照组口服安慰剂 ,疗程 12个月 ,观察治疗前后心率、室性心律失常和心率变异性的变化。结果 :比索洛尔组室性心律失常明显减少 ,心率变异性参数显著改善。结论 :长期使用比索洛尔可降低CHF恶性室性心律失常的发生 ,改善心率变异性     

卡维地洛治疗老年慢性心力衰竭的临床疗效观察

目的：观察卡维地洛治疗老年慢性充血心力衰竭（CHF）的临床疗效及副作用。方法：72例老年CHF患者随机分为卡维地洛组（治疗组）和常规治疗组（对照组），各36例。对照组使用洋地黄、利尿剂、血管紧张素转换酶抑制剂、硝酸酯类等药物治疗。治疗组在常规治疗的基础上加用卡维地洛5mg／d，只要能耐受尽可能递增到10～20mg／d，疗程20周。每周测量血压、心率，评定心功能，治疗前后检查超声心动图。结果：治疗组左室射血分数（LVEF）明显升高（P〈0．001），心功能分级、左室舒张末期内径（LVEDD）、心肌耗氧指数和收缩末期内径（LVESD）明显降低（P〈0．01），心率减慢，血压降低（P〈0．01）．与对照组比较差异有显著性（P〈0．05）。结论：卡维地洛治疗心力衰竭改善心功能，改善左室重塑，安全有效。     

卡维地洛对缺血性心脏病心衰并慢性心房颤动者运动时心率的影响

目的观察卡维地洛对缺血性心脏病心衰（心功能NYHAⅡ-Ⅲ级）并慢性心房纤颠（Af）者心率的影响。方法96例缺血性心脏病心功能Ⅱ-Ⅲ级合并慢性Af者随机分为卡雏地洛组（A组,48例）和对照组（B组,48例）。A组在常规治疗基础上加用卡雏地洛,开始剂量3．125mg,2次／日,每2周剂量加倍,6周后达目标剂量12．5mg 2次／日,至研究结束（总疗程12周）。B组维持常规治疗。结果 A组患者治疗3个月后,静息及运动时心率均明显下降（P〈0．01）,运动平板总时间增加（P〈0．01）,心功能分级改善;B组无改变。结论卡雏地洛可改善缺血性心脏病心衰伴慢性Af者的静息及运动心率,改善长期预后。     

卡维地洛联合螺内酯治疗慢性心室重构性心力衰竭的研究

目的研究卡维地洛联合螺内酯治疗慢性心室重构性心力衰竭疗效。方法将60例明确诊断心功能不全的患者随机分成治疗组和对照组各30例,对照组患者给予常规治疗（利尿剂、血管紧张素转化酶抑制剂,必要时给予洋地黄类药物）。观察组在常规治疗的基础上加用卡维地洛12．5～50．0mg/d和螺内酯20～40mg/d。疗程均为3个月。治疗3个月后按NYHA心功能分级标准评价心功能。治疗前、后分别测定心率、血压等,并行超声心动图检查,测定左室射血分数（LVEF）、每搏输出量（SV）、心脏指数（CI）。结果两组患者临床疗效间差异有非常显著性意义（P＜0．01）。两组患者治疗前、后血压、心率、LVEF、SV、CI间差异均有非常显著性意义（P＜0．01）。结论卡维地洛联合螺内酯治疗慢性心室重构性心力衰竭较常规治疗能更有效地改善患者的心功能,提高患者的治愈率。     

卡维地洛治疗轻中度稳定性慢性心力衰竭耐受性和安全性研究

目的：评估卡维地洛治疗轻中度稳定性慢性心力衰竭的I临床耐受性和安全性。方法：482例符合轻中度慢性心衰标准的患者在常规治疗后，病情基本稳定的基础上加用卡维地洛。卡维地洛从小剂量3．125mg每日两次开始，每两周递增一次，直至靶剂量25mg每天2次或最大耐受剂量。治疗前后分别对心功能(NYHA)分级、心衰评分、血压、心率等体征及实验室(血常规，肝肾功能及心电图等)检查进行检测，评判疗效、耐受性及安全性。结果：用卡维地洛治疗后心功能明显改善，心衰评分下降，提示生活质量改善，同时不良反应少，安全性好。60％的患者可以达到推荐靶剂量。结论：卡维地洛治疗轻中度慢性稳定性心衰耐受性和安全性良好。     

小剂量卡维地洛治疗慢性心力衰竭的疗效观察

目的:探讨小剂量卡维地洛治疗慢性心力衰竭的疗效。方法:90例慢性心力衰竭患者被随机分为两组:卡维地洛组(45例,在原有治疗的基础上加用卡维地洛,起始剂量为3.125mg,2次/d,持续两周,无不良反应则加至6.25mg,2次/d,直到6个月)。对照组(45例,进行常规治疗)。分别检测两组患者治疗前后心率(HR),左室射血分数(EF),左室舒张末期内径(LVDED),左室收缩末期内径(LVESD),心胸比例及心功能变化。结果:与常规治疗组相比卡维地洛组患者的HR变慢,LVEF增加,LVDED,LVESD及心胸比减少,心功能改善(P<0.05～<0.01),总有效率达91%。结论:卡维地洛治疗慢性心功能不全能安全、有效。     

卡维地洛治疗老年心力衰竭的有效性和安全性

目的：探讨卡维地洛治疗老年充血性心力衰竭（CHF）患者的有效性和安全性。方法：60岁以上老年CHF患者86例，在心衰症状已基本缓解，常规治疗基础上加用卡维地洛2．5mg，2次／d，以后根据患者耐受情况在4～6周内渐增到病人能耐受的最大剂量或达到目标剂量20mg，2次／d。维持剂量治疗3个月。观察治疗前及维持剂量治疗3个月后心率、血压、血生化及心功能的变化。结果：治疗后心率、血压均明显下降（P〈0．01），心搏量、心脏指数、心排血量、左室射血分数均明显增加（P〈0．01或P〈0．05），左房内径、左室收缩末期内径、左室舒张末期内径均明显降低（P〈0．01）；而各项生化指标均无明显改变（P〉0．05）。结论：卡维地洛治疗老年心力衰竭可明显改善心功能并且耐受性良好。     

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.