慢性激活天门冬氨酸受体对心室复极变异性储备和心律失常的影响

目的 研究慢性激活天门冬氨酸（N-methyl-d-aspartate,NMDA）受体对心室复极变异性和储备的影响,探讨其诱发室性心律失常的可能机制.方法 36只成年雄性Wistar大鼠分为：对照组（CTL组）、NMDA受体激动剂组（N组）和NMDA受体激动剂＋抑制剂组（N＋M组）.在Langerdorff灌流下,行不同频率的S1S1和短阵快速（Burst）刺激左心室前壁和后壁;记录单向动作电位复极到90％的时限（MAPD90）的动态变化,计算短时限变异（STV）、电交替阈值和室性心律失常的诱发率.结果 与CTL组相比,以不同周长刺激时,N组MAPD90和STV的动态变化幅度显著增大;诱发电交替的起搏周长显著增高[（111.67±2.97）ms对（88.33±2.41）ms,P＜0.01];刺激完成前的STV明显增大[（12.18±0.81）ms对（3.61±0.29）ms,P＜0.01];N组的室性心律失常诱发率和持续性室性心律失常比例均高于CTL组：S1S1模式：83.33％对25.00％,P=0.02和75.00％对8.33％,P＜0.01;Burst模式：100％对25％P＜0.01和83.33％对25.00％,P=0.02.N＋M组的上述变化与CTL组相近,差异无统计学意义（P＞0.05）.结论 慢性激活NMDA受体明显增加室性心律失常的易感性,可能与心脏复极变异性增大和复极储备降低有关.     

大剂量静脉用胺碘酮治疗顽固性、持续性室性心律失常的临床疗效及安全性

目的：评价静脉用胺碘酮（ａｍｉｏｄａｒｏｎｅ）对顽固性、持续性室性心动过速（ＳＶＴ）、心室颤动（ＶＦ）患者的临床疗效。方法：２４例ＳＶＴ和（或）ＶＦ患者，其中男１９例，女５例，平均年龄４９．２±１２．４岁；冠心病陈旧性心肌梗死１４例，心肌病７例，心肌炎２例，先天性心脏病１例。静脉注射胺碘酮首剂３～５ｍｇ／ｋｇ，１０分钟内注入，继之以１．０～１．５ｍｇ／ｍｉｎ维持静脉滴注，第１个２４小时总量平均２１６５．０±３８５．４ｍｇ（包括口服量），以后依病情渐减，维持静脉滴注平均４．２±２．５天。静脉应用同时加用口服胺碘酮６００～１２００ｍｇ／ｄ。第１次负荷量后，若心律失常控制不理想，可每隔１５～３０分钟再给１．５～３．０ｍｇ／ｋｇ的追加负荷量。疗效判断以ＳＶＴ和（或）ＶＦ消失为有效。结果：总有效率８３．３％。２例静脉用胺碘酮期间出现窦性心动过缓、窦性停搏及一过性Ⅱ度房室传导阻滞。经减量后恢复。结论：静脉应用大剂量胺碘酮治疗快速性室性心律失常安全有效。     

Cardiac Remodeling: Concepts,Clinical Impact,Pathophysiological Mechanisms and Pharmacologic Treatment

Cardiac remodeling is defined as a group of molecular, cellular and interstitial changes that manifest clinically as changes in size, mass, geometry and function of the heart after injury. The process results in poor prognosis because of its association with ventricular dysfunction and malignant arrhythmias. Here, we discuss the concepts and clinical implications of cardiac remodeling, and the pathophysiological role of different factors, including cell death, energy metabolism, oxidative stress, inflammation, collagen, contractile proteins, calcium transport, geometry and neurohormonal activation. Finally, the article describes the pharmacological treatment of cardiac remodeling, which can be divided into three different stages of strategies: consolidated, promising and potential strategies.     

Ventricular oversensing in 518 patients with implanted cardiac defibrillators: incidence, complications, and solutions.

The present study evaluates the incidence of various complications in implanted cardiac defibrillators (ICD) therapy due to ventricular oversensing (VO) and its complications. From June 1998 to May 2005, we retrospectively screened 518 patients (1085.6 patient years) for the occurrence of VO episodes (441 male, 77 female). The overall incidence was 7.3% (n = 38) with inappropriate shock deliveries accounting for 2.3% (n = 12). All VO episodes were caused by either T-wave oversensing (n = 10), myopotentials (n = 8), electrode failure (n = 5), interference with electromagnetic fields (n = 3), double-counting (n = 4), pacemaker interactions (n = 2), or others (n = 2). There were five life-threatening events due to inappropriate ICD reaction. In eight (22%) cases, ICD reprogramming was able to avoid further oversensing episodes (e.g. adaptation of sensitivity, T-wave suppression feature), 13 (35%) patients had to undergo invasive procedures (e.g. electrode replacing) to suppress VO, 16 (43%) were told to avoid the trigger situation, and one demanded to deactivate all ICD therapies because of inappropriate shock delivery. Our data demonstrate that VO is a rare complication, but might lead to life-threatening events. In most cases, VO episodes could be prevented by appropriate ICD reprogramming or avoidance of the initiating trigger.     

室性心动过速起源点标测与电消融及手术治疗

作者对８例室性心动过速（ＶＴ）患者进行９次ＶＴ起源点标测与电消融及手术治疗，其中１例直流电导管消融手术（ＤＣＣＡ）后１５个月复发，再次行消融术。８例中，１例为开胸术中心外膜标测，１例由体表ＥＣＧ定位，其余均为导管电极心内膜标测。８例共标出９个ＶＴ起源点，左室４个，右室５个。１例在开胸术中施行心外膜ＤＣＣＡ，２例手术切除ＶＴ起源点，其余５例６个起源点施行ＤＣＣＡ，其中３例次先行导管射频消融术（ＲＦＣＡ），不成功者而改用ＤＣＣＡ。结果显示，１例心内膜ＤＣＣＡ后１５个月ＶＴ复发，进行第２次心内膜ＤＣＣＡ后控制（术中先施行ＲＦＣＡ无效），２例分别施行心外膜与心内膜ＤＣＣＡ后仍发ＶＴ，分别服美西律与维拉帕米即可控制。前者随访１９个月、后者１２个月未再发作，其余５例随访１４～３４个月（２１．６±７．６）均未服药而无ＶＴ发作。这提示，对于顽固性ＶＴ患者，只要准确定位ＶＴ起源点，电消融或外科手术可望获得满意疗效。     

Oxidative stress and hyperuricaemia: pathophysiology,clinical relevance,and therapeutic implications in chronic heart failure

Heart failure (HF) is a state of chronic deterioration of oxidative mechanisms due to enhanced oxidative stress and consequent subcellular alterations. In this condition, oxidant‐producing enzymes, in particular xanthine oxidase (XO), the major cardiovascular source of reactive oxygen species (ROS), are up‐regulated. Growing evidence shows that this impaired oxidative metabolism due to enhanced ROS release is implicated in the development of cardiac hypertrophy, myocardial fibrosis, left ventricular remodelling, and contractility impairment responsible for worsening of cardiac function in CHF. Uric acid (UA) has long been linked with cardiovascular diseases, and hyperuricaemia is a common finding in patients with CHF. Hyperuricaemia is associated with impairment of peripheral blood flow and reduced vasodilator capacity, which relate closely to clinical status and reduced exercise capacity. Recent studies also suggest an association between UA levels and parameters of diastolic function; more importantly, UA has emerged as a strong independent prognostic factor in patients with CHF. In this review, we describe the up‐to‐date experimental and clinical studies that have begun to test whether the inhibition of XO translates into meaningful beneficial pathophysiological changes. This treatment gives evidence that myocardial energy, endothelial dysfunction, and vasodilator reactivity to exercise are improved by reducing markers of oxidative stress responsible for vascular dysfunction, so it represents an interesting therapeutic alternative for better outcome in CHF patients.     

Using a Human Cardiopulmonary Model to Study and Predict Normal and Diseased Ventricular Mechanics, Septal Interaction, and Atrio-Ventricular Blood Flow Patterns

We upgraded our human cardiopulmonary (CP) model with additional data that enables it to more accurately simulate normal physiology. We then tested its ability to explain human disease by changing two parameter values that decrease ventricular compliance, and found that it could predict many of the hemodynamic, gas exchange, and autonomic abnormalities found in patients with left ventricular diastolic dysfunction (LVDD). The newly incorporated information includes high-fidelity pressure tracings simultaneously recorded from the RV and LV of a normal human in a cardiac catheterization laboratory, Doppler echocardiographic inlet flow velocity patterns, measures of right and left ventricular impedance, and atrial volumes. The revised cardiovascular section details the hemodynamics of a normal subject to the extent that it can now explain the effects of septal compliance on ventricular interaction, the differences in left and right ventricular pressure development, and venous blood gas mixing in the right atrium. The model can isolate the highly interrelated features of normal and abnormal physiology, and simultaneously demonstrate their interaction in a manner that would be very difficult or impossible using an intact organism. It may therefore help physicians and scientists understand, diagnose, and improve their treatment of complicated cardiovascular and pulmonary diseases. It could also simulate the hemodynamic and respiratory effects of ventricular and pulmonary assist devices, and thus help with their development.     

第22例:临床表现胸闷憋气、全身水肿

<正>患者女性,67岁。主因"胸闷憋气、全身水肿4个月余"于2009年8月14日入院。患者4个多月前出现胸闷憋气、全身水肿,并逐渐出现声音嘶哑、双下肢无力,外院CT提示双侧胸腔积液,超声心动图提示左心室后壁及室间隔增厚,     

心室间隔缺损心电图心室肥厚与肺动脉压力、缺损大小和分流量的对比分析

目的：分析８３例心室间隔缺损（ＶＳＤ）患者术前心电图改变与血流动力学及缺损大小之间的关系，为ＶＳＤ术前提供初步预测性意见。方法：依据心电图分为正常、左心室肥厚、右心室肥厚和双心室肥厚４组，与右心导管检查所测肺动脉压力和阻力、左向右分流量和术中所见缺损大小、心室壁厚度进行对比。结果：心电图为左心室肥厚、心室间隔为中小缺损且呈中大分流量者，肺动脉压力多为轻中度增高；心电图为右心室肥厚和双心室肥厚，心室间隔多为中大缺损且分流量大者多有重度肺动脉高压，右心室肥厚，肺总阻力增高较双心室肥厚者严重。与术中所见心室壁肥厚比较，心电图诊断左、右心室肥厚符合率较高，分别为１００．０％及８５．７％，但心电图正常者中有７８．６％术中所见为左心室肥厚。结论：ＶＳＤ心电图改变可以间接评估其血液动力学改变及缺损大小。     

Refractory ventricular tachycardia secondary to cardiac sarcoid: Electrophysiologic characteristics, mapping, and ablation

BACKGROUND: Cardiac sarcoidosis is a recognized cause of ventricular tachycardia (VT) and sudden death that has not been well studied. OBJECTIVES: The purpose of this study was to describe the clinical characteristics of a consecutive series of eight patients with recurrent monomorphic VT due to cardiac sarcoidosis and to define the electrophysiologic characteristics of the VT and its electrophysiologic substrate. METHODS/RESULTS: Of 98 patents with nonischemic cardiomyopathy and VT referred for ablation over a 7-year period, sarcoid was the etiology in 8%. Mean age was 42 +/- 8 years, and all but one patient had a reduced left ventricular ejection fraction (mean 34% +/- 15%). VT was the initial manifestation of sarcoid disease in 5 of 8 cases based on retrospective analysis. All patients had not responded to therapy with multiple antiarrhythmic drugs (mean 2.5 +/- 1). Cardiac biopsy initially was negative in 3 of 7 patients, and in 2 patients the diagnosis was not made until posttransplant examination of the heart. Two patients (25%) had a previous presumptive diagnosis of arrhythmogenic right ventricular dysplasia. Electrophysiologic study revealed evidence of scar-related reentry with multiple monomorphic VTs induced (4 +/- 2 VTs per patient) with both right bundle branch block and left bundle branch block QRS configurations. Areas of low-voltage scar were present in the right ventricle in all 8 of 8 patients, in the left ventricle in 5 (63%) of 8 patients, and in the epicardium in 2 patients undergoing epicardial mapping. Ablation abolished one or more VTs in 6 (75%) of 8 patients, but other VTs remained inducible in all but one patient. Postablation, some form of sustained VT recurred in 6 of 8 patients within 6 months. However, at longer follow-up (range 6 months to 7 years), 4 of 8 patients currently are free of VT with antiarrhythmic drugs and immunosuppression. Cardiac transplantation eventually was required in 5 of 8 patients because of either recurrent VT (n = 4) or heart failure (n = 1). CONCLUSION: Sarcoid is an important diagnostic consideration in scar-related VT. Sarcoid can be misdiagnosed as idiopathic or arrhythmogenic right ventricular cardiomyopathy. Arrhythmia control can be difficult, although ablation can be helpful in some patients.     

室性心动过速患者QT离散度变化的临床意义

目的　探讨室性心动过速 (VT)患者 QT离散度 (QTd)变化的意义。方法　对正常对照组 (35例 )和 VT组 (31例 )记录 12导联同步心电图 ,人工测量 QT间期 ,计算 QTd。结果　与对照组相比 ,VT组 12导联QTd明显增加 (P<0 .0 1) ,但两组之间存在很大交叉 ,无法建立正常参考值 ;QT间期明显延长 (P<0 .0 1) ,两组QTmax多见于 V2 、V3、V4 和 V5导联 (分别为 75 .0 %、77.8% ) ,两组 QTmax、QTmin导联分布无显著差异 (P>0 .0 5 )。结论　 VT患者的 QTd不能代表心肌复极的区域性差异 ,仅可作为心肌复极异常简单、粗略的指标。     

Synergistic effect of amlodipine and atorvastatin on blood pressure,left ventricular remodeling,and C-reactive protein in hypertensive patients with primary hypercholesterolemia

Our aim in this study was to investigate the changes of serum high-sensitive C-reactive protein (hs-CRP) and uric acid (UA), and evaluate the synergistic effect of amlodipine and atorvastatin on blood pressure and left ventricular remodeling in hypertensive patients with primary hypercholesterolemia. One hundred and twenty-six hypertensive patients with hypercholesterolemia were randomized into amlodipine group (10 mg/day, group A, n = 65) and amlodipine (10 mg/day) plus atorvastatin group (20 mg/day, group B, n = 61), treated for 4 months continuously. Serum concentrations of total cholesterol, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, triglycerides, hs-CRP, and UA were determined, and blood pressure of both groups was examined before and after treatment. Left ventricular posterior wall thickness and interventricular spectum thickness were measured by echocardiography, and left ventricular mass index (LVMI) was calculated. After 4-months of treatment with atorvastatin, serum concentrations of total cholesterol, low-density lipoprotein cholesterol, triglycerides, hs-CRP, and UA were significantly decreased in group B (P < 0.05, P < 0.01), while serum concentrations of high-density lipoprotein cholesterol was elevated (P < 0.05). Meanwhile, systolic blood pressure and diastolic blood pressure were reduced in both groups (P < 0.05), and blood pressure in group B was markedly lower than that in group A after treatment (P < 0.05). Compared with that before treatment, LVMI in both groups decreased (P < 0.05), to a significantly lower degree in group B than in group A (P < 0.05). Atorvastatin can decrease serum concentrations of hs-CRP and UA. The amlodipine-atorvastatin combination markedly reduces blood pressure and reverses left ventricular hypertrophy more than amlodipine monotherapy. The positive effect suggests that in hypertensive and hypercholesterolemic patients, the combination of amlodipine and atorvastatin could be the treatment of choice.     

束支传导阻滞患者Q—T,J—T离散度与室性心律失常的关系

为探讨左、右束支传导阻滞患者Q-T_d、J-T_d与室性心律失常之间的关系,观察63例右束支传导阻滞、30例左束支传导阻滞并与30例正常QRS波群者作对照。结果显示:束支传导阻滞两组的Q-T_d、J-T_d值比对照组显著增高,差异有非常显著意义(P<0.01);左束支传导阻滞组的Q-T_d、J-T_d值高于右束支传导阻滞组,但两者Q-T_d差异无显著意义(P>0.05),而两者J-T_d差异有显著意义(P<0.05)。提示束支传导阻滞时J-T_d更能反映心肌复极情况,J-T_d值较高的左束支传导阻滞组临床上高危室性心律失常发生率较高。     

Adult Congenital Pulmonary Valve Replacement: A Simple,Effective, and Reproducible Technique

Pulmonary valve replacement is a relatively uncommon operation in adults, with the exception of those patients operated on previously for congenital heart disease. We present a technique for pulmonary valve replacement and right ventricular outflow tract augmentation. It has been utilized in over 50 consecutive patients. This technique is simple, effective, and easily reproducible. The postoperative hemodynamics, echocardiographic data, and outcomes have been excellent.