心脏传导系统淀粉样变

目的 研究心脏淀粉样变患者出现心律失常心力衰竭与心传导系统淀粉样变的关系。方法 用本组建立的心脏传导系统检查法,刚果红染色,偏振光显微镜观察了６例淀粉样变的心脏传导系统,结果 ６例心脏淀粉样变者,心传导系统病变以窦房的是重要,房室传导系统轻,后者有由近（房室结）至远部（左束支）逐渐加重倾向,其中３例有窦性心动过缓和传导阻滞者,心传导系统病变广布严重,结论 心传导系统淀粉产变可以是心律失常的病理基础     

A novel explanation for the cause of atrial fibrillation seen in atherosclerotic coronary artery disease: “Downstream inflammation” hypothesis

Atrial fibrillation is a frequent arrhythmia, and atherosclerotic coronary artery disease remains as the most common etiological factor underlying atrial fibrillation, along with systemic hypertension. The relationship between uncomplicated coronary artery disease and atrial fibrillation is not explained satisfactorily. Inflammation is now recognized as an important pathogenetic mechanism for both disorders. We hypothesise that inflammation originated from atherosclerotic coronary arteries may disseminate downstream to atrial tissue and initiate or stabilize atrial fibrillation. Studies conducted with drugs bearing anti-inflammatory properties such as hydroxymethylglutaryl coenzyme A inhibitors decrease frequency of both conditions. Such a relationship may become a novel therapeutic target to prevent this arrhythmia or decrease the frequency of paroxysms.     

Incidentally found,growing congenital aneurysm of the left atrium

A left atrial aneurysm is a very rare cardiac anomaly that usually develops in the left atrial appendage. It usually develops congenitally, and has a risk of life-threatening complications. Here, we report a case of a growing aneurysm of the left atrium that was incidentally found in a 42-yr-old woman. Eighteen years prior, an abnormal cardiomegaly was found on a chest radiography for a pre-operative study. The chest radiography at this time demonstrated a more prominent cardiomegaly than the previous radiography findings. The left atrial aneurysm was diagnosed by echocardiography and cardiac catheterization. Although asymptomatic, she underwent a successful surgical excision to allay the possibilities of rupture, arrhythmia, heart failure, or thromboembolism. The surgical findings demonstrated an 8 x 15 cm sized saccular aneurysm at the left atrial appendage, and the pathologic findings showed three myocardial layers. The patient has been asymptomatic during the 15 months of follow-up. In conclusion, a congenital left atrial aneurysm can grow with time, even in asymptomatic cases, and an aneurysmectomy is a curative treatment, which can eliminate the potential complications.     

Nonreentrant atrial tachycardia occurs independently of hypertrophic cardiomyopathy in RASopathy patients

Multifocal atrial tachycardia (MAT) has a well‐known association with Costello syndrome, but is rarely described with related RAS/MAPK pathway disorders (RASopathies). We report 11 patients with RASopathies (Costello, Noonan, and Noonan syndrome with multiple lentigines [formerly LEOPARD syndrome]) and nonreentrant atrial tachycardias (MAT and ectopic atrial tachycardia) demonstrating overlap in cardiac arrhythmia phenotype. Similar overlap is seen in RASopathies with respect to skeletal, musculoskeletal and cutaneous abnormalities, dysmorphic facial features, and neurodevelopmental deficits. Nonreentrant atrial tachycardias may cause cardiac compromise if sinus rhythm is not restored expeditiously. Typical first‐line supraventricular tachycardia anti‐arrhythmics (propranolol and digoxin) were generally not effective in restoring or maintaining sinus rhythm in this cohort, while flecainide or amiodarone alone or in concert with propranolol were effective anti‐arrhythmic agents for acute and chronic use. Atrial tachycardia resolved in all patients. However, a 4‐month‐old boy from the cohort was found asystolic (with concurrent cellulitis) and a second patient underwent cardiac transplant for heart failure complicated by recalcitrant atrial arrhythmia. While propranolol alone frequently failed to convert or maintain sinus rhythm, fleccainide or amiodarone, occasionally in combination with propranolol, was effective for RASopathy patient treatment for nonreentrant atrial arrhythmia. Our analysis shows that RASopathy patients may have nonreentrant atrial tachycardia with and without associated cardiac hypertrophy. While nonreentrant arrhythmia has been traditionally associated with Costello syndrome, this work provides an expanded view of RASopathy cardiac arrhythmia phenotype as we demonstrate mutant proteins throughout this signaling pathway can also give rise to ectopic and/or MAT.     

Lewy bodies in the sinoatrial nodal ganglion: clinicopathological studies

Lewy bodies (LB) are characteristic pathological findings for idiopathic Parkinson disease, and extracranial organs have also been known to exhibit these structures. Clinically, the possible involvement of LB in cardiac dysfunction has attracted attention based on the findings of studies using [123I] metaiodobenzyl guanidine (MIBG) scintigraphy. The purpose of the present study was to investigate the possible involvement of LB in heart disease. A total of 40 autopsy cases consisting of Lewy body disease and Parkinson syndrome were examined. The former were cases with intracranial LB regardless of clinical symptoms, and the latter were cases with parkinsonism but without intracranial LB. The presence of heart disease or an atrial arrhythmia and the results of an MIBG scintigraphy study were clinically examined. The sinoatrial node was examined microscopically and immunohistochemically. The results showed that heart disease and atrial arrhythmia complications were more frequent in cases with Lewy body disease than in cases with Parkinson syndrome and that LB were frequently found in extracranial organs, especially in the sinoatrial nodal ganglion, in cases with Lewy body disease. In the current report, we hypothesized that neuronal changes involving LB in the sinoatrial nodal ganglion may cause arrhythmia and ischemic heart disease as a result of vasoconstriction.     

KB—R7943改善大鼠心肌缺血—再灌注损伤室性心律失常的作用

目的：研究Na^ -Ca^ 交换抑制剂KB－R7943（2－[2-4(4-Nitrobenzyloxy)phenyl]cthyl]isothiourea methanesulphonate)对大鼠心肌缺血－再灌注损伤致室性心律失常的抑制作用。方法：制备大鼠离体左右心房,研究KB－R7943对其心肌及心率的影响,采用离体血管平滑肌张力记录不研究KB－R7943对大鼠胸主动脉血管平滑肌张力作用的影响,利用大鼠离体和在体心肌缺血－再灌注损伤（ischemia/reperfusion,I/R)致心律失常模型研究KB－R7943的抗心律失常。结果：KB－R7943对大鼠心肌收缩力、心率及血管平滑张力作用的影响均较弱,但它可有效地降低大鼠离体和在体心肌I／R后室早、室速、室颤的发生率和持续时间。结论：KB－R7943有较强的抗I／R性心律失常作用,但对大鼠正常心血管功能活动无明显影响。     

Risk factors for an intraoperative arrhythmia during esophagectomy

PURPOSE: Arrhythmias after an esophagectomy (most commonly atrial fibrillation) are a significant contributing factor to patient morbidity. However, the significance of an intraoperative arrhythmia is not completely understood. The aim of this retrospective study was to determine the occurrence and risk factors for developing intraoperative arrhythmias in patients undergoing an esophagectomy. MATERIALS AND METHODS: We reviewed the records of 427 patients who underwent a transthoracic esophagectomy between 2001 and 2005. Variables such as age, sex, hypertension, diabetes, cardiac disease, preoperative pulmonary function test (PFT) results, cancer level, combined radiochemotherapy, intrathoracic cavity adhesions and anastomosis site, hemoglobin, central venous pressure (CVP), fluid balance, serum potassium level, dose of vasopressors, temperature, and combined general and epidural anesthesia were analyzed as risk factors for the occurrence of an arrhythmia. We defined this arrhythmia as one not originating from the sinus node. RESULTS: The incidence of intraoperative arrhythmia in this subset of patients was 17.1%, with a 37.2% reoccurrence rate during the first three postoperative days. Univariate and multivariate analysis revealed the presence of heart disease, poor PFTs, cervical anastomosis, elevated CVP, and higher ephedrine doses to be independent predictors of the development of an intraoperative arrhythmia. CONCLUSION: The incidence of intraoperative arrhythmia during esophagectomy was 17.1% with a 37.2% of reoccurrence rate.     

Cardiac responses to exercise in the dog before and after destruction of the sinoatrial node

Summary Chronotropic and dromotropic responses to treadmill exercise were compared in conscious dogs prior to and following excision of the sinoatrial node (SAN). The initial junctional rhythm accompanying removal of the SAN region was replaced within hours to days by subsidiary atrial pacemaker (SAP) foci located in the inferior right atrium along the sulcus terminalis. With SAN intact, cardiac acceleration was immediate at onset of exercise and the tachycardia was directly proportional to work intensity. Atrioventricular (AV) conduction concurrently accelerated during exercise as manifest by shortening in P-R and atrioventricular (A-V) intervals. Following SAN excision, subsidiary atrial pacemaker foci likewise demonstrated prompt tachycardias during exercise, although heart rate was significantly reduced at rest and during steady state exercise. In the SAP state, tachycardia during exercise was related to work intensity and was mediated by changes in cardiac autonomic nerve activity. Combined propranolol-atropine blockade increased heart rate at rest in the SAP state, and significantly attenuated the tachycardia accompanying treadmill exercise. Following SAN excision the P-R (A-V) interval was significantly reduced in the resting animal. In response to exercise, AV conduction time decreased in the SAP state, though the absolute levels during steady state exercise were not significantly different from prior control runs with SAN intact. Blood pressure response to exercise was similar during both SAN and SAP states. We conclude that following an initial unstable period, SAP foci maintain adequate heart rate increases in response to dynamic exercise, primarily mediated via autonomic nerve regulation. Supported by NIH Grants HL 27595, HL 27664, HL 28205, and HL 32392     

Atrial fibrillation from the pathologist’s perspective

Atrial fibrillation (AF), the most common sustained cardiac arrhythmia encountered in clinical practice, is associated with increased morbidity and mortality. Electrophysiologically, it is characterized by a high rate of asynchronous atrial cell depolarization causing a loss of atrial contractile function and irregular ventricular rates. For a long time, AF was considered as a pure functional disorder without any structural background. Only in recent years, have new mapping and imaging techniques identified atrial locations, which are very often involved in the initiation and maintenance of this supraventricular arrhythmia (i.e. the distal portion of the pulmonary veins and the surrounding atrial myocardium). Morphological analysis of these myocardial sites has demonstrated significant structural remodeling as well as paved the way for further knowledge of AF natural history, pathogenesis, and treatment. This architectural myocardial disarrangement is induced by the arrhythmia itself and the very frequently associated cardiovascular disorders. At the same time, the structural remodeling is also capable of sustaining AF, thereby creating a sort of pathogenetic vicious circle. This review focuses on current understanding about the structural and genetic bases of AF with reference to their classification, pathogenesis, and clinical implications.     

糖尿病心肌离子通道重构的研究进展

糖尿病心血管并发症是患者死亡的主要原因,其中重要的临床表现是与猝死相关的心律失常发生率较高。糖尿病患者心电图常出现与心律失常相关的QT间期延长,且心电图的异常可不伴随其它危险因素而独立存在。实验研究也显示糖尿病动物模型的QT间期延长对应心室肌细胞动作电位时     

Intravenous magnesium for cardiac arrhythmias: jack of all trades.

Intravenous magnesium has been used to prevent and treat many different types of cardiac arrhythmia. It has diverse electrophysiological actions on the conduction system of the heart; including prolonging sinus node recovery time, and reducing automaticity, atrioventricular nodal conduction, antegrade and retrograde conduction over an accessory pathway, and His-ventricular conduction. Intravenous magnesium can also homogenise transmural ventricular repolarisation. Because of its unique and diverse electrophysiological actions, intravenous magnesium has been reported to be useful in preventing atrial fibrillation and ventricular arrhythmias after cardiac and thoracic surgery; in reducing the ventricular response in acute onset atrial fibrillation, including for patients with Wolff-Parkinson-White syndrome; in the treatment of digoxin induced supraventricular and ventricular arrhythmias, multifocal atrial tachycardia, and polymorphic ventricular tachycardia or ventricular fibrillation from drug overdoses. Intravenous magnesium is, however, not useful in monomorphic ventricular tachycardia and shock-resistant ventricular fibrillation. Large randomised controlled studies are needed to confirm whether intravenous magnesium can improve patient centre outcomes in different cardiac arrhythmias.     

THE HISTOPATHOLOGICAL SUBSTRATUM FOR ATRIAL FIBRILLATION IN MAN

Quantitative studies on the histological sections of the atria including sinoatrial (SA) node, SA junction and internodal preferential pathways in 12 hearts with long-term atrial fibrillation (Af group) and in 43 hearts with no arrhythmia (control group) have been carried out. The control group was subdivided Into two age-groups, the younger and older over 50 years for the age-matched comparison with the Af group. In the Af group, markedly impaired contiguity of the SA junction, severe fibrosis and lipomatosis of atria were common precipitating factors. Regarding the ratio of SA nodal cells to the area of SA node, and patency of SA node artery, there were no significant difference between the Af group and age-matched (older) control group. In comparison between the two control groups, decreased SA nodal cells, stenosis of SA node artery, impaired contiguity of the SA junction, fibrosis and lipomatosis of atria were more prominent in the majority of the older group than that of the younger. These findings suggest that the pathological lesions of the SA junction and the atrial myocardium in the Af group were the exaggerated aging changes, and these lesions may be the main anatomic substratum for Af.     

Detection of atrial-flutter and atrial-fibrillation waveforms by fetal magnetocardiogram

Two cases of fetal tachycardia are reported: atrial flutter and fibrillation. The waveforms from each case were detected by fetal magnetocardiograms (FMCGs) using a 64-channel superconducting quantum interference device (SQUID) system. Because the magnitude of supraventricular arrhythmia signals is very weak, two subtraction methods were used to detect the fetal MCG waveforms: subtraction of the maternal MCG signal, and subtraction of the fetal QRS complex signal. It was found that atrial-flutter waveforms showed a cyclic pattern and that atrial-fibrillation waveforms showed f-waves with a random atrial rhythm. Fast Fourier transform analysis determined the main frequency of the atrial flutter to be about 7 Hz, and the frequency distribution of atrial fibrillation consisted of small, broad peaks. To visualise the current pattern, current-arrow maps, which simplify the observation of pseudo-current patterns in fetal hearts, of the averaged atrial flutter and fibrillation waveforms were produced. The map of the atrial flutter had a circular pattern, indicating a re-entry circuit, and the map of the atrial fibrillation indicated one wavelet, which was produced by a micro-re-entry circuit. It is thus concluded that an FMCG can detect supraventricular arrhythmia, which can be characterised by re-entry circuits, in fetuses.     

Structure-function relationship in the AV junction

In the normal heart, the atrioventricular node (AVN) is part of the sole pathway between the atria and ventricles. Under normal physiological conditions, the AVN controls appropriate frequency-dependent delay of contractions. The AVN also plays an important role in pathology: it protects ventricles during atrial tachyarrhythmia, and during sinoatrial node failure an AV junctional pacemaker can drive the heart. Finally, the AV junction provides an anatomical substrate for reentry. Using fluorescent imaging with voltage-sensitive dyes and immunohistochemistry, we have investigated the structure-function relationship of the AV junction during normal conduction, reentry, and junctional rhythm. We identified molecular and structural heterogeneity that provides a substrate for the dual-pathway AVN conduction. We observed heterogeneity of expression of three isoforms of connexins: Cx43, Cx45, and Cx40. We identified the site of origin of junctional rhythm at the posterior extension of the AV node in 79% (n = 14) of the studied hearts. This structure was similar to the compact AV node as determined by morphologic and molecular investigations. In particular, both the posterior extension and the compact node express the pacemaking channel HCN4 (responsible for the I(F) current) and neurofilament 160. In the rabbit heart, AV junction conduction, reentrant arrhythmia, and spontaneous rhythm are governed by heterogeneity of expression of several isoforms of gap junctions and ion channels. Uniform neurofilament expression suggests that AV nodal posterior extensions are an integral part of the cardiac pacemaking and conduction system. On the other hand, differential expression of Cx isoforms in this region provides an explanation of longitudinal dissociation, dual-pathway electrophysiology, and AV nodal reentrant arrhythmogenesis.     

Determinants of successful direct current cardioversion for atrial fibrillation and flutter: the importance of rapid referral.

Direct current (DC) cardioversion is an effective means of restoring sinus rhythm in patients with atrial fibrillation or flutter; however, the existing literature contains conflicting evidence on which factors are useful predictors of success. In a study of 171 patients undergoing DC cardioversion, we found that duration of arrhythmia prior to DC cardioversion was the only significant predictor of both successful cardioversion and subsequent maintenance of sinus rhythm (P < 0.001). Rapid DC cardioversion after the onset of atrial fibrillation or flutter significantly increases the likelihood of a successful outcome in both the short-term and long-term.     

人窦房结中突触素增龄性变化的定量研究

为了探讨正常人窦房结中突触素增龄性变化的规律 ,用免疫组织化学方法显示窦房结中的突触素 ,并用计算机图像分析技术测量突触素的免疫阳性物面积。结果显示 :窦房结中的突触素阳性物在 1岁以前较少 ,1岁以后显著增多 ,并在 1～ 2 0岁年龄组达到最多 ,其后随年龄增长而减少 ,70岁以后降到最低。提示窦房结中的神经组织在生理状态下存在着增龄性变化     

The Role of the Crista Terminalis in Atrial Flutter and Fibrillation: A Computer Modeling Study

Although atrial fibrillation is a common arrhythmia, the underlying mechanisms are incompletely understood. Recent studies have determined the role of the crista terminalis in the mechanisms of a simpler arrhythmia, atrial flutter. We hypothesize that as transverse coupling across the crista terminalis increases, the activation pattern that results is less like typical atrial flutter and more like atrial fibrillation. 6480 Van Capelle elements were coupled in an icosahedron, simulating the right atrium. Atrial simulations were created which incorporated no heterogeneity, heterogeneous coupling, heterogeneous effective refractory periods, and both heterogeneous coupling and effective refractory periods. When the entire crista terminalis was uncoupled, typical atrial flutter occurred. When transverse coupling allowed activation to propagate across the crista terminalis, the flutter cycle length decreased (p < 0.0001). In addition, when heterogeneity was present, both the coefficient of variation of cycle length and the number of activation wavelets increased (p < 0.0001). Thus, a more rapid reentrant circuit in the superior right atrium drove fibrillatory activity in the remainder of the atrium, as predicted by the mother wavelet hypothesis. While awaiting in vivo validation, our study indicates that transverse coupling along the crista terminalis may play an important role in the development of atrial fibrillation from atrial flutter. © 2000 Biomedical Engineering Society. PAC00: 8719Hh, 8710+e     

Characterization of stretch-activated ion currents in isolated atrial myocytes from human hearts

To explore further the mechanisms that may underlie cardiac arrhythmia, we analysed stretch-activated ion currents in human atrial myocytes. Longitudinal stretch of freshly isolated atrial myocytes prolonged the duration of action potentials, depolarized the resting membrane potential and caused extra action potentials. Under voltage-clamp conditions, the amplitude of stretch-induced transmembrane currents increased reversibly with the intensity of stretch. Stretch-activated currents ( I(SAC)) had a reversal potential of 0 mV and were insensitive to substitution of Cl(-) with aspartate ions in the extracellular fluid. I(SAC) was suppressed by 5 micro M gadolinium (Gd(3+)). Furthermore, mechanical stretch decreased transmembrane ion fluxes through L-type calcium channels (I(Ca,L)). This reduction of I(Ca,L) was inhibited by dialysing the cells for 5 min with 5 mM BAPTA prior to application of stretch. In contrast, both BAPTA and removal of Ca(2+) from the extracellular bathing solution had no significant effect on stretch activation of I(SAC). These findings suggest that non-selective cation channels in human atrial myocytes are sensitive to mechanical stimulation. We propose that activation of transmembrane influx of cations, preferentially Na(+), by local stretch may play a role in cardiac arrhythmia.     

Long-term Prognosis of Paroxysmal Atrial Fibrillation and Predictors for Progression to Persistnt or Chronic Atrial Fibrillation in the Korean Population

Little is known about the long-term prognosis of or predictors for the different clinical types of atrial fibrillation (AF) in Korean populations. The aim of this study was to validate a risk stratification to assess the probability of AF progression from paroxysmal AF (PAF) to persistent AF (PeAF) or permanent AF. A total of 434 patients with PAF were consecutively enrolled (mean age; 71.7 ± 10.7 yr, 60.6% male). PeAF was defined as episodes that are sustained > 7 days and not self-terminating, while permanent AF was defined as an ongoing long-term episode. Atrial arrhythmia during follow-up was defined as atrial premature complex, atrial tachycardia, and atrial flutter. During a mean follow-up of 72.7 ± 58.3 months, 168 patients (38.7%) with PAF progressed to PeAF or permanent AF. The mean annual AF progression was 10.7% per year. In univariate analysis, age at diagnosis, body mass index, atrial arrhythmia during follow-up, left ventricular ejection fraction, concentric left ventricular hypertrophy, left atrial diameter (LAD), and severe mitral regurgitation (MR) were significantly associated with AF progression. In multivariate analysis, age at diagnosis (P = 0.009), atrial arrhythmia during follow-up (P = 0.015), LAD (P = 0.002) and MR grade (P = 0.026) were independent risk factors for AF progression. Patients with younger age at diagnosis, atrial arrhythmia during follow-up, larger left atrial chamber size, and severe MR grade are more likely to progress to PeAF or permanent AF, suggesting more intensive medical therapy with close clinical follow-up would be required in those patients.     

计算机模拟建模及应用：微波消融治疗心房颤动的温度场

背景：心房颤动是临床上最为常见的持续性心律失常,微波消融是治疗房颤的一种新技术,在国内外临床应用时间短,经验不足。 目的：对国内外微波消融治疗心房颤动温度场的研究现状及新进展作一综述。 方法：应用计算机检索CNKI、EI、SCI数据库中关于微波消融温度场的文章,在标题和摘要中以“消融,心房颤动,微波,温度场”或“ablation,atrial fibrillation,microwave, thermal field”为检索词进行检索。 结果与结论：微波导管消融术对引起心律失常的关键部位(即靶点)进行精细标测,使靶点及邻近的心肌组织发生凝固性坏死,以破坏心动过速的病灶及折返途径,从而消除心律失常。在尽量减少对正常组织伤害的同时,保证消融切割线的连续性,对于房颤消融至关重要。实现温度场的计算机模拟能够全面反映温度场的分布规律,医护人员可以在热疗手术进行之前对治疗过程有比较直观的认识,提出比较详细的手术规划,并且可以在术中根据部分参数修正模拟结果和加热的时间与强度,达到理想的治疗效果。