Electrophysiological, Rate Dependent, and Autonomic Effects of the Class III Antiarrhythmic Almokalant After Myocardial Infarction in the Pig

Ventricular arrhythmias remain a major problem, in particular in patients with left ventricular dysfunction or heart failure. In this group of patients, Class I drugs were shown to be ineffective, and they even increased mortality during chronic treatment. New antiarrhythmic agents should preferably not only have pure antiarrhythmic effects, but should also be free from adverse autonomic properties. In the present study, the electrophysiological, rate dependent and autonomic effects of intravenously administered almokalant, a new Class III antiarrhythmic drug, were investigated in nine pigs surviving a myocardial infarction. The ventricular effective refractory period (VERP) increased after almokalant (loading dose: 0.05 μmoLkg ^?1 .min^?1, continuous infusion: 0.0025 uμmol/kg^?1.min^?1) from 292 ± 25 to 308 ± 13 ms (pacing cycle length [PCL] 500 ms + 1 extrasystole [ES]), from 249 ± 19 to 261 ± 16 ms (PCL 400 ms +1ES), and from 209 ± 18 to 219 ± 18ms (PCL 300 ms +1ES). The VERPs increased most after three ES at PCL 400 ms: from 167 ± 27 to 186 ± 29 ms (P < 0.05) and at PCL 300 ms: from 159 ± 29 to 174 ± 27 ms (P < 0.05). The ventricular monophasic action potential durations (MAPD) were similarly prolonged and the ratio VERP/MAPD did not change. Prolongation of MAPD after almokalant remained present at short pacing cycle lengths. Before almokalant infusion, sustained monomorphic ventricular tachycardia (VT) was inducible in two pigs, and nonsustained VT in a third animal. After almokalant, only one pig remained inducible. Two weeks after myocardial infarction, heart rate variability and baroreflex sensitivity were reduced. Furthermore, subsequent electrophysiological testing transiently reduced these parameters of autonomic activity. During almokalant however, no changes in autonomic functions were observed after programmed stimulation. Heart rate variability decreased after myocardial infarction from 6.3 ± 2.5 ms to 5.4 ± 4,2 ms (P = NS}. After programmed stimulation, it further decreased to 2.8 ± 2.0 ms (P = 0.028). Almokalant infusion prevented autonomic deterioration: 3.3 ± 2.2 ms before stimulation and 3.3 ± 1.3 after stimulation (P = NS). In postinfarct pigs, almokalant prolongs VERP and MAPD at shorter pacing cycle lengths. The results indicate absence of reverse rate dependence and of adverse autonomic changes.     

Electrophysiological Effects of E 4031, a Drug with Selective Class III Properties, in Man

We studied the electrophysiological effects ofE 4037, given in a dose ascending manner (1.5, 3.0, and 6.0 μg/kg over 5 min followed by 0.1, 0.2, and 0.4 μg/kg per min for 60 min, respectively) to 19 volunteers. There were significant, dose related linear increases in QT and QT_C intervals, in atrial functional and effective refractory periods (ERPs) at a paced cycle length of 400 ms, and in ventricular functional and ERPs at a paced cycle length of 600 ms. There was no significant change in the AH and HV intervals or QRS duration. No significant proarrhythmic or other side effects were encountered during the administration of the drug. E 4031 prolongs atrial and ventricular refractoriness without significantly affecting AV or intraventricular conduction, consistent with selective Class III properties. At the doses used in the present study, intravenous infusion of E 4031 appears to be safe and well tolerated.     

Results of Electrophysiological Testing and Long-Term Follow-Up in Patients Sustaining Cardiac Arrest Only While Receiving Type IA Antiarrhythmic Agents

Therapeutic management of patients sustaining a cardiac arrest while receiving antiarrhythmic agents can be difficult since the role of the drug in possibly facilitating the arrhythmia is often difficult to define. To determine if the response to programmed stimulation could give insight into which patients may have experienced a drug-induced cardiac arrest, we studied 29 patients (61 +/- 9 years) with no prior history of sustained ventricular tachyarrhythmias (VT) who suffered a cardiac arrest only while receiving type Ia antiarrhythmic agents. Patients with documented myocardial infarction, acute ischemia, electrolyte abnormalities, or torsade de pointes were excluded from the study. Twenty-four patients had coronary artery disease with prior myocardial infarction (ejection fraction 28% +/- 9%) and five patients had idiopathic dilated cardiomyopathy (ejection fraction 31% +/- 6%). During baseline electrophysiological testing, 19 patients (66%) had inducible sustained ventricular arrhythmias: uniform VT, n = 14 (group I), polymorphic VT or ventricular fibrillation, n = 5 (group II). Ten patients (group III) had no inducible sustained ventricular arrhythmias. To determine if rechallenge with a type Ia agent could facilitate induction of a sustained ventricular arrhythmia in group III, eight patients underwent ten electrophysiological studies during therapy with either procainamide or quinidine. Only two patients developed sustained VT in response to programmed stimulation. Patients in groups I and II received therapy guided by electrophysiological testing, including antiarrhythmic agents alone (n = 8), subendocardial resection (n = 4), or an implantable cardioverter defibrillator (n = 7). Patients in group III received antiarrhythmic agents empirically (n = 3), or for treatment of atrial tachyarrhythmias (n = 2) or nonsustained VT (n = 1). In addition, four patients in group III received an implantable cardioverter defibrillator. During a mean follow-up of 28 +/- 27 months (range: 1 day-84 months) 13 patients died suddenly or received a defibrillator shock preceded by syncope or presyncope: group I: n = 5; group II: n = 2; group III: n = 6. In conclusion: (1) most patients sustaining a cardiac arrest only in the presence of type Ia antiarrhythmic agents have inducible sustained VT in the absence of antiarrhythmic agents, and (2) the risk of recurrent VT persists in patients without inducible sustained arrhythmias in the drug-free state, regardless of whether they manifest inducible arrhythmias after rechallenge with a type Ia agent.     

The Effect of Bidisomide (SC-40230), a New Class Ia/Ib Antiarrhythmic Agent, on Defihrillation Energy Requirements in Dogs with Healed Myocardial Infarctions

Bidisomide is a Class Ia/Ib antiarrhythmic agent with activity against ventricular and supraventricular arrhythmias. The potential for bidisomide to increase defibrillation threshold (DFT) was tested in anesthetized dogs with healed left ventricular infards (≥ 10 days). Defibrillation patches were attached to each ventricle and shocks were delivered via an external cardioverter/defibrillator. Three groups were studied: placebo (saline), canine therapeutic bidisomide (TB, 2–5 μg/mL plasma concentration) and supratherapeutic bidisomide (STB, 6–14 μg/mL). Each animal received only one treatment. An abbreviated DFT curve was determined before and after treatment. Heart rate, blood pressure, PR, QRS, infarct size, and hematocrit were also measured be/ore and after treatment. DFT was significantly increased (average + 3 to +5 joules [J], P < 0.05) by TB and STB. TB (5/5) did not increase DFT beyond 40 J. In 6/7 experiments, STB did not increase DFT beyond 40 J. Placebo (n = 6) had no significant effect on DFT. Infarct size (x = 11% of the left ventricle) was not significantly different between groups. Heart rate and QRS were not significantly altered but blood pressure was significantly decreased (16%-31% systolic, 29%-45% diastolic) and hematocrit was significantly increased (19% to 25%) in oil groups. PR was significantly increased by STB only. Conclusion: therapeutic and supratherapeutic doses of bidisomide slightly but significantly increased DFT (3–5 J) in a canine infarcted heart model.     

Sotalol: From "Just Another Beta Blocker" to "The Prototype of Class III Antidysrhythmic Compound"

Sotalol is a beta-blocking drug devoid of membrane stabilizing properties, as well as intrinsic sympathomimetic actions, or cardioselectivity. In addition, sotalol prolongs atrial and ventricular repolarization (Class III antiarrhythmic activity). It appears to have less myocardial depressant effect than other beta-blocking agents. Given orally, bioavailability of the drug reaches 100%. Sotalol's plasma half-life is 15 hours (range 7–18) and is dependent only on renal function. In clinical practice, it has been found effective in the suppression of nearly all supraventricular and ventricular dysrrhythmias except those related to prolonged ventricular repolarization. Most common adverse effects are dyspnea, bradycardia, and fatigue, which results in drug termination in 16% of the cases. Torsades de pointes usually associated with bradycardia and drug induced QTc prolongation has been reported in 1.9%–3.5% of the patients receiving sotalol. This complication may be reduced by limiting the dose (< 640 mg/day) especially in patients with impaired renal function. In addition hypokalemia must be avoided. To sum up, the combination of Class II and Class III effects may carry additional benefits. However, further studies are required to test such hypotheses.     

Comparison in the Same Patient of Aberrant Conduction and Bundle Branch Reentry After Dofetilide, a New Selective Class III Antiarrhythmic Agent

Dofetilide may induce aberrant intraventricular conduction due to its Class III effect. This report describes an atrial fibrillation patient in whom intraventricular conduction was studied before and after dofetilide using multiple endocardial recordings. Dofetilide provoked aberrant conduction during atrial fibrillation, and aberrancy could be mimicked with programmed atrial stimulation after restoration of sinus rhythm. However, during right ventricular slimulation, isolated bundle branch reentrant beats were recorded after induction of critical retrograde conduction delays. This occurred in the setting of relatively large differences in refractoriness between the right bundle branch and the right ventricular myocardium. This favored distal retrograde bundle branch block during ventricular extrastimulation, in turn enhancing bundle branch reentry. This potendal proarrhythmic mechanism deserves close attention in the further deveiopmeni of dofetilide and also of other new "pure" Class III agents.     

Cumulative Effects of Amiodarone on Inducibility of Ventricular Tachycardia: Implications for Electrophysiological Testing

To determine whether the slow onset of action of amiodarone might result in a delayed effect on the inducibility of sustained ventricular arrhythmias, 45 patients with ischemic heart disease and inducible sustained monomorphic ventricular tachycardia were prospectively studied. Each patient had at least one initial repeat study on amiodarone and those with persistently inducible arrhythmias were rescheduled for further studies over the following 24 weeks. After 2-3 weeks of amiodarone therapy, nine patients no longer had inducible tachycardias, and tachycardia in another eight patients (18%) later became noninducible. Using life-table methods, analysis based on the results of the first re-study showed 18-month recurrence rates of 43% in the inducible vs 17% in the noninducible groups (p = 0.056). When the results of additional testing were then used to reclassify patients, the recurrence rates for these two groups were 50% and 17%, respectively (p = 0.004). Observation of blood pressure and level of consciousness during induced arrhythmias was also predictive of clinical tolerance in patients having recurrences; 16 of 19 patients experienced symptoms of similar severity to those produced during testing. We conclude: (1) early testing of amiodarone may result in misclassification of some patients as remaining inducible; (2) re-testing at a later time more accurately predicts tachycardia recurrence; (3) observation of hemodynamic response also provides important prognostic information.     

The Novel Class III Antiarrhythmic Agent MS-551 Blocks the Cardiac Inward Rectifier With Greater Potency Than Sotalol or E-4031: Possible Relevance to Reverse Use Dependence

BACKGROUND: The tendency for the electrophysiologic effect of class III antiarrhythmic agents (action potential prolongation) to be diminished at faster heart rates represents a major drawback of this class of drug and is usually referred to as "reverse use dependence." A novel class III agent, MS-551, has recently been reported to exhibit less reverse use dependence than E-4031. We set out to investigate whether this observation may be due to differential blockade of the inward rectifier current (i(K1)) by these drugs. METHODS AND RESULTS: We recorded i(K1) using single channel methods and cell attached patch configurations, with standard patch clamp technology. Neither E-4031 nor racemic sotalol in concentrations up to 100 μM had any significant effect on the open probability or kinetics of i(K1) without altering the single-channel conductance. Openings to subconductance levels were abolished in three of six patches in which they had been frequently present in the absence of drug. MS-551 had no effect on mean channel open time but increased the slower component of the closed time. CONCLUSIONS: MS-551, unlike E-4031 and sotalol, appears to produce significant blockade of the inwardly rectifying potassium channel at clinically relevant concentrations. We propose that this might provide a partial explanation for the observed differences in their response to rate changes.     

Clinical Electrophysiological Effects of Intravenous Recainam: An Antiarrhythmic Drug Under Investigation for the Treatment of Ventricular and Supraventricular Arrhythmias

This open-label, multicenter study was designed to assess the electrophysiological properties of intravenous recainam, an investigational Class I antiarrhythmic agent. In 25 patients undergoing electrophysiological studies for the evaluation of arrhythmias, recainam was administered intravenously in a loading infusion (0.1 mg/kg/min) for 40 minutes, followed by a maintenance infusion (0.02 mg/kg/min) until the completion of the study. Electrophysiological measurements were obtained at baseline, 30 minutes after initiation of the loading infusion, and 30 minutes after termination of the infusion during washout. Conduction intervals, refractory periods, and sinus node recovery times were measured during sinus rhythm and during atrial or ventricular pacing. Vital signs were obtained and recorded before, during, and after recainam infusion. The results showed no change in mean arterial pressure, but heart rate increased slightly by 4 beats/min following recainam infusion. Recainam produced a generalized slowing of intracardiac conduction. The mean intraatrial conduction time, measured at an atrial paced cycle length of 600 msec, increased during recainam loading infusion by 44%, from 38.8% +/- 2.8 to 53.0 +/- 5.4 msec; intranodal conduction time increased by 10%, from 102.0 +/- 5.5 to 112.1 +/- 5.2 msec; and infranodal conduction time increased by 31% from 53.1 +/- 3.0 to 70.7 +/- 3.8 msec. Slowed conduction persisted during washout. The mean right atrial effective refractory period was significantly prolonged (+7% at 600 msec cycle length and +8% at 450 msec cycle length, P less than 0.05 and P less than 0.01, respectively) during recainam loading and remained so during washout.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of Isoflurane on Electrophysiological Measurements in Children with the Wolff-Parkinson-White Syndrome

This study was designed to assess the effects of isoflurane (ISO) on the electrophysiological properties of the accessory pathway, atrium, ventricle, and AV node in children with the Wolff-Parkinson-White (WPW) syndrome. The results of programmed electrical stimulation were analyzed in 51 patients (4 months to 17 years of age) with WPW. The study population was divided into two groups. Twenty-seven patients received local anesthesia and intramuscular injection of meperidine, promethazine, and chlorpromazine (MPC group). Twenty-four patients received general anesthesia with ISO inhalation (ISO group). We compared the antegrade effective refractory period of the accessory pathway (antegrade APERP), ventricular effective refractory period (VERP), atrial effective refractory period (AERP), AH interval, and cycle length of circus movement tachycardia (CMT-CL) in 12 pairs of age and sex matched patients selected from the MPC and ISO groups. Of the 12 pairs of age and sex matched patients, antegrade APERP in patients who received ISO (299 ± 17 ms, mean ± SEM) was significantly longer as compared with matched patients in the MPC group (262 ± 5 ms, P < 0.025). The VERP and AERP in patients from the ISO group were significantly prolonged compared with the MPC patients (239 ± 7 vs 210 ± 8 ms, P < 0.025, and 228 ± 11 vs 180 ± 6 ms, P < 0.01, respectively). There was no significant difference in the AH interval or CMT-CL between the two subgroups. Thus, ISO prolongs the antegrade APERPs as well as the effective refractory periods of atrial and ventricular muscle in children with WPW, while the AH interval and CMT-CL appear to be unaffected. Care must be taken in interpreting measurements of the antegrade APERP made in patients under general anesthesia for RF ablation of accessory pathways.     

Increased Pacing Threshold After an Automatic Defibrillator Shock in Dogs: Effects of Class I and Class II Antiarrhythmic Drugs

A high energy shock delivered by an automatic defibrillator may interfere with pacemaker function. To provide insight into the changes that occur in the threshold for ventricular pacing after the shock from an automatic defibrillator, we measured the time to capture during asynchronous ventricular pacing in dogs from endocardial or epicardial sites, after a 30 joule shock was delivered via conventional automatic defibrillator (AICD) patch electrodes. After a 30 joule shock, there was a transient loss of ventricular capture. The duration of capture loss was related to current strength. During endocardial pacing at threshold current, the time to capture was 4.9 +/- 1.2 s, whereas at current values twice threshold the time to capture from endocardial pacing was 2.2 +/- 0.9 s. No difference was found between endocardial and epicardial pacing sites in the time to capture. To ascertain the mechanism of capture loss we: (1) examined the effects of converting the pacing catheter to a current sink (transiently shunting to ground); (2) altered excitability by an infusion of flecainide; (3) blocked sympathetic input (propranolol). No change in time to capture was noted by shunting the pacer to ground. After an infusion of flecainide the time to capture from endocardial pacing was significantly prolonged to 14.9 +/- 2.2 s at the threshold value (P less than .01) and 5.6 +/- 2.1 s at twice threshold (P less than .05). Conversely, intravenous propranolol had no effect on the time to capture after shock from endocardial pacing. These data indicate that there is a transient increase in pacing threshold after the shock from an automatic defibrillator.(ABSTRACT TRUNCATED AT 250 WORDS)     

Prediction of Antiarrhythmic Efficacy of Class I and III Agents in Patients with Ventricular Tachycardia by Signal-Averaged ECG Analysis

The effects of procainamide and dofetilide (pure Class III antiarrhythmic agent) on the signal-averaged ECG (SAECG) were examined in relation to the results of programmed ventricular stimulation studies in 25 patients with inducible sustained monomorphic ventricular tachycardia. Procainamide prolonged significantly the total QRS and low amplitude signal durations (140 ± 31 msec vs 166 ± 48 msec, P < 0.0001; 50 ± 25 msec vs 65 ± 38 msec, P < 0.002, respectively) whereas the root mean square voltage of the last 40 msec of the QRS complex was significantly reduced (22 ± 21 (iV vs 13 ± 12 p-V, P < 0,006). Procainamide was effective (prevention of the inducibility of sustained ventricular tachycardia or prolongation of the cycle length of ventricular tachycardia by > 100 msec) in 15 of 27 drug trials. Of the procainamide induced SAECG changes, the fractional prolongation of the total QRS duration was the best parameter that identified effectively treated patients (24%± 16% in responders vs 10%± 11% in nonresponders, P < 0.014). Afractional prolongation of the total QRS duration by > 15% identified effectively treated patients with a sensitivity of 87%, specificity of 81%, and an overall predictive accuracy of 84%. Dofetilide did not change the SAECG, and no SAECG parameter predicted the results of programmed ventricular stimulation. The effects of both drugs on the spectral analysis (area ratios) and on the spectral temporal mapping (the values of normality factor) of the SAECG were not consistent. In conclusion, antiarrhythmic efficacy of procainamide can be predicted by the degree of drug induced prolongation of the signal-averaged QRS complex. Dofetilide does not significantly affect the SAECG, and its efficacy cannot be predicted by the SAECG analysis.     

The Ventricular Excitability-Interval Relationship in Early Diastole in Humans: The Influence of the Electrode Configuration During Bipolar Stimulation

The purpose of this study was to determine the relationship between ventricular excitability and the extrastimulus (S2) coupling interval in early diastole in humans. The influence of the electrode configuration during bipolar stimulation was examined. Ventricular strength-interval curves were constructed using an eight beat drive train at a cycle length of 600 msec, 2-msec decrements in the S2 coupling interval, and 0.2-mA increments in the current intensity of S2 at each coupling interval. A transient dip in the excitation threshold was observed in early diastole during bipolar pacing when the distal electrode was the anode in six of 17 patients (35%). In contrast, this type of dip was not observed when the distal electrode was the cathode. The excitation threshold at the trough of the dip ranged from 1.0 to 2.2 mA. Unipolar strength-interval curves indicated that a dip occurred with anodal but not cathodal pacing. We postulated that the dip might interfere with the accurate determination of the ventricular effective refractory period by resulting in transient loss of ventricular capture during decremental scanning of diastole with S2. A gap in ventricular capture was produced in all six patients who demonstrated a dip in the bipolar strength-interval curve by selecting an S2 current intensity that fell within the dip. In conclusion, the bipolar strength-interval curve may display an early diastolic dip in the excitation threshold, depending on the electrode configuration.(ABSTRACT TRUNCATED AT 250 WORDS)     

广东省三级医院护理人力资源分析

目的对广东省内三级医院护理人员相关信息进行调查研究,了解护理人力资源管理政策模型实施的基础。方法采取发文的形式．分别于2007年度及2008年度对65家和69家三级医院进行调查。调查内容主要包括：病床使用率、医院护士总数、病房护士数量、病房护士与床位的比例、监护病房与床位的比例、合同护士的数量、有护理专业大专以上学历的比例等,用SAS9．13统计软件录入及分析数据。结果2年均调查的54家医院中病床数明显增加,2008年与2007年相比,病床平均使用率增加,床护比未达标比例仍然较大,合同护士比例占较大比重,护理人员学历不断提高。2008年调查结果,护士离职率〉10％的医院占4．3％;护士离职率介于5％～10％之间的医院占27．5％。结论广东省三级医院依然存在护理人力资源不足的问题,调查医院中不同程度存在护士离职的现象,护士队伍稳定仍然是迫切需要解决的问题,探讨高效的护理人力资源管理模式势在必行。     

Antiarrhythmic Effects of VVI Pacing at Physiologic Rates: A Crossover Controlled Evaluation

Ventricular pacing can prevent bradycardia-dependent ventricular ectopic activity (VEA) and is helpful in some cases of drug-refractory venfricuiar tachycardia (VT). This study is a prospective evaluation of VVI pacing for the control of VEA not related to underlying bradycardia, drug side-effects, or prolonged QT interval syndromes. Twenty-nine patients undergoing serial electrophysioiogic-pharmacoiogic testing for VT control were studied. Eighteen of these patients (12 men; meon age = 60.1) both completed ihe protocol and had sufficient VEA for analysis. Coronary disease was present in 13 patients, cardiomyopathy in two patients, and one patient each had myocarditis, mitral valve prolapse, and no structural heart disease. Ambulatory (Holter) monitor recordings during VVI pacing were compared with control recordings made in the absence of pacing, VVI pacing rates were 10–15 bpm above the mean daily heart rate (mean = 92 bpm; range = 63–110). Hours from paced recordings were paired with hours from control (prior to analysis) according to time of day to reduce the effects of spontaneous variability in VEA frequency. Overall, VVI pacing reduced ventricular premature complexes (VPGs) 26% from 331 to 245/hour (p < 0.001). During pacing, couplets (pairs, successive VPGs) were reduced from 6.95 to 1.03/hour (p < 0.000001) and VT (≥3 successive VPCs) from 0.89 to 0.045 episodes/hour (p < 0.003). Of 13 patients with couplets, 11 had ≥50% reduction and five had ≥90% reduction. Baseline VT was eliminated in four out of nine patients during pacing. Pacing did not increase VEA significantly in any patient. In this group of patients, reduction of VEA by VVI pacing was significant and was comparable to pharmacologic interventions. Higher forms of VEA fcouplets and VT) appeared to respond better than single VPCs. Further studies may define patients with VEA who can benefit from pacing     

Effects of Left Atrial Dilatation on the Endocardial Atrial Defibrillation Threshold: A Study in an Ovine Model of Pacing Induced Dilated Cardiomyopathy

Left atrial (LA) dilatation is a common finding in patients with chronic atrial fibrillation (AF). Progressive dilatation may alter the atrial defibrillation threshold (ADFT). In our study, epicardial electrodes were implanted on the LA free wall and right ventricular apex of eight adult sheep. Large surface area, coiled endocardial electrodes were positioned in the coronary sinus and right atrium (RA). LA dilatation was induced by rapid ventricular pacing (190 beats/min) for 6 weeks and echocardiographically assessed weekly along with the ADFT (under propofol anesthesia). LA effective refractory period (ERP) was measured every 2–3 days using a standard extra stimulus technique and 400 ms drive. The AF cycle length (AFCL) was assessed from LA electrograms. During the 6 weeks of pacing the mean LA area increased from 6.1 ± 1.5 to 21.3 ± 2.4 cm². There were no significant changes in the mean ADFT (122 ± 15 V), circuit impedance (46 ± 5 Ω), or LA AFCL (136 ± 23 ms). There was a significant increase in the mean LA ERP (106 ± 10 ms at day 0, and 120 ± 13 ms at day 42 of pacing). In this study, using chronically implanted defibrillation leads, the minimal energy requirements for successful AF were not significantly altered by ongoing left atrial dilatation. This finding is a further endorsement of the efficiency of the coronary sinus/RA shock vector. Furthermore, the apparent stability of the AF present may be a further indication of a link between the type of AF and the ADFT.     

上海市某三级甲等医院患者就医心态的现状调查

目的调查并了解三级甲等医院门急诊及住院患者就医心态的现状。方法便利抽样法选择上海市某三级甲等医院2015年3-5月收治的441例门急诊及住院患者为研究对象,自制患者就医心态调查问卷对其进行调查。结果患者就医心态复杂多样,表现在医疗信任度较好、治疗效果预期过高、就诊急切度高、对医疗费用的满意度不高、紧张和焦虑心理、就医找熟人心理及较理性认识不愉快就医经历等。结论医护人员应充分了解患者的就医心态、需求及影响因素,并采取针对性的措施,同时应加强医患沟通,减少医患矛盾与纠纷的发生。     

Dependency on Atrial Electrophysiological Properties of Appearance of Paroxysmal Atrial Fibrillation in Patients with Wolff-Parkinson-White Syndrome: Evidence from Atrial Vulnerability Before and After Radiofrequency Catheter Ablation and Surgical Cryoablation

The pathogenesis of paroxysmal atrial fibrillation in patients with Wolff-Parkinson-White syndrome and the effects of elimination of accessory pathways on the appearance of atrial fibrillation are still controversial. Fifty-four patients with Wolff-Parkinson-White syndrome were classified into three groups: a No AFgroup (n = 24), patients without paroxysmal atrial fibrillation; an RF-AF Group (n =12), patients with paroxysmal atrial fibrillation whose accessory pathways were eliminated using radiofrequency catheter ablation; and a Cryo-AF Group (n = 18), patients with paroxysmal atrial fibrillation whose accessory pathways were eliminated with surgical Cryoablation. The electrophysiological characteristics of each group were evaluated prior to and following the elimination of their accessory pathways. As indices of atrial vulnerability, the presence of fragmented atrial activity and repetitive atrial firing zones were assessed. Deducibility of atrial fibrillation was significantly reduced following ablation of accessory pathways in the Cryo-AF group (83.3%-5.6%, P < 0.0001), while it was unchanged in the RF-AF group (83.3%-75%). In preablation studies, the effective refractory periods of the atrium in the RF-AF group and the Cryo-AF group were significantly shorter compared with the No AF group (204 ± 18 ms, 197 ± 16 ms vs 246 ± 44 ms, respectively, P < 0.0001). Following ablation, the effective refractory period for patients in the Cryo-AF group was significantly prolonged compared with before ablation (197 ± 16 ms to 232 ± 24 ms, P < 0.0001). As a result of this prolongation of the effective refractory period of the atrium, the fragmented atrial activity and repetitive atrial response zones narrowed following ablation in the Cryo-AF group, but not in the RF-AF group. Therefore, the pathogenesis of atrial fibrillation in patients with Wolff-Parkinson-White syndrome may depend on the refractory period of the atrium rather than on the presence of accessory pathways.     

快速心房起搏对家兔心房肌L型钙离子通道的影响及氯沙坦干预的研究

目的 探讨以人工心脏起搏的方法制备家兔急性心房纤颤(atrial fibrillation,AF)模型时心房发生电重构的机制和干预方法.方法 家兔45只随机分为生理盐水(NS)组、生理盐水起搏(NSP)组、氯沙坦起搏(LP)组.观测每组基础状态、快速心房起搏时心房有效不应期(AERP)及心房肌L-型钙通道的电流密度(ICa-L),并进行统计学处理.结果 [1]快速起搏时NSP组较NS组各个基础周长下的AERP均显著下降(P＜0.01);NSP组快速起搏6小时和8小时与NS组AERP的差距随着基础周长的下降而减少.[2]而快速起搏8小时后LP组AERP的下降较NSP组显著减轻(P＜0.01);LP组快速起搏后与NS组AERP的差距随着基础周长的下降未见减少趋势.[3]NSP组较NS组心房肌ICa-L降低;LP组较NS组和NSP组心房肌ICa-L差异无统计学意义(P＞0.05);而LP组较NSP组心房肌ICa-L的标准差显著降低(P＜0.05).结论 快速心房起搏可引起AERP缩短及AERP频率适应性不良为特征的心房肌电重构.氯沙坦可以抑制这种电重构及心房肌ICa-L离散度增加,从而降低AF的发生.     

Summation and Inhibition by Ultrarapid Train Pulses in Dogs: Effects of Frequency and Duration of Trains, Lidocaine, and Beta Blockade

To test whether summation and inhibition of excitation by ultrarapid train pulses were modified by frequency and duration of trains, using lidocaine and beta blockade, the strength-interval relationship was determined with a single extrastimulus and train pulses (100 and 200 Hz) in 28 anesthetized, open-chest dogs. The effective refractory period (ERP) determined at greater than or equal to 5 mA was shorter for trains than for single stimulus (summation). Summation determined at 15 mA increased progressively as the duration of trains was increased to 50 msec after which it reached a plateau. ERP determined at less than or equal to 2 mA was longer with train pulses than with single stimulus (inhibition). Inhibition for 200 Hz trains increased linearly with train duration up to 200 msec, while for 100 Hz trains it became constant when the duration was greater than or equal to 80 msec. Lidocaine (plasma concentration: 2.6 +/- 1.0 micrograms/mL) did not affect inhibition and summation in 11 dogs. Propranolol (1 mg/kg, iv) increased summation at 15 mA (n = 7, 30 +/- 10 vs 46 +/- 11 msec with 100 Hz trains, P less than 0.01), but did not affect inhibition (37 +/- 26 vs 29 +/- 17 msec, NS). In conclusion, (1) effect of frequency of train pulses was more on inhibition than on summation; (2) lidocaine did not affect inhibition and summation; and (3) propranolol increased summation but not inhibition.