Lignocaine Therapy after Acute Myocardial Infarction

Thirty-five patients with ventricular dysrhythmias and seven with other dysrhythmias after acute myocardial infarction were treated with intravenous lignocaine.Satisfactory initial suppression of ventricular ectopic beats was achieved in 27 (82%) of 33 patients after either a 50-mg. bolus or a 50-mg. bolus followed by a 100-mg. bolus of intravenous 2% lignocaine. Continuous suppression of ventricular ectopic beats was accomplished in 21 (78%) of these 27 patients by continuous intravenous lignocaine infusions of 1 to 2 mg. per minute. Recurrence of ventricular ectopic beats occurred in four patients despite lignocaine infusion rates of up to 6 mg. per minute. Six patients with ventricular ectopic beats developed ventricular fibrillation despite satisfactory initial suppression of their dysrhythmia by lignocaine. In three of them ventricular fibrillation supervened while they were receiving a lignocaine infusion and two subsequently died. Unheralded ventricular fibrillation occurred in three other patients between four and seven days after completing the full course of lignocaine therapy.Toxic effects of lignocaine were minimal in patients receiving 1 to 2 mg. per minute.     

Acceleration of ventricular rate by amiodarone in atrial fibrillation associated with the Wolff-Parkinson-White syndrome

Amiodarone has proved to be a valuable drug in atrial fibrillation associated with the Wolff-Parkinson-White syndrome. When it was administered to a patient with this syndrome in atrial fibrillation, who had previously suffered an inferior myocardial infarction, the ventricular rate accelerated from 170 to 230 beats/minute.This unusual case emphasises the need for full electrophysiological assessment of patients with the Wolff-Parkinson-White syndrome for whom amiodarone treatment is being considered.     

A mathematical model of human atrioventricular nodal function incorporating concealed conduction

This work develops a mathematical model for the atrioventricular (AV) node in the human heart, based on recordings of electrical activity in the atria (the upper chambers of the heart) and the ventricles (the lower chambers of the heart). Intracardiac recordings of the atrial and ventricular activities were recorded from one patient with atrial flutter and one with atrial fibrillation. During these arrhythmias, not all beats in the atria are conducted to the ventricles. Some are blocked (concealed). However, the blocked beats can affect the properties of the AV node. The activation times of the atrial events were regarded as inputs to a mathematical model of conduction in the AV node, including a representation of AV nodal concealment. The model output was compared to the recorded ventricular response to search for and identify the best possible parameter combinations of the model. Good agreement between the distribution of interbeat intervals in the model and data for durations of 5 min was achieved. A model of AV nodal behavior during atrial flutter and atrial fibrillation could potentially help to understand the relative roles of atrial input activity and intrinsic AV nodal properties in determining the ventricular response.     

Mechano-electric feedback and atrial fibrillation

Atrial fibrillation frequently occurs under conditions associated with atrial dilatation suggesting a role of mechano-electric feedback in atrial arrhythmogenesis. Although atrial arrhythmias may be due both to abnormal focal activity and reentrant mechanisms, the majority of sustained atrial arrhythmias have been ascribed to reentrant activity. Atrial stretch may contribute to focal arrhythmias by inducing afterdepolarizations and to reentrant arrhythmias by increasing the atrial surface, by shortening the refractory period and/or slowing the conduction velocity and by increasing their spatial dispersion. Experimental and clinical studies have demonstrated that changes in mechanical loading conditions may modulate the electrophysiological properties of the atria. These studies have, for the most part, involved the effects of acute stretch on atrial refractoriness. While studies in humans and intact animals yield divergent results due to the variety of loading conditions and neurohumoral influences, experimental studies in isolated preparations clearly show that atrial refractory period and action potential duration at early levels of repolarization shorten by acute atrial dilatation. Both experimental and human studies have shown that acute atrial stretch is arrhythmogenic and may induce triggered premature beats and atrial fibrillation.     

A Novel pacing option in patients with endomyocardial fibrosis: A case series

Endomyocardial fibrosis (EMF) is characterized by fibrous tissue deposition on the endocardial surface leading to impaired filling of one or both ventricles, resulting in either right or left heart failure or both. Although Sinus node dysfunction and tachyarrhythmia - atrial fibrillation, ventricular tachycardia, have been commonly reported, complete heart block (CHB) necessitating a pacemaker is rare in EMF. Transvenous pacing is technically limited by fibrotic obliteration of the affected ventricle that results in poor lead parameters, and alternative pacing strategy like epicardial pacing may be required in many. We report three cases of EMF, who were treated with an alternative pacing strategy.     

Atrial Rate And Rhythm Abnormalities In A Patient With Hyperkalemia

A 67 year old man presented with a serum potassium of 7.7 mEq/L and slow atrial flutter with variable A-V block and peaked T waves. Initial treatment for hyperkalemia was followed by an increase in the atrial flutter rate to 300 beats per minute. After hemodialysis the rhythm converted to sinus.     

Cardiac gene expression profiling – the quest for an atrium-specific biomarker

Biomarkers are gaining increasing interest to predict risk but also to aid in diagnostics. Tissue-specific biomarkers are of utmost importance to detect diseases of respective organs. As of yet there are no atriumspecific biomarkers for risk stratification of atrial disease, such as atrial fibrillation. Bioinformatics such as mRNA microarrays can help to detect tissue-enriched and possibly tissue-specific expressed genes that can be targets for biomarkers. We describe an approach to identify genes preferably expressed in atrial cardiomyocytes compared with ventricular cardiomyocytes by RNA microarray and confirmed by quantitative real-time polymerase chain reaction. By this approach we identified several atrium-enriched genes but also ventricle-enriched genes. As expected atrial natriuretic peptide (ANP) mRNA showed higher expression in atrial cardiomyocytes while with adrenergic stimulation expression was almost as high in ventricular as in atrial cells. Brain-type natriuretic peptide (BNP), however, was not different between atrial and ventricular cells giving a possible explanation for increased levels of NT-proBNP in atrial fibrillation patients. Interesting identified candidates are serpine1 and ltbp2 as atrium-enriched genes whereas alpha-adrenergic receptor subtype 1b and S100A1 expression was significantly higher in ventricular cells. The identified genes need to be confirmed in human tissue and might ultimately be tested as potential biomarkers for atrial stress. (Neth Heart J 2010;18:610–4.)     

Atrial pacing, the forgotten pacing mode

In patients with sick sinus syndrome and normal atrioventricular conduction, physiological pacing can be accomplished with either a single chamber atrial pacemaker AAI/R or a dual chamber pacemaker DDD/R. The single chamber device has the advantages of simpler implantation and lower initial costs, while the dual chamber device offers protection in case atrioventricular conduction disturbances develop in the future. When rigorous attention is paid to the pre-implantation selection criteria, the incidence of reported second- or third-degree atrioventricular block varied between 0.4 and 1.8% per annum. Medical practice, however, has shifted to predominant implantation of DDD/R pacemakers in more than 95% of patients with sick sinus syndrome. Recent publications have reported an increase in left atrial diameter, decrease in left ventricular fractional shortening and increased incidence of atrial fibrillation in patients with DDD/R pacing as compared with patients with single chamber atrial devices. These changes were proportional to the percentage of ventricular paced beats. New algorithms in dual chamber devices have been developed in order to minimise ventricular stimulation. These are being evaluated at present. In my opinion there is still a place for atrial pacing in selected patients with sick sinus syndrome with a minimum risk of developing complete atrioventricular block. (Neth Heart J 2008;16(suppl 1): S25-S27.)     

Ganglionic Plexus Ablation During Pulmonary Vein Isolation - Predisposing to Ventricular Arrhythmias?

Catheter ablation is increasingly used to treat patients with atrial fibrillation (AF). Ablation of ganglionic plexi is often performed to reduce vagal innervation and has been shown to confer a better long-term outcome in terms of AF recurrence. We report a case of a patient having AF ablation with a profound vagal response, suggesting ganglionic plexus ablation, who subsequently developed ventricular fibrillation after programmed ventricular stimulation. Reduced vagal modulation is known to predispose to ventricular arrhythmias and vagal denervation following AF ablation may predispose to ventricular arrhythmias and requires further study.     

Direction-dependent conduction abnormalities in a canine model of atrial fibrillation due to chronic atrial dilatation

Chronic rapid atrial pacing (RAP) leads to changes that perpetuate atrial fibrillation (AF). Chronic atrial dilatation due to mitral regurgitation (MR) also increases AF inducibility, but it is not clear whether the underlying mechanism is similar. Therefore, we have investigated atrial electrophysiology in a canine MR model (mitral valve avulsion, 1 mo) using high-resolution optical mapping and compared it with control dogs and with the canine RAP model (6-8 wk of atrial pacing at 600 beats/min, atrioventricular block, and ventricular pacing at 100 beats/min). At followup, optical action potentials were recorded using a 16 x 16 photodiode array from 2 x 2-cm left atrial (LA) and right atrial (RA) areas in perfused preparations, with pacing electrodes around the field of view to study direction dependency of conduction. Action potential duration at 80% repolarization (APD(80)) was not different between control and MR but was reduced in RAP atria. Conduction velocities during normal pacing were not different between groups. However, the MR LA showed increased conduction heterogeneity during pacing at short cycle lengths and during premature extrastimuli, which frequently caused pronounced regional conduction slowing. Conduction in the MR LA during extrastimulation also displayed a marked dependence on propagation direction. These phenomena were not observed in the MR RA and in control and RAP atria. Thus both models form distinctly different AF substrates; in RAP dogs, the decrease in APD(80) may stabilize reentry. In MR dogs, regional LA conduction slowing and increased directional dependency, allowing unidirectional conduction block and preferential paths of conduction, may account for increased AF inducibility.     

Unusual Tachycardia Association In A patient Without Structural Heart Disease

We report an unusual association of persistent atrial flutter and bundle branch re-entrant ventricular tachycardia in a young patient without structural heart disease. Atrial flutter masked the infra-Hisian conduction disease, was fundamentally dependent on a long PR interval, and could be a possible trigger of ventricular tachycardia.     

HL-1细胞培养及房颤细胞模型的建立

目的:利用HL-1细胞建立快速起搏模型,对心房颤动(atrial fibrillation,AF)早期的重构现象进行初步研究。方法:培养HL-1细胞,建立快速电场刺激起搏细胞模型,利用全细胞膜片钳技术记录刺激前后HL-1细胞的动作电位周期,透射电镜观察细胞超微结构的变化。结果:将细胞接种于培养皿中,72 h后细胞呈融合状态,全细胞膜片钳记录培养HL-1细胞及经电场刺激(600次/min,1 V/cm)24 h后的心房肌细胞的动作电位周期,动作电位周期分别为106 ms,45 ms,刺激前后差异有统计学意义(P0.05)。透射电镜观察到刺激后HL-1细胞超微结构发生去分化改变。结论:经快速起搏24 h后,HL-1细胞发生了电及结构重构;利用HL-1细胞建立快速起搏的房颤模型,可以对房颤早期的重构机制进行研究。     

Effect of atrio-ventricular conduction on the appearance of supraventricular arrhythmia and thrombotic complications in patients with chronic stimulation of cardiac ventricles in sick sinus syndrome]

Two hundred three patients with sick sinus node disease were treated with continuous ventricular stimulation between 1981 and 1985. To 1988, 168 patients aged between 26 and 88 years were followed-up for 5.1 years on the average. All these patients were divided into two groups: I (93 patients) with sinusal bradycardia, and group II (93 patients) with brady-tachycardia. Ventriculo-atrial conduction was seen in 82.61% of patients of group I in whom the implantation of electric stimulator produced the attacks of atrial fibrillation, and in 44.23% of patients without such attacks (p < 0.01); in 80.77% of patients of group II in whom atrial fibrillation became stable with time, and in 50.57% with intermittent atrial fibrillation (p < 0.01) ventriculo-atrial conduction was noted. It may be concluded, that the presence of ventriculo-atrial conduction in patients with prolonged stimulation of the cardiac ventricles favor the occurrence and stabilization of the paroxysmal atrial fibrillation and thrombotic complications.     

The role of stretch-activated channels in atrial fibrillation and the impact of intracellular acidosis

The incidence of atrial fibrillation correlates with increasing atrial size. The electrical consequences of atrial stretch contribute to both the initiation and maintenance of atrial fibrillation. It is suggested that altered calcium handling and stretch-activated channel activity could explain the experimental findings of stretch-induced depolarisation, shortened refractoriness, slowed conduction and increased heterogeneity of refractoriness and conduction. Stretch-activated channel blocking agents protect against these pro-arrhythmic effects. Gadolinium, GsMTx-4 toxin and streptomycin prevent the stretch-related vulnerability to atrial fibrillation without altering the drop in refractory period associated with stretch. Changes the activity of two-pore K+ channels, which are sensitive to stretch and pH but not gadolinium, could underlie the drop in refractoriness. Intracellular acidosis induced with propionate amplified the change in refractoriness with stretch in the isolated rabbit heart model in keeping with the clinical observation of increased propensity to atrial fibrillation with acidosis. We propose that activation of non-specific cation stretch-activated channels provides the triggers for acute atrial fibrillation with high atrial pressure while activation of atrial two-pore K+ channels shortens atrial refractory period and increases heterogeneity of refractoriness, providing the substrate for atrial fibrillation to be sustained. Stretch-activated channel blockade represents an exciting target for future antiarrhythmic drugs.     

Atrial Pacing to Control Heart Rate and Rhythm in Acute Cardiac Conditions

Increasing the heart rate by a bedside atrial pacing technique was successfully utilized to treat serious cardiac arrhythmia or failure in 13 patients. Nine of these had ventricular arrhythmia refractory to drugs. Seven had evidence of sinus node depression or disease since their sinus pacemaker was below 70 beats per minute under decompensated conditions. In five, coronary artery disease was associated with the bradycardia and in two, digitalis toxicity was related to depression of the intrinsic pacemaker rate. Two patients in the coronary group required implantation of a permanent demand ventricular pacemaker. Hemodynamic studies were performed in seven patients. Only one patient had no increase in cardiac output with pacing rates above his resting rate. The other six patients showed an increase in cardiac output from 22 to 81% at paced rates between 70 and 125/minute. The duration of pacing ranged from one hour to 14 days and averaged five days.     

Magnesium Therapy for Intractable Ventricular Tachyarrhythmias in Normomagnesemic Patients

Intractable ventricular tachyarrhythmia associated with hypomagnesemia responds well to magnesium given intravenously. Two patients with recurrent ventricular tachycardia and ventricular fibrillation associated with normal serum magnesium levels and resistant to treatment with potassium chloride, lidocaine and bretylium tosylate responded dramatically to the administration of magnesium sulfate. A third patient in whom the serum magnesium level was unknown also showed dramatic response to magnesium therapy.Magnesium depletion probably interferes with sodium-potassium adenosine triphosphatase enzyme activity and causes ionic imbalance and electrical instability of purkinje''s fibers. Without obvious magnesium depletion this element in high concentration may still prolong transient inward current, prolong the effective refractory period, increase the membrane potential and control ventricular tachyarrhythmia.When ventricular fibrillation or malignant ventricular tachycardia cannot be controlled with lidocaine and other conventional drugs, we recommend infusing magnesium sulfate, 2 to 3 grams in one minute, followed by 10 grams over five hours.     

持续正压通气治疗阻塞性睡眠呼吸暂停综合征并发心房纤颤的临床研究

目的:研究持续正压通气治疗阻塞性睡眠呼吸暂停综合征(OSAHS)并发心房纤颤的临床疗效。方法:选取2013年1月到2014年1月我院收治的OSAHS并发心房纤颤患者60例,按照随机数字表法将患者分为实验组和对照组,每组30例。对照组给予常规治疗,实验组在对照组的基础上给予持续正压通气治疗,两组均治疗1年。分析治疗前、后两组心率(HR)、血氧饱和度(SPO2)、左心射血分数(LVEF)、脑钠肽(BNP),并比较两组心房纤颤转复率、复发率和不良反应。结果:治疗后实验组HR、SPO2、LVEF以及BNP显著优于对照组,两组比较差异具有统计学意义(P0.05);治疗后实验组心房纤颤转复率显著高于对照组,心房纤颤复发率显著低于对照组,两组比较差异具有统计学意义(P0.05);两组不良反应发生率比较无统计学意义(P0.05)。结论:持续正压通气治疗OSAHS并发心房纤颤具有较好的效果,有利于改善心功能,提高心房纤颤转复率降低房纤颤复发率。     

起搏器术后新发房性心律失常的影响因素分析

目的:探讨起搏器术后新发房性心律失常的发生情况及其相关影响因素。方法:选择2006年1月至2007年12月于沈阳军区总医院首次植入永久起搏器的107例患者,男性50例,平均年龄65.0±11.9岁,术前通过追问病史及相关检查均排除房性心律失常(房颤、房扑、房速),术后平均随访3.9年,观察新发房性心律失常情况。按术后是否出现房性心律失常,将患者分为新发房性心律失常组和无房性心律失常组,比较两组患者术前和术后心脏超声结果的变化、心室起搏比例、起搏部位及起搏模式,并通过logistic回归分析起搏器术后发生房性心律失常的影响因素。结果:新发房性心律失常组26例(24.3%),其中房颤17例(15.9%),房扑2例(1.9%),房速7例(6.5%);无房性心律失常组81例。与无房性心律失常组比较,新发房性心律失常组左房内径明显增加(P=0.040)、二尖瓣返流程度较重(P=0.032)及左室射血分数明显下降(P=0.001),心室起搏百分比(VP%)显著升高(P=0.017)。心尖部起搏患者房性心律失常的发生率明显高于间隔部起搏(33.3%vs 16.9%,P<0.05),双腔起搏组患者房性心律失常发生率明显低于单腔起搏器组(18.7%vs 37.5%,P<0.05)。Logistic回归分析显示术后新发房性心律失常的发生与高比例的心室起搏(P=0.006)、VVI(R)起搏模式(P=0.014)及右心室起搏电极导线植于心尖部(P=0.024)显著相关。结论:起搏模式、心室起搏百分比、起搏部位是起搏器术后发生房性心律失常的影响因素。     

Three-dimensional electroanatomical mapping for non-pulmonary vein foci in a patient with complete situs inversus and dextrocardia

In patients with atrial fibrillation (AF) having congenital anatomical abnormalities, such as complete situs inversus and dextrocardia, pulmonary vein isolation (PVI) ablation can be performed safety using a three-dimensional electroanatomical mapping system. However, it is not clear whether a three-dimensional electroanatomical mapping system can be used to detect non-PV ectopic beats initiating AF in patients with complete situs inversus and dextrocardia. Here, we report a 21-year-old man with complete situs inversus and dextrocardia, who showed AF caused by non-PV ectopic beats. We successfully detected the origin of the triggered activity from the non-PV foci using three-dimensional electroanatomical mapping.     

Dual chamber pacing mode in an atrial antitachycardia pacing device without a ventricular lead – A necessary evil

We present a case of a single chamber atrial pacemaker implanted for sinus node dysfunction and treatment of macroreentrant atrial tachycardias with atrial antitachycardia pacing. The patient presented with sustained atrial tachycardia above the detection rate, however, the device was unable to detect the tachycardia and did not deliver the programmed therapy. We discuss the nuances of the atrial tachyarrhythmia detection algorithms, and the programming strategies to maximize detection of atrial arrhythmias in a single chamber atrial pacemaker.