Dual Atrioventricular Nodal Nonreentrant Tachycardia with Alternating 1:1 and 1:2 AV Conduction: Mechanistic Hypotheses and Total Suppression Using Right Atrial Pacing

Dual atrioventricular (AV) nodal nonreentrant tachycardia is an uncommon arrhythmia with several pattern types. The primary therapy is ablation of the slow AV nodal pathway. A rare pattern type demonstrates alternating 1:2 and 1:1 AV ratios with longer PR intervals during 1:1 conduction. We report the second intracardiac study of this variant and the first case of using right atrial pacing as the ultimate therapy for any pattern type.     

Beta1 and beta2-adrenergic receptor polymorphisms and idiopathic ventricular arrhythmias

Introduction: Idiopathic ventricular arrhythmias commonly refer to ventricular tachycardia (VT) and/or frequent/monomorphic premature ventricular contractions (PVC) in patients with structurally normal heart. Activation of sympathetic tone has been shown to play an important role in the provocation and maintenance of these arrhythmias. We investigated whether common single nucleotide polymorphisms in the β₁ and β₂‐adrenergic receptors are associated with idiopathic ventricular arrhythmias. Methods: A total of 143 unrelated patients presenting with idiopathic ventricular arrhythmias were prospectively included in a case‐control association study. Patient population was matched by age and gender to the unrelated, healthy control subjects (N = 307). All study subjects were of Turkish (Anatolian Caucasian) descent. Allele and genotype frequencies of the Gly389Arg and Ser49Gly polymorphisms of the β₁‐adrenergic receptor and Arg16Gly, Gln27Glu, and Thr164Ile polymorphisms of the β₂‐adrenergic receptor were compared between patient population and control subjects. The genotype frequencies were in Hardy‐Weinberg equilibrium. Results: Patients with idiopathic ventricular arrhythmias had higher frequency of Arg389Arg genotype (22.4% vs 1.6%, P < 0.001), Arg389Gly49 (5.24% vs 0.73%, P = 0.005), and Arg389Ser49 (36.7% vs 13.6%, P < 0.001) haplotypes of the β₁‐adrenergic receptor, and higher frequency of Gly16Gly (31.5% vs 13.4%, P < 0.001), Glu27Glu genotypes (18.2% vs 10.1%, P = 0.006) and Gly16Gln27Thr164 (15.3% vs 7.4%, P = 0.002), Gly16Glu27Thr164 (13.1% vs 7%, P = 0.004), and Gly16Glu27Ile164 (13.2% vs 6%, P = 0.002) haplotypes of the β₂‐adrenergic receptor compared to control subjects. Conclusion: Our data suggest that common single nucleotide polymorphisms in the β₁ and β₂‐adrenergic receptors are significantly associated with idiopathic ventricular arrhythmias in Turkish population.     

Spontaneous transition of 2:1 atrioventricular block to 1:1 atrioventricular conduction during atrioventricular nodal reentrant tachycardia: evidence supporting the intra-Hisian or infra-Hisian area as the site of block

INTRODUCTION: The incidence of spontaneous transition of 2:1 AV block to 1:1 AV conduction during AV nodal reentrant tachycardia has not been well reported. Among previous studies, controversy also existed about the site of the 2:1 AV block during AV nodal reentrant tachycardia. METHODS AND RESULTS: In patients with 2:1 AV block during AV nodal reentrant tachycardia, the incidence of spontaneous transition of 2:1 AV block to 1:1 AV conduction and change of electrophysiologic properties during spontaneous transition were analyzed. Among the 20 patients with 2:1 AV block during AV nodal reentrant tachycardia, a His-bundle potential was absent in blocked beats during 2:1 AV block in 8 patients, and the maximal amplitude of the His-bundle potential in the blocked beats was the same as that in the conducted beats in 4 patients and was significantly smaller than that in the conducted beats in 8 patients (0.49 +/- 0.25 mV vs 0.16 +/- 0.07 mV, P = 0.007). Spontaneous transition of 2:1 AV block to 1:1 AV conduction occurred in 15 (75%) of 20 patients with 2:1 AV block during AV nodal reentrant tachycardia. Spontaneous transition of 2:1 AV block to 1:1 AV conduction was associated with transient right and/or left bundle branch block. The 1:1 AV conduction with transient bundle branch block was associated with significant His-ventricular (HV) interval prolongation (66 +/- 19 ms) compared with 2:1 AV block (44 +/- 6 ms, P < 0.01) and 1:1 AV conduction without bundle branch block (43 +/- 6 ms, P < 0.01). CONCLUSION: The 2:1 AV block during AV nodal reentrant tachycardia is functional; the level of block is demonstrated to be within or below the His bundle in a majority of patients with 2:1 AV block during AV nodal reentrant tachycardia, and a minority are possibly high in the junction between the AV node and His bundle.     

Atrial flutter with 1: 1 conduction after administration of the antimalarial drug mefloquine

Antimalarial drugs are well known for their cardiovascular toxicity. Quinine, the most famous antimalarial agent, mostly causes bradycardia. Quinidine, its dextrorotatory isomer, may cause 1: 1 atrioventricular (AV) conduction during atrial flutter. The newly developed drug mefloquine was reported to have fewer cardiac side effects. We describe a 63-year-old male patient with atrial flutter in whom mefloquine use was associated with 1: 1 AV conduction, and who then responded to therapy with digoxin and sotalol. The patient had a history of palpitations. This case report emphasizes that mefloquine should be used with caution in patients with a history of palpitations or underlying heart disease.     

Coexistence of 2 types of atrial tachycardias and right ventricular outflow tract tachycardia

Double tachycardia is a relatively uncommon type of tachycardia. In this report, we discuss a 68-year-old woman with history of frequent palpitations. Electrophysiologic study revealed that narrow QRS tachycardias from 2 origins and 1 wide QRS tachycardia were induced and each of the tachycardias was induced by the other. We found that 2 focal atrial tachycardias and 1 ventricular tachycardia originated from right ventricular outflow tract. All of these tachycardias were successfully ablated during one session, and no recurrence appeared during 10 months of follow-up.     

Elimination of AV Nodal Reentrant Tachycardia with 2:1 VA Block by Posteroseptal Ablation

AV Nodal Reentrant Tachycardia. AV nodal reentry capable of VA block during tachycardia was successfully eliminated using a posteroseptal ablation pulse delivered well away from the site of earliest atrial activation during tachycardia. A possible explanation is that the arrhythmia represented typical AV nodal reentrant tachycardia with transient intra atrial conduction block during tachycardia.     

Sustained intra-atrial reentrant tachycardia. Electrophysiologic study of 20 cases

Twenty cases of sustained tachycardia due to intra-atrial reentry were investigated in patients aged 17 to 80 years (mean 47). The average frequency of the tachycardia was 128.6/min (extremes 95 and 180). Three modes of onset of the tachycardia were observed: atrial extra-stimulus (19 times), progressively accelerated atrial pacing (9 times) and atrial escape beat (10 times). The tachycardia was stopped in all cases by a premature stimulation. When spontaneous, the termination was either sudden (10 times) or preceded by a progressive slowing (9 times) or an alternating phenomenon of long-short cycle (13 times). Precise atrial mapping allowed to localize the first atrial depolarization less frequently in the sinus node area (1 case) than in the mean right atrium (21 cases), the low right atrium (2 cases), the interatrial septum (2 cases), and the left atrium (4 cases). The macroscopic size of the reentry circuit was demonstrated in only 3 cases. A junctional reentry was accurately ruled out in all cases thanks to the existence of a second or third-degree AV or VA black, or by studying the sequence of retrograde atrial activation. A true junctional reciprocating tachycardia was associated with the intra-atrial reentry in 2 cases.     

Differentiating wide complex tachycardias: A historical perspective

One of the most critical and challenging skills is the distinction of wide complex tachycardias into ventricular tachycardia or supraventricular wide complex tachycardia. Prompt and accurate differentiation of wide complex tachycardias naturally influences short- and long-term management decisions and may directly affect patient outcomes. Currently, there are many useful electrocardiographic criteria and algorithms designed to distinguish ventricular tachycardia and supraventricular wide complex tachycardia accurately; however, no single approach guarantees diagnostic certainty. In this review, we offer an in-depth analysis of available methods to differentiate wide complex tachycardias by retrospectively examining its rich literature base – one that spans several decades.     

Automatic wide complex tachycardia differentiation using mathematically synthesized vectorcardiogram signals

BackgroundAutomated wide complex tachycardia (WCT) differentiation into ventricular tachycardia (VT) and supraventricular wide complex tachycardia (SWCT) may be accomplished using novel calculations that quantify the extent of mean electrical vector changes between the WCT and baseline electrocardiogram (ECG). At present, it is unknown whether quantifying mean electrical vector changes within three orthogonal vectorcardiogram (VCG) leads (X, Y, and Z leads) can improve automated VT and SWCT classification.MethodsA derivation cohort of paired WCT and baseline ECGs was used to derive five logistic regression models: (i) one novel WCT differentiation model (i.e., VCG Model), (ii) three previously developed WCT differentiation models (i.e., WCT Formula, VT Prediction Model, and WCT Formula II), and (iii) one “all‐inclusive” model (i.e., Hybrid Model). A separate validation cohort of paired WCT and baseline ECGs was used to trial and compare each model''s performance.ResultsThe VCG Model, composed of WCT QRS duration, baseline QRS duration, absolute change in QRS duration, X‐lead QRS amplitude change, Y‐lead QRS amplitude change, and Z‐lead QRS amplitude change, demonstrated effective WCT differentiation (area under the curve [AUC] 0.94) for the derivation cohort. For the validation cohort, the diagnostic performance of the VCG Model (AUC 0.94) was similar to that achieved by the WCT Formula (AUC 0.95), VT Prediction Model (AUC 0.91), WCT Formula II (AUC 0.94), and Hybrid Model (AUC 0.95).ConclusionCustom calculations derived from mathematically synthesized VCG signals may be used to formulate an effective means to differentiate WCTs automatically.     

Mayo Clinic VT calculator: A practical tool for accurate wide complex tachycardia differentiation

The discrimination of ventricular tachycardia (VT) versus supraventricular wide complex tachycardia (SWCT) via 12-lead electrocardiogram (ECG) is crucial for achieving appropriate, high-quality, and cost-effective care in patients presenting with wide QRS complex tachycardia (WCT). Decades of rigorous research have brought forth an expanding arsenal of applicable manual algorithm methods for differentiating WCTs. However, these algorithms are limited by their heavy reliance on the ECG interpreter for their proper execution. Herein, we introduce the Mayo Clinic ventricular tachycardia calculator (MC-VTcalc) as a novel generalizable, accurate, and easy-to-use means to estimate VT probability independent of ECG interpreter competency. The MC-VTcalc, through the use of web-based and mobile device platforms, only requires the entry of computerized measurements (i.e., QRS duration, QRS axis, and T-wave axis) that are routinely displayed on standard 12-lead ECG recordings.     

Current Algorithms for the Diagnosis of wide QRS Complex Tachycardias

The differential diagnosis of a regular, monomorphic wide QRS complex tachycardia (WCT) mechanism represents a great diagnostic dilemma commonly encountered by the practicing physician, which has important implications for acute arrhythmia management, further work-up, prognosis and chronic management as well. This comprehensive review discusses the causes and differential diagnosis of WCT, and since the ECG remains the cornerstone of WCT differential diagnosis, focuses on the application and diagnostic value of different ECG criteria and algorithms in this setting and also provides a practical clinical approach to patients with WCTs.     

国产心脏射频治疗仪治疗阵发性心动过速

报告用我们与西安黄河机器制造厂共同研制的DS92H心脏射频治疗仪,对阵发性心动过速患者47例进行50次射频消融术的结果.前7例次采用美国USCI公司标准电极导管(标准组),无1例成功,其中3例以后改用大头导管.46例采用美国Mansfield公司大头导管(大头组),其中房室结快道消融术(AAVN)10例,房室旁道消融术(AAP)32例(4例左侧游离壁旁道用单大头导管法),室速起源点消融术(AVT)4例.除4例AVT与2例AAP外,均获成功.大头组AAVN与AAP总成功率为95%.成功病例的操作总时间为0.7～5.2(平均2.0)h,且随经验积累,时间缩短.除AAVN1例术后Ⅲ°房室传导阻滞而植入水入起搏器,AAP1例轻度主动脉瓣返流外,无严重并发症.术后随访1～9月(平均5.3月).AAP组3例复发,复发率9.4%;AAVN组无复发.     

Inappropriate sinus tachycardia (1ST): management by radiofrequency modification of sinus node

Background: Inappropriate sinus tachycardia (IST) is a rare form of supraventricular arrhythmia. It can cause disabling symptoms and may be refractory to medical treatment. In symptomatic drug refractory patients, sinus node excision or total ablation of the sinus node with permanent pacemaker implantation was the only therapeutic option. Recently, radiofrequency (RF) modification of the sinus node has been reported to be an effective treatment for this condition. Aim: To present our experience with sinus node modification using RF energy in the management of 1ST Methods: Between 1989> to 1996 three patients (two females and one male), aged 28–36 years were diagnosed with symptomatic IST All had failed multiple drugs and hence underwent sinus node modification using RF. In the first two patients, the site of RF application was guided by anatomical landmarks using fluoroscopy to localise the presumed most superior portion of the crista terminalis and also the earliest site of atrial activation. In fhe third patient, a 20 pole electrode catheter was used to map the crista terminalis and guide the ablation. Success was defined by 20–30% reduction in the heart rate with normal atrial activation sequence after ablation. Results: The three patients described here had IST by clinical, electrocardiographic and electrophysiological criteria and were refractory to multiple antiarrhythmic drugs. The number of RF applications were 11, 15, and three applied at the site of earliest atrial activation for the control of heart rates. Patient 3 had a early recurrence at one month and underwent repeat sinus node modification (five RF applications). All three patients who underwent RF modification of the sinus node had a successful outcome. The procedure was uncomplicated and the patients remain asymptomatic during follow up (20, 12 and three months) with satisfactory control of heart rate, although one patient requires atenolol which was previously ineffective. Conclusions: RF modification of the sinus node is feasible and effective for IST, and should be the treatment of choice in patients refractory to medical therapy.     

R-Wave Peak Time at Lead II in Adults With Ventricular Premature Beats,Bundle Branch Block and Left Anterior Fascicular Block

Background

Recently, the R-wave peak time (RWPT) at lead II was reported to be a helpful and simple tool for differentiating wide QRS complex tachycardias with a RWPT ≥ 50 ms for ventricular tachycardia diagnosis. Our previous study showed that the duration of RWPT at lead II in adults was ≈29 ms. However, the effects of ventricular premature beats (VPBs), bundle branch block (BBB) or left anterior fascicular block (LAFB) on RWPT at lead II remain unknown.

Griffith法Brugada法诊断宽QRS性室上性心动过速

为了解Griffith法和Brugada法诊断宽QRS性室上性心动过速（SVT）的价值，选择34例心电图表现为宽QRS心动过速者，其中SVT25例，室性心动过速（VT）9例，均经心脏电生理检查证实，采用上述两法进行了比较和综合分析。结果发现，Griffith法诊断SVT的敏感性、特异性和假阴性率分别为76％、77．8％和24％；而Brugada法的则分别为80％、88．9％和20％；两者合用时分别为84％、88．9％和16％。4例SVT为右侧旁路前传者均不符合诊断标准。认为，Griffith法和Brusada法或二者合用对SVT合并原有束支阻滞或室内差异性传导者有较高的诊断价值，而对预激旁路前传的SVT诊断价值低。     

Brugada法联合Steurer法在宽QRS波心动过速鉴别诊断中的价值

为评价Brugada法联合Steurer法在宽QRS波心动过速 (WRT)鉴别诊断中的应用价值及存在的缺陷。对 1 0 1例WRT[室性心动过速 (VT) 5 8例 ,室上性心动过速 (SVT) 43例 ]进行分析。结果 :Brugada法诊断VT灵敏度、特异度、准确性分别为 85 .7%、89.5 %、87.1 % ;联合Steurer法后灵敏度、特异度、准确性分别升至 91 .5 %、90 .5 %、91 .1 %。进一步分析显示 :Brugada法对器质性原因所致VT、右束支阻滞型 (RBBB)特发性VT(IVT)、SVT伴室内差异性传导 (AC)或原有单侧束支阻滞 (BBB)者诊断符合率高 ( 95 .8%～ 1 0 0 .0 % ) ;对左束支阻滞型 (LBBB)特发性VT、SVT伴原有双支阻滞、心肌坏死或心肌梗死伴宽QRS波SVT及预激综合征伴旁道前传型SVT(WPW SVT)诊断的符合率低 ( 0～ 5 0 .0 % )。联合Steurer法可使WPW伴旁道前传型SVT得以明确诊断 ,但对前三者无鉴别意义 ,故不适合在前三者中应用。结论 :Brugada法联合Steurer法能提高WPW伴旁道前传型SVT的鉴别能力 ,是目前鉴别WRT的重要方法。