心室晚电位对冠状动脉搭桥术后室性心律失常的预测

目的 研究冠状动脉搭桥术前后心室晚电位(VLP)的变化，评价术前VLP阳性对术后发生室性心律失常的预测价值。方法 采取冠状动脉搭桥术患者40例。其中心肌梗塞(M1)病史组31例，无MI病史组9例。室壁瘤组7例，非室壁瘤组33例。观测冠状动脉搭桥术前及术后2周VLP的变化。结果 1．MI及室壁瘤患者术前FQRS显著高于，LAS显著低于非MI及非室壁瘤患者(P<0．05)；VLP阳性率高于非MI及非室壁瘤患者。2．术后VLP阳性率显著低于术前(P=0．025)，VLP转阴率为75％。3．术前VLP阳性患者术后发生室性心律失常例数显著高于术前VLP阴性患者(P=0．03)。结论：1．M1及室壁榴患者VLP阳性率高提示其存在折返性室性心律失常的电生理基础。2．冠状动脉搭桥及室壁瘤切除术后VLP转阴提示外科手术不仅能够改善梗塞区域局部心肌的血供，而且切断了潜在的折近径路，从而减少了VLP及室性心律失常的发生。3．术前VLP阳性是预测术后室性心律失常的独立指标(敏感性71．43％，特异性78．79％，阳性准确率41．67％，阴性准确率92．86％)，据此指导临床预防应用抗心律失常药物。     

心肌梗塞的心室晚电位研究

本文对50例心肌梗塞(MI)病人的心室晚电位(VLP)检测结果进行定性与定量分析:(1)MI组与正常组之间存在着显著性差异(P<0.001),提示VLP是一种病理性的电活动;(2)不同部位MI的VLP阳性检出率下壁为38％、前壁为35％、前间壁为33％、前侧壁为20％,提示下壁MIVLP的阳性检出率较高。此外,根据对VLP定量分析的结果发现,下壁、前间壁MI对反映传导和电压的指标均敏感。而前壁、前侧壁MI仅对反映传导的指标敏感,其机理需进一步探讨;(3)急性心肌梗塞与陈旧性心肌梗塞组都有形成VLP的可能,但前者检出率相对较高。由此提出应根据不同发生机制而采取针对性较强的防止电不稳定的措施;(4)MI伴室性心律失常(VA)组与不伴VA组之间存在着显著性差异(P<0.001),提示VLP阳性者VA的发生率较高。     

不同体位检测对心室晚电位的影响(摘要)

近年来,广泛应用心室晚电位(VLP)预测危重心律失常,若能将Holter信息与信号平均心电图(SAECG)相结合,在不同的体位、状态和时间检测发生心肌缺血时或室性心律失常(VA)发生时的VLP,可能对高危VA的研究更有裨益。目前,动态心电图磁带记     

倍他乐克对心室晚电位的影响

心室晚电位(VLP)与折返性心律失常(AV)密切相关,在预测恶性心律失常事件中具有重要意义。抗心律失常药物对VLP的影响亦日益引起人们的重视。本文就倍他乐克对VLP的影响进行临床实验研究,旨在探讨倍他乐克在抗心律失常治疗中的影响及临床意义。 资料和方法:     

心室晚电位、心率变异对急性心肌梗死患者心律失常事件发生的预测价值

目的 了解心率变异(HRV)、心室晚电位(VLP)在预测急性心肌梗死(AMI)预后的价值。方法 40例AMI患者HRV(SDNN)、VLP测定,与40例正常人进行对比分析。结果 AMI组SDNN(87.9±25.07ms)与对照组(13.37±35.96ms)比较明显减低(P<0.001),AMI组VLP阳性(11例)与正常组(1例)比较明显增高(P<0.01)。梗塞患者室性心律失常事件组与非事件组HRV(SDNN)、VLP比较相差显著(P<0.005)。对心律失常事件发生预测方面,HRV特异性为93.55％,相对危险性为10.50,VLP敏感性为44.4％。二者结合特异性、相对危险性增加。结论 二项指标均有独立的预测价值,如同时检测可望提高阳性预测值。     

倍他乐克对心室晚电位的影响

心室晚电位(VLP)与折返性心律失常(AV)密切相关，在预测恶性心律失常事件中具有重要意义。抗心律失常药物对VLP的影响亦日益引起人们的重视．本就倍他乐克对VLP的影响进行临床实验研究，旨在探讨倍他乐克在抗心律失常治疗中的影响及临床意义。     

糖尿病合并冠心病患者室性心律失常和心室晚电位以及QT间期离散度的变化

目的　探讨 2型糖尿病 (T2DM )合并冠心病 (CHD)患者室性心律失常 (VA)和心室晚电位 (VLP)与QT间期离散度 (QTcd)的变化。　方法　对选择性冠状动脉造影阳性的 186例单纯CHD与 178例T2DM合并CHD患者的VA阳性率、VLP阳性率与QTcd进行比较分析。　结果　T2DM合并CHD组VA的阳性率、VLP的阳性率明显高于CHD组 (P <0 0 1) ,QTcd明显增加 (P <0 0 1)。　结论　CHD患者VA的阳性率、VLP阳性率与QTcd增加不仅与CHD血管病变有关 ,且与DM所致心脏血管结构和功能改变有密切关系.     

心律平治疗充血性心力衰竭合并室性心律失常的疗效与安全性

目的　观察心律平治疗充血性心力衰竭 ( CHF)合并室性心律失常 ( VA)的疗效与安全性。方法　将 80例 CHF合并 VA患者随机分成两组 ,均停用抗心律失常药物 5个半衰期 ,两组病人抗心力衰竭治疗相同 ,试验组应用心律平抗心律失常 ,对照组不使用抗心律失常药物 ,疗程 4周 ,观察临床疗效、室性心律失常及左心室射血分数 ( L VEF)变化。结果　治疗后试验组临床疗效低于对照组 ( P<0 .0 1) ,VA减少两组差异无显著性 ( P>0 .0 5 ) ,对照组 L VEF值增加优于试验组 ( P<0 .0 5 ) ,试验组有 6例出现新的心律失常 ,停用心律平后恢复。结论　 CHF合并 VA时不宜应用心律平     

急性心肌梗塞溶栓治疗后心室晚电位转阴的机理及意义

临床研究发现,各种溶栓治疗都不同程度地降低了急性心肌梗塞(AMI)患者病死率。心室晚电位(VLP)是心肌梗塞后心律失常发生的强烈预兆。新近,许多作者对AMI溶栓治疗后心室晚电位转阴的机理及意义进行探讨。现综述如下:1 溶栓治疗前VLP转阴的机理 溶栓治疗后VLP转阴确切机理尚未完全明了,     

抗心律失常药物治疗的新药热点

近半个世纪以来,抗心律失常药物(AAD)的新药研发整体进展缓慢,鲜有新药上市。但近几年来,AAD的新分类和新靶点不断涌现,促进了AAD的研发热度;同时,传统药物的作用机制和途径也更加明确,定位更加清晰,提升了临床医生对心律失常患者精准治疗的能力。     

长效二氢奎尼丁、普罗帕酮、美托洛尔对心室晚电位影响的临床研究

通过短期观察信号平均心电图（ＳＡ－ＥＣＧ）的重复性及比较心室晚电位（ＶＬＰ）阳性患者服药前后ＳＡ－ＥＣＧ指标变化，以了解长效二氢奎尼丁（ｓéｒéｃｏｒ）、普罗帕酮、美托洛尔对ＶＬＰ阳性患者ＳＡ－ＥＣＧ指标的影响，及是否具有逆转ＶＬＰ的作用，结果表明：（１）ＳＡ－ＥＣＧ各定量指标的重复性良好，ＶＬＰ阳性组自然转阴率仅为７．７％。（２）ｓｅｒｅｃｏｒ不能逆转ＶＬＰ，而具有选择性延长ＱＲＳ终末部４０μＶ的低振幅信号持续时间（ＬＡＳ）的作用。（３）普罗帕酮不能逆转ＶＬＰ，仅延长滤波后ＱＲＳ－时限（ＱＲＳ－Ｄ）。（４）美托洛尔显著逆转ＶＬＰ，使ＱＲＳ－Ｄ、ＬＡＳ缩短，综合导联滤波的ＱＲＳ终末４０ｍｓ处综合向量电压（ＲＭＳ_（４０））增加。讨论了三种抗心律失常药物对ＶＬＰ影响的不同效应。     

Efficacy of antiarrhythmic drugs in patients with arrhythmogenic right ventricular disease. Results in patients with inducible and noninducible ventricular tachycardia.

BACKGROUND. Ventricular tachyarrhythmias are the major clinical manifestation of arrhythmogenic right ventricular disease. Although antiarrhythmic therapy has been widely advocated, there is only limited information available on the efficacy of antiarrhythmic drugs in these patients. METHODS AND RESULTS. The short- and long-term efficacies of various antiarrhythmic agents were retrospectively and prospectively analyzed in 81 patients (mean age, 39 +/- 14 years; range, 16-68 years; 61.7% males) with arrhythmogenic right ventricular disease. In 42 patients with inducible ventricular tachycardia during programmed ventricular stimulation, the following efficacy rates were obtained: class Ia and Ib drugs (n = 18), 5.6%; class Ic drugs (n = 25), 12%; beta-blockers (n = 8), 0%; sotalol (n = 38), 68.4%; amiodarone (n = 13), 15.4%; verapamil (n = 5), 0%; and drug combinations (n = 26), 15.4%. Only one of the 10 patients not responding to sotalol was treated effectively by amiodarone, whereas the remaining nine patients proved to be drug refractory toward all other drugs tested (3.8 +/- 2.3 drugs, including amiodarone in five cases) and underwent nonpharmacological therapy. During a follow-up of 34 +/- 25 months, three of the 31 patients (9.7%) discharged on pharmacological therapy had nonfatal recurrences of ventricular tachycardia after 0.5, 51, and 63 months, respectively. In 39 patients with noninducible ventricular tachycardia during programmed ventricular stimulation, the following efficacy rates were observed: class Ia and Ib drugs (n = 16), 0%; class Ic agents (n = 23), 17.4%; beta-blockers (n = 7), 28.6%; sotalol (n = 35), 82.8%; amiodarone (n = 4), 25%; verapamil (n = 24), 50%; and drug combinations (n = 11), 9.1%. During a follow-up of 14 +/- 13 months, four of 33 patients (12.1%) discharged on antiarrhythmic drugs had nonfatal relapses of their clinical ventricular arrhythmia. CONCLUSIONS. Thus, in arrhythmogenic right ventricular disease, sotalol proved to be highly effective in patients with inducible as well as noninducible ventricular tachycardia. Patients with inducible ventricular tachycardia not responding to sotalol are likely to not respond to other antiarrhythmic drugs and should be considered for nonpharmacological therapy without further drug testing. Amiodarone did not prove to be more effective than sotalol and may not be an alternative because of frequent side effects during long-term therapy, especially in young patients. Verapamil and beta-blockers were effective in a considerable number of patients with noninducible ventricular tachycardia and may be a therapeutic alternative in this subgroup. Class I agents appear to be rarely effective in the treatment of both inducible and noninducible ventricular tachycardia in arrhythmogenic right ventricular disease.     

Long-term survival of patients with malignant ventricular arrhythmia treated with antiarrhythmic drugs

The protective effect of antiarrhythmic agents for patients with malignant ventricular arrhythmia (defined as noninfarction ventricular fibrillation or sustained hemodynamically compromising ventricular tachycardia) remains uncertain. We have analyzed survival among 123 such patients (98 males, 25 females, average age 53.6 years) dependent on the abolition of antiarrhythmic drugs of salvos of ventricular tachycardia and R-on-T ventricular premature beats (Lown grades 4B and 5). Over an average follow-up of 29.6 months there were 35 deaths (11.2 percent annual mortality rate) of whom 23 patients succumbed suddenly (8.2 percent annual mortality rate). Among 98 patients in whom antiarrhythmic drugs abolished grades 4B and 5 ventricular premature beats, only 6 sudden deaths occurred for a 2.3 percent annual mortality rate. Of the 25 patients in whom advanced ventricular premature beats were not controlled, 17 died suddenly. Seventy-nine patients had left ventricular studies suitable for analysis. Among 44 patients with left ventricular dysfunction, control of ventricular premature beats was a critical element predicting survival. The annual sudden death rate for the 12 noncontrolled patients with left ventricular dysfunction was 41 percent contrasting with only 3.1 percent for the 32 patients with similar abnormalities in ventricular function in whom advanced ventricular premature beats were abolished. It is concluded that antiarrhythmic drugs can protect against the recurrence of life-threatening arrhythmias in patients who have manifest ventricular fibrillation or ventricular tachycardia and that abolition of certain advanced grades of ventricular premature beats provides an effective therapeutic objective.     

Contemporary real life cardioversion of atrial fibrillation: Results from the multinational RHYTHM-AF study

Aims

Electrical and pharmacological cardioversion (ECV, PCV) are important treatment options for symptomatic patients with recent onset atrial fibrillation (AF). RHYTHM-AF is an international registry of present-day cardioversion providing information that is not currently available on country differences and acute and long-term arrhythmia outcomes of ECV and PCV.

Methods and results

3940 patients were enrolled, of whom 75% underwent CV. All patients were followed for 2 months. There were large variations concerning mode of CV used, ECV being heterogeneous. A choice of PCV drug depended on the clinical patient profile. Sinus rhythm was restored in 89.7% of patients by ECV and in 69.1% after PCV. Among patients not undergoing CV during admission, 34% spontaneously converted to sinus rhythm within 24 h. ECV was most successful in patients pretreated with antiarrhythmic drugs (mostly amiodarone). PCV was enhanced by class Ic antiarrhythmic drugs; conversion rate on amiodarone was similar to that seen with rate control drugs. Female patients and those with paroxysmal and first detected AF as well as those without previous ECV responded well to PCV. The median duration of hospital stay was 16.2 and 24.0 h for ECV and PCV patients, respectively. There were very few CV-related complications regardless of mode of CV. Chronic maintenance of sinus rhythm was enhanced in patients on chronic antiarrhythmic drugs, beta-blockers or inhibitors of the renin–angiotensin system.

Conclusions

Mode of CV varied significantly, but both PCV and ECV were safe and effective. Class Ic drugs were most effective conversion drugs, but amiodarone is used most frequently despite providing merely rate control rather than shorten time to conversion.     

Prediction of results of antiarrhythmic drug therapy in patients with malignant ventricular tachyarrhythmias, based on the prognostic value of left ventricular contractility parameters

In 44 patients (3 women and 41 men, mean age 54 +/- 11 years) with malignant ventricular tachyarrhythmias (MVT) we assessed dependence of results of testing of antiarrhythmic drugs and efficacy of their long term use for prevention of recurrences of MVT on topography of derangement of local left ventricular (LV) contractility. Regional LV contractility was assessed with transthoracic echocardiography and radionuclide ventriculography (RNV). Testing of antiarrhythmic drugs was performed under control of repetitive intracardiac electrophysiological studies. Duration of follow-up was 28 (13 - 61) months. According to ROC-analysis most precise markers of positive results of drug testing were values of local ejection fraction (EF) in apical LV segment (10th segment on RNV) above 55%. Signs predisposing to absence of MVT recurrences during long term use of antiarrhythmic drugs were lack of mitral regurgitation (above I degree) according to echocardiography data, values of local EF in segment of lateral LV wall (4th segment on RNV) exceeding 42%, or value of LV end diastolic volume less than 365 ml according to RNV data. Parameters of local LV contractility are most precise markers of results of the use of antiarrhythmic drugs in patients with MVT, their diagnostic value is hair than that of global LVEF. Efficacy of antiarrhythmic drugs at electrophysiologic testing and long term follow-up are associated with different parameters of local LV contractility.     

Effects of antiarrhythmic drugs on canine ventricular arrhythmia models: Which electrophysiological characteristics of drugs are related to their effectiveness?

In order to compare and clarify the effects of various antiarrhythmic drugs when given as monotherapy, we reevaluated our previous data on antiarrhythmic drugs and recalculated antiarrhythmic plasma concentrations of drugs for several canine arrhythmia models. We used three spontaneously occurring arrhythmias: a) digitalis-, b) two-stage coronary ligation-, and c) adrenaline-induced arrhythmias. All antiarrhythmic drugs of class I suppressed digitalis arrhythmia, and, except for lidocaine, also suppressed coronary ligation arrhythmia. Class II antiarrhythmic drugs, beta blockers, and class IV antiarrhythmic drugs, Ca antagonists, had common features of effectiveness and suppressed adrenaline arrhythmia in relatively low concentrations. Class III drugs were not effective on these three arrhythmias. Differences among the antiarrhythmic effects of class I drugs could not be explained by their subclassification based either on action potential duration or kinetic properties of dissociation or association with Na channels. New triggered arrhythmia models in vivo and in vitro canine hearts were developed, and drug effects were not the same as those on the three spontaneously occurring arrhythmia models.     

Recent antiarrhythmic drugs

Clinical failure of antiarrhythmic drugs often occurs in practice. Therefore, there is a need for new, effective and long-acting drugs with a wide therapeutic range and a low level of toxicity. Most new class I compounds block the fast sodium ion inward current of myocardial cells. According to their effects on the recovery kinetics of the sodium ion channel, these drugs are classified into 3 groups: IA (intermediate — cibenzoline, pirmenol, hydroxy-3-S-dihydroquinidine, quinacainol); IB (fast — tocainide, moricizine); IC (slow — flecainide, encainide, propafenone, lorcainide, indecainide, recainam and penticainide). Class IC drugs greatly depress intracardiac conduction and are the most potent antiarrhythmic compounds able to suppress ventricular premature beats. However, it is doubtful that longterm suppression of ventricular arrhythmias will improve survival of the patients. Some new drugs have been developed belonging to other classes: class II, esmolol, a new ultrashort-acting β blocker; class III, N-acetyl-procainamide and sotalol, which prolong duration of the action potential and increase ventricular refractoriness; class IV, the mixed sodium ion-eakaum ion-potassium ion antagonist, bepridil. The pharmacologic properties and the clinical effects of these new antiarrhythmic drugs are reviewed.

However, future therapeutic trends will depend on the results of large multicenter clinical secondary prevention trials such as the Cardiac Arrhythmia Suppression Trial. New antiarrhythmic drugs with original electrophysiologic profiles and minimal adverse effects must prove their ability not only to suppress arrhythmias but also to reduce sudden cardiac death rate.     

Natural history of potentially lethal ventricular arrhythmias in patients treated with long-term antiarrhythmic drug therapy

To examine the natural history of long-term anti-arrhythmic therapy in patients with benign and potentially lethal ventricular premature complexes (VPCs), 28 patients with initial efficacy with moricizine (greater than 75% suppression of baseline mean VPCs/hr and greater than 90% suppression of repetitive VPCs) were prospectively followed for 1 to 56 (mean +/- standard deviation 25 +/- 17) months. Patients were examined during baseline placebo, anti-arrhythmic drug therapy and intermittent pulsed-placebo reexamination periods. The mean VPCs of all patients at baseline entry were 233 +/- 47 VPCs/hr, and after moricizine therapy 14 +/- 4 VPCs/hr. Follow-up demonstrated that antiarrhythmic efficacy decreased to 75% at 12 months and to 62% at 24 months. Loss of antiarrhythmic drug efficacy most commonly occurred as a "transient" event (10 patients [36%]), and efficacy was spontaneously reestablished without a change in antiarrhythmic therapy. In contrast, increased dose titration of moricizine was necessary to reestablish antiarrhythmic suppression efficacy in 4 patients (14%), and 4 patients (14%) lost antiarrhythmic drug responsiveness during follow-up. Spontaneous decrease in baseline VPCs resulted in discontinuation of antiarrhythmic therapy in 3 patients, and increase in baseline VPCs was associated with a loss of antiarrhythmic response in 2 patients. Late proarrhythmic effects (2 patients, 7%), delayed side effects necessitating drug withdrawal (6 patients, 21%) and medical events (4 patients, 14%) occurred during 56 months of follow-up. Individual serum moricizine levels remained in the therapeutic range throughout the study and did not correlate with changes in antiarrhythmic efficacy.(ABSTRACT TRUNCATED AT 250 WORDS)     

Blockade of 2,4-dinitrophenol induced ATP sensitive potassium current in guinea pig ventricular myocytes by class I antiarrhythmic drugs.

OBJECTIVE: The aim was to assess the effects of various antiarrhythmic drugs on 2,4-dinitrophenol (DNP) induced outward current (IDNP), presumably the ATP sensitive K+ current (IK,ATP) of isolated cardiac cells and to discuss mechanisms involved in the hypoglycaemia which occurs in patients on these drugs. METHODS: The quasi-steady state current-voltage relationship from the isolated guinea pig ventricular cells was measured using whole cell voltage clamp techniques with a ramp pulse programme. The effects of seven different antiarrhythmic drugs on IDNP were examined. Action potentials were elicited at a rate of 0.2 Hz by an intracellular current injection. RESULTS: DNP (50 mumol.litre-1) increased the quasi-steady state outward current at potentials positive to about -60 mV. This current (IDNP) was completely inhibited by the subsequent application of glibenclamide (1 mumol.litre-1), thereby suggesting that the IDNP is probably IK,ATP. Cibenzoline (10 mumol.litre-1, class Ia), disopyramide (30 mumol.litre-1, class Ia), and procainamide (100 mumol.litre-1, class Ia) significantly inhibited the IDNP by 95.5(SD 11.3)%, 77.8(21.2)%, and 76.4(23.9)% respectively. Flecainide (class 1c) inhibited the IDNP by 66.9(23.9)% at 10 mumol.litre-1 but not at 2 mumol.litre-1. Mexiletine (30 mumol.litre-1, class Ib), pilsicainide (50 mumol.litre-1, class Ic), and E4031 (10 mumol.litre-1, class III) at concentrations as high as approximately fivefold the clinically effective blood levels, did not suppress IDNP. Except for 10 mumol.litre-1 flecainide, all the concentrations listed above which blocked IDNP were within twofold of the clinical blood concentrations documented to be effective for suppression of arrhythmias. Cibenzoline, disopyramide, and procainamide, but not flecainide, belong to class Ia antiarrhythmic drugs. All these class Ia antiarrhythmic drugs "shortened" the action potential duration of guinea pig ventricular cells, an opposite change to that noted for multicellular preparations, eg, guinea pig papillary muscles. CONCLUSIONS: Class Ia antiarrhythmic drugs (cibenzoline, disopyramide, and procainamide) inhibit IDNP (presumably IK,ATP) in guinea pig ventricular cells within a range of therapeutic concentrations. This inhibitory effect of IK,ATP can probably explain the hypoglycaemia which occurs in some patients receiving these drugs, and the prolongation of the action potential duration alleged to occur in "superfused" papillary muscles.