Surgical atrioventricular disconnection in Wolff-Parkinson-White syndrome

Surgical atrioventricular disconnection is a possible means of treating patients with severe paroxysmal arrhythmias resistant to medical treatment due to the Wolff-Parkinson-White syndrome. Between 1971 and April 1982 we operated 50 patients (38 men and 12 women) with the WPW syndrome. Thirty seven patients were operated for arrhythmias (paroxysmal tachycardia) resistant to medical therapy or with a high risk of sudden death. Thirteen patients had associated cardiac disease with less severe arrhythmias (aortic valve disease: 6 cases; mitral and aortic valve disease: 3 cases; mitral valve disease: 3 cases, and atrial septal defect: 1 case). The causes of paroxysmal tachycardia were atrial fibrillation (13 cases), atrial flutter (2 cases), orthodromic reciprocating tachycardia (30 cases), with associated atrial fibrillation in 9 cases, and with associated atrial flutter in 4 cases. Antidromic reciprocating tachycardia was present in 2 cases. In 3 cases, the preexcitation was a chance finding. Electrophysiological studies performed before and after antiarrhythmic drug administration showed type A WPW (LV preexcitation) in 23 cases, and type B WPW (RV preexcitation) in 20 cases. The ECG was normal in the horizontal plane in 7 cases. The atrioventricular accessory pathway was permeable in both directions in 39 cases; in 9 cases the pathway was permeable only in the retrograde direction and in 2 cases it was permeable only in the anterograde direction. In 7 patients an atrio-hisian short circuit was demonstrated. The site of the accessory conduction pathway was located by epicardial mapping, the first surgical stage, in the left lateral region of the atrioventricular junction (28 cases), in the right lateral region (6 cases), in the posterior septal region (15 cases) (right sided in 4 cases, left sided in 11 cases), and in the anterior septal region (1 case). The accessory pathway (so-called Bundle of Kent) was interrupted by atrioventricular disconnection. Six patients died during surgery, mainly at the beginning of the series; the operative risk is now low (1 death in the last 34 cases: 2,95%). Complete interruption of the accessory pathway was obtained in 38 cases, 1 of which had to be reoperated. Three patients had an incomplete result due to partial interruption or the presence of a second accessory pathway. However, these patients no longer have severe arrhythmias. Surgical section failed in 3 cases, but the patients are now controlled by medical therapy.(ABSTRACT TRUNCATED AT 400 WORDS)     

Electrophysiological characteristics of asymptomatic Wolff-Parkinson-White syndromes]

The management of the Wolff-Parkinson-White syndrome (WPW) is controversial especially when the patient is asymptomatic. The aim of this study was to evaluate the electrophysiological characteristics of such patients. Thirty two asymptomatic subjects with overt WPW on the surface ECG aged 14 to 68 years (average 36 +/- 15 years) underwent endocavitary or oesophageal electrophysiological study with the following protocol: programmed atrial stimulation using 1 or 2 extrastimuli over 3 cycles to evaluate the induction of paroxysmal junctional tachycardia and atrial fibrillation; atrial pacing at increasing frequencies to assess the shortest cycle conducted by the bundle of Kent. This protocol was repeated during intravenous infusion of 20 to 30 mg of Isoproterenol. Four electrophysiological characteristics were identified: the incidence of induction of junctional tachycardia was very low (2 cases, 6%); the incidence of induction of atrial fibrillation or tachycardia was similar to that of symptomatic WPW (9 cases 30%); the incidence of rapid conduction via the bundle of Kent (cycle conducted by the Kent less than 250 ms under basal conditions less than 200 ms with Isoproterenol) was 19% (6 cases); the incidence of potentially serious forms of WPW with rapid conduction in the bundle of Kent and atrial vulnerability (induction of atrial fibrillation at a frequency less than the Wenckebach point by programmed atrial stimulation) was similar to that in symptomatic WPW, 3 cases (10%). In conclusion, the asymptomatic character of the WPW is very probably due to the absence of junctional tachycardias. Nevertheless, these patients are at risk of atrial fibrillation with an incidence of potentially serious forms of 10%.(ABSTRACT TRUNCATED AT 250 WORDS)     

Usefulness of invasive and non-invasive electrophysiologic studies in the selection of antiarrhythmic drugs for the patients with paroxysmal supraventricular tachyarrhythmia

A comparison of the effects of several antiarrhythmic agents was made in a study of 70 patients - 15 with manifest Wolff-Parkinson-White (WPW) syndrome, 17 with concealed WPW syndrome, 18 with AV nodal re-entrant tachycardia, 14 with paroxysmal atrial fibrillation and 6 with paroxysmal atrial flutter - employing intracardiac stimulation and esophageal pacing. For the termination of paroxysmal supraventricular tachycardia, intravenous administration of verapamil or aprindine was more effective than that of disopyramide or procainamide. In AV nodal re-entrant tachycardia, verapamil was the most effective for termination. In the manifest WPW syndrome, disopyramide or aprindine was indicated especially for patients with the accessory pathways of the short antegrade refractory period, because these drugs lengthened the refractory period of the accessory pathways. For the purpose of converting atrial fibrillation or flutter to the sinus rhythm, type IA drugs such as disopyramide were indicated. However, verapamil was effective for slowing down the ventricular rate in atrial fibrillation or flutter except in cases of manifest WPW syndrome. A 6-month follow-up study showed that oral administration of verapamil was also useful for putting a stop to the attacks in 24 out of 32 patients with paroxysmal supraventricular tachycardia, while oral disopyramide prevented the recurrence of atrial fibrillation in only 4 of 10 patients.     

Value of transesophageal programmed atrial stimulation in the evaluation of unexplained cerebrovascular accidents

Certain embolic cerebrovascular accidents can be explained by the development of paroxysmal atrial fibrillation. When noninvasive complementary investigations are negative, programmed atrial stimulation can be proposed to detect increased atrial vulnerability. The objective of this study was to evaluate the reliability of this method performed via a transoesophageal approach in 59 subjects presenting with an embolic cerebrovascular accident and who were in sinus rhythm at the time of the accident. Seven of these patients had a history of paroxysmal atrial fibrillation (AF) or atrial tachycardia (AT) (group I). Three of these seven patients also presented AV nodal reentrant junctional tachycardia. The other 52 patients had no history of arrhythmia and their Holter recording did not reveal any episodes of sustained atrial tachycardia (group II). Transoesophageal programmed atrial stimulation used up to 2 extrastimuli under baseline conditions and during Isuprel infusion. The following results were obtained: sustained atrial tachycardia (> 1 min) was induced in all patients of group 1, 3 of them also presented inducible junctional tachycardias. 14 patients of group II (27%) presented inducible supraventricular tachycardia: atrial tachycardia in 7 cases. Patients in group II with inducible AT presented either heart disease (n = 3) or minor abnormalities on the Holter recording (runs of atrial premature complexes or sinus pauses (n = 3). Two of these patients subsequently developed sustained atrial fibrillation during follow-up. In 25 patients with normal Holter recording and no heart disease, programmed atrial stimulation induced junctional tachycardia in 4 cases. In conclusion, transoesophageal electrophysiological investigation is a useful way to identify various forms of supraventricular tachycardia able to explain an embolic cerebrovascular accident. The considerable incidence of inducible AV nodal reentrant junctional tachycardia must be emphasized, while the incidence of atrial fibrillation is much lower than during intracardiac investigations.     

Usefulness of transesophageal electrophysiological study during the ergometric test in the evaluation of supraventricular paroxysmal tachycardia occurring during exertion

Transesophageal electrophysiologic study has recently been proposed for the evaluation of supraventricular arrhythmias. In this report we present 13 cases, with palpitations occurring only during effort, due to a suspected supraventricular tachycardia, in which the usefulness of the transesophageal electrophysiologic study performed during stress test was evaluated. Of these 13 patients, nine were male and four were female, mean age was 29 yrs. Twelve cases had no heart disease, one had a moderate mitral valve insufficiency. Nine cases had a normal ECG, four had a WPW pattern. In 9/13 cases no significant arrhythmia was ever documented, in 1/13 ventricular premature beats were present in the basal ECG, in 1/13 a atrial fibrillation and in 2/13 a supraventricular reciprocating tachycardia was recorded. In all cases a maximal exercise test and a 24-hour Holter monitoring were performed. In all pts a transesophageal electrophysiologic study was performed both at rest and during extra-stimuli and incremental atrial pacing. The end point of transesophageal study was the induction of a sustained (greater than 30") supraventricular tachycardia. RESULTS. Maximal exercise test was negative in 11/13 cases; it showed ventricular premature beats in one case and initiated a supraventricular tachycardia in one. The 24 hour Holter monitoring was negative in 12/13 cases while it showed frequent ventricular premature beats in one. Resting transesophageal electrophysiologic study revealed dual A-V nodal pathways in six pts: in one of them a junctional re-entry was induced; in two a single echo beat was observed, while in three no reentry was observed. In three cases a supraventricular tachycardia was induced which was sustained in one and unsustained (7" and 24") in two cases. In 4 cases transesophageal electrophysiologic study gave no information. Transesophageal stimulation during exercise induced a greater than 30" reciprocating tachycardia in all patients, at work loads of 30-180 watts. Six pts had an intranodal tachycardia (V-A less than 70 msec) a further six pts had a atrioventricular tachycardia involving a Kent bundle (V-A greater than or equal to 70 msec), which was concealed in two, and one had a atrial tachycardia. In four cases (3 with intranodal and 1 with atrioventricular tachycardia), exercise transesophageal study was repeated after chronic therapy with betablockers (sotalol 240 mg/die or metoprolol 200 mg/die). In all cases, after therapy, the induced tachycardia had a longer cycle and in two cases it was induced at a higher work load. In a further two cases flecainide (200 mg/die) was tested. In one case (with atrial tachycardia), the arrhythmia was no longer inducible after therapy, in another case (with intranodal tachycardia) the drug had no effect. CONCLUSIONS. In patients with paroxysmal supraventricular tachyarrhythmias occurring during effort the basal ECG is normal or shows a WPW pattern. The maximal exercise test and 24 hour Holter monitoring give no information in over 90% of cases.(ABSTRACT TRUNCATED AT 400 WORDS)     

Predictors of atrial rhythm after atrioventricular node ablation for the treatment of paroxysmal atrial arrhythmias

OBJECTIVE: To assess the natural history of the atrial rhythm of patients with paroxysmal atrial arrhythmias undergoing atrioventricular node ablation and permanent pacemaker implantation. DESIGN AND SETTING: A retrospective cohort study of consecutive patients identified from the pacemaker database and electrophysiology records of a tertiary referral hospital. PATIENTS: 62 consecutive patients with paroxysmal atrial arrhythmias undergoing atrioventricular node ablation and permanent pacemaker implantation between 1988 and July 1996. MAIN OUTCOME MEASURES: (1) Atrial rhythm on final follow up ECG, classified as either ordered (sinus rhythm or atrial pacing) or disordered (atrial fibrillation, atrial flutter or atrial tachycardia). (2) Chronic atrial fibrillation, defined as a disordered rhythm on two consecutive ECGs (or throughout a 24 hour Holter recording) with no ordered rhythm subsequently documented. RESULTS: Survival analysis showed that 75% of patients progressed to chronic atrial fibrillation by 2584 days (86 months). On multiple logistic regression analysis a history of electrical cardioversion, increasing patient age, and VVI pacing were associated with the development of chronic atrial fibrillation. A history of electrical cardioversion and increasing patient age were associated with a disordered atrial rhythm on the final follow up ECG. CONCLUSIONS: Patients with paroxysmal atrial arrhythmias are at high risk of developing chronic atrial fibrillation. A history of direct current cardioversion.     

Prediction of a fatal atrial fibrillation in patients with asymptomatic Wolff-Parkinson-White pattern

Paroxysmal atrial fibrillation (PAF) in patients with manifest WPW syndrome can be a life-threatening arrhythmia by deterioration into ventricular fibrillation. In patients with asymptomatic WPW pattern, the first PAF may lead to ventricular fibrillation or sudden death. Therefore, the purpose of this study was to predict a fatal PAF in patients with asymptomatic WPW pattern. The patient population was divided into two groups: (1) 145 patients with manifest WPW syndrome, excluding intermittent ones (32 with an episode of PAF, 49 with AV reciprocating tachycardia alone, and 64 without any episode of paroxysmal tachyarrhythmia), and (2) mixed group of patients with and without WPW syndrome (36 with an episode of PAF and 66 without PAF). The results were as follows: (1) (a) out of 32 patients with WPW syndrome and PAF, 8 patients were observed to have both the shortest preexcited R-R interval of less than 200 msec during PAF and the shortest antegrade effective refractory period of the accessory pathway (ERP-AP) of less than 250 msec, 7 of whom had dizziness or syncope during PAF and 2 died suddenly during the follow-up period; (b) 21 (32.8%) out of 64 patients with asymptomatic WPW pattern showed the shortest antegrade ERP-AP less than 250 msec; (2) patients with PAF had a higher tendency to develop repetitive atrial firing (RAF), as well as fragmented atrial activity (FAA), which were induced using programmed atrial stimulation.(ABSTRACT TRUNCATED AT 250 WORDS)     

Mechanisms for atrial fibrillation in patients with Wolff-Parkinson-White syndrome

INTRODUCTION: Paroxysmal atrial fibrillation (PAF) frequently occurs in patients with Wolff-Parkinson-White (WPW) syndrome. To elucidate the mechanisms for PAF, we performed electrophysiologic studies (EPS) before and after ablation of accessory pathways (APs). METHODS AND RESULTS: We investigated 24 patients with WPW syndrome who had AV reciprocating tachycardia and prior PAF and had undergone successful ablation of APs. Patients in whom atrial fibrillation (AF) was induced by EPS at day 7 after ablation were considered the inducible AF group (n = 14), and patients in whom AF was not induced by EPS at day 7 after ablation were considered the noninducible AF group (n = 10). Fifteen patients with AV nodal reentrant tachycardia (AVNRT) but without PAF who underwent ablation of the slow AV nodal pathways served as the control group (AVNRT group). Maximal atrial conduction delay and conduction delay zone, which are indices of atrial vulnerability, were measured before and after ablation. Before ablation, maximal atrial conduction delay and conduction delay zone were significantly greater (P < 0.0001 and P < 0.0001, respectively) in the two WPW syndrome groups than in the AVNRT group, indicating increased atrial vulnerability in WPW syndrome with PAF. After ablation, these parameters did not change in the inducible AF group, whereas they were significantly (P < 0.0001) decreased in the noninducible AF group and were not different from those in the AVNRT group, indicating normalized atrial vulnerability in the noninducible AF group after ablation. The prospective study demonstrated that PAF recurred only in the inducible AF group during long-term follow-up (17+/-7 months). CONCLUSION: The findings of this study suggest that there are two mechanisms of PAF in patients with WPW syndrome: one mechanism is reversible and AP-dependent atrial vulnerability, and the other is intrinsic and AP-independent atrial vulnerability.     

P波离散度对脑卒中患者并发阵发性房颤及预后的预测价值

目的 探讨P波离散度对脑卒中患者发生阵发性房颤及预后的预测价值.方法 选择72例脑卒中患者,根据有无阵发性房颤分为A组（伴有阵发性房颤）36例和B组（不伴有阵发性房颤）36例,两组患者均行12导联心电图及彩色多普勒超声心动图,24h动态心电图检测,分别测量心电图P波最大时限（Pmax）、P波最小时限（Pmin）,计算P波离散度（Pd）、左心房内径（LAD）、左心室射血分数（LVEF）,并进行比较.结果 两组间P波最大时限（Pmax）、P波离散度（Pd）、左心房内径（LAD）、左心室射血分数（LVEF）、频发房早、短阵房速比较,差异有统计学意义（P＜0.05）.结论 P波离散度是预测脑卒中患者并发阵发性房颤的可靠指标,对预后观测有一定意义.     

Wolff-Parkinson-White syndrome presenting in atrial fibrillation

A case of atrial fibrillation in a patient with Wolff-Parkinson-White (WPW) syndrome is presented. In this case, the patient's ECG initially was misread as ventricular tachycardia. The therapy was appropriate for the actual condition, although electrical cardioversion and defibrillation eventually were required. The treatment of WPW with atrial fibrillation in this case consisted of lidocaine and procainamide. Verapamil, propranolol, and digoxin, which normally are indicated for WPW with tachyarrhythmias, are contraindicated for WPW with atrial fibrillation.     

间歇性预激综合征动态心电图分析

目的探讨间歇性预激综合征的动态心电图特点和发病机制,为临床提供有价值信息。方法对近几年来我院动态心电图检查中记录到的22例间歇性预激综合征患者进行回顾性分析。结果间歇性预激综合征发生率为21.9%,其中12例（54.5%）呈频率依赖性发作;7例（31.8%）呈非频率依赖性发作;5例（22.7%）夜间发作较显著。8例（36.4%）伴有阵发性室上性心动过速（均在白天发作）,1例（4.5%）伴心房纤颤。9例（40.9%）常规心电图未见典型预激图形表现。结论本研究间歇性预激综合征主要表现为频率依赖性、非频率依赖性和夜间发作明显等几种类型;并发的心律失常主要为前向性房室折返性心动过速和心房纤颤;常规心电图检出率较低,推荐常规使用动态心电图检查,以提高检出率。     

Mechanism and prediction of sudden cardiac death in arrhythmia patients using electrophysiological studies

Thirty nine cases, in which sudden cardiac death (SCD) was suspected, were studied to evaluate the mechanism and the prediction of SCD in arrhythmia-patients using electrophysiological studies (EPS). The 39 cases (28 male and 11 female) were located by surveying 2098 patients who underwent EPS for the evaluation of arrhythmias. Age at time of EPS ranged from 4 to 86 years, average 50.5 years. Time from EPS to death was 2 to 163 months, average 27.9 months. Underlying heart disease was: dilated cardiomyopathy in 11, old myocardial infarction in 5, ischemic heart disease in 5, hypertensive heart disease in 5, valvular heart disease in 3, hypertrophic cardiomyopathy in 2, arrhythmogenic right ventricular dysplasia in 1, myocarditis in 1, sarcoidosis in 1, cor pulmonale in 1, and no obvious heart disease in 4. Fifteen had a permanent pacemaker implanted. SCD in cases without a permanent pacemaker (24 cases): 2 had chronic complete A-V block (one BH block, one HV block), 1 had advanced A-V block (HV block), 3 had bundle branch block with first degree HV block, 9 had ventricular tachycardia (VT), 3 had sick sinus syndrome (SSS), 3 had paroxysmal atrial flutter, 1 had WPW syndrome and paroxysmal atrial fibrillation, 1 had paroxysmal atrial tachycardia, and 3 had premature ventricular beats and first degree HV block. SCD in cases with permanent pacemaker (15 cases): 5 had SSS, and 10 had A-V block. In 3 of the 5 with SSS and 7 of the 10 with A-V block, VT was found before pacemaker implantation. In our study, brady and tachyarrhythmias coexisted in 25 cases (64%).(ABSTRACT TRUNCATED AT 250 WORDS)     

血压变异性与心房颤动相关性研究

［］ 目的 探讨血压变异性(BPV)对心房颤动发生及左心结构的影响。方法 随机选取我科2013年6月至2015年10月就诊患者120例患者,其中永久性房颤40例,持续性房颤40例,阵发性房颤40例,选取同期住院的窦性心律患者40例,测24h动态心电图、动态血压、超声心动图对160例患者检测,比较四组患者血压变异性及左房内径。 结果 心房颤动组的血压变异性、左房内径较正常对照组明显增加,房颤组内比较,永久性房颤组较持续性房颤组、阵发性房颤组血压变异性明显增大。 结论 心房颤动的患者血压变异性明显增加,且心房颤动的严重程度与血压变异性呈正相关。#$NL［关键词］心房颤动;血压变异性;左房内径     

Ventricular fibrillation as a primary manifestation of Wolff–Parkinson–White syndrome

Wolff–Parkinson–White syndrome (WPW) is defined as a condition involving an accessory pathway associated with symptoms. A typical ECG pattern of a pre-excitation shows a short PQ interval, presence of delta wave and a broad QRS complex on surface ECG. The underlying mechanism involves an accessory pathway, which enables conduction of a depolarization wave from atria to ventricles bypassing the AV node and predisposes to arrhythmias and sudden cardiac death. The most common arrhythmia in patients with WPW syndrome is atrioventricular reentrant tachycardia. However, it is not present in all patients with pre-excitation [1], [2], [3], [4]. Up to 1/3 of patients with AVRT experience atrial fibrillation, which may be conducted to ventricular myocardium via the accessory pathway and lead to a life-threatening ventricular fibrillation. The most effective treatment of the WPW syndrome is a radiofrequency catheter ablation [2], [5], [6], [7], [8]. This paper describes a case of a 40-year-old woman after a cardiopulmonary resuscitation for ventricular fibrillation, which was a primary manifestation of the WPW syndrome. It focuses on pathophysiology, clinical pattern and treatment possibilities of patients with WPW syndrome.     

Anti-arrhythmia efficacy of propafenone per os in the prevention of paroxysmal supraventricular arrhythmia resistant to class Ia agents

The efficacy of orally administered propafenone in the prevention of paroxysmal supraventricular dysrhythmias (atrial fibrillation, atrial tachysystole, reciprocal tachycardia) resistant to Vaughan-Williams class Ia drugs was investigated in 10 patients. Propafenone controlled dysrhythmia very well in 4 out of the ten patients, and satisfactorily in another one at a dosage ranging from 450 to 900 mg/day in 3 or 4 divided doses; this result was documented using continuous 24 hr. Holter ECG monitoring. Among the 5 clinical failures, 1 patient had atrial fibrillation primarily at night, and another poorly tolerated this agent which led to interrupt therapy.     

Significance of supraventricular arrhythmias induced by electrophysiologic studies

The clinical history and the findings on Holter monitoring of767 patients (without evidence of ventricular pre-excitationon the ECG) were compared with the results of electrophysiologicalstudies to assess the significance of supraventricular arrhythmiasinduced by intracardiac study. The studies were undertaken todetermine the cause of syncope, conduction disturbances or tachycardia. In 570 patients (group 1) supraventricular arrhythmias werenot induced. On Holter monitoring, 36 (6%) had evidence of supraventriculartachycardias, including atrial flutter, atrial fibrillationand paroxysmal junctional tachycardia. In 86 patients (group 2) one atrial extrastimulus induced aparoxysmal junctional tachycardia; 79 (82%) of these patientshad had spontaneous supraventricular tachycardia (SVT). In 111 patients (group 3) another type of SVT was induced: (a) The movement of the catheter induced atrial flutter or fibrillationin nine patients, eight (89%) of whom had spontaneous SVT. (b) Atrial pacing at a rate less than 200 bpm induced atrialflutter or fibrillation in 14 patients of whom nine (64%) hadSVT. (c) Ventricular pacing induced SVT in 15 patients, of whom 14(64%) had SVT. (d) An atrial extrastimulus during sinus rhythm induced atrialechoes in 62 patients, 47 (76%) of whom had SVT. (e) The atrial extrastimulus during sinus rhythm induced atrialtachycardia in 11 patients, nine (82%) of whom had SVT.     

Prevalence of inducible paroxysmal supraventricular tachycardia during esophageal electrophysiologic study in patients with unexplained stroke

BACKGROUND: The relationships between stroke and atrial tachycardia or atrial fibrillation were previously reported. Electrophysiological study is one of the means, used to detect and evaluate these atrial tachyarrhythmias. But, some other arrhythmias as paroxysmal supraventricular tachycardia, can be induced during electrophysiologic study and their significance in stroke is unknown. The aim of the study was to assess the significance of inducible paroxysmal supraventricular tachycardia (PSVT) in stroke. METHODS: One hundred thirty seven patients, aged 61+/-12 years had unexplained stroke (group I) and were compared to 60 subjects aged 45+/-18.5 years without stroke and history of tachycardia (group II); Holter monitoring (HM), echocardiogram and esophageal electrophysiologic study (EPS) in basal state and after isoproterenol were performed. RESULTS: Heart disease was noted in 19 group I patients (14%) and 10 group II patients (17%). In group I, atrial fibrillation or tachycardia (AF-AT) was induced in 20 patients (15%) and PSVT was induced in 19 patients (14%) aged 66+/-12 years. In group II, AF/AT was induced in 3 patients (5%); no group II patient had induced PSVT. After 3+/-1 years, in group I, one of 98 patients without induced arrhythmias had new strokes and 2 had AF; 5 patients with induced AT/AF developed AF; 5 patients with induced PSVT had PSVT's, requiring ablation in 4 of them; 1 died from a new stroke; one had a second non-fatal stroke and 3 patients developed AF (16%). In group II, there were no events. CONCLUSION: In 14% of patients with unexplained stroke, PSVT was inducible during esophageal electrophysiologic study. Further studies are warranted to assess the significance of this finding in patients with unexplained stroke.     

Doppler predictors of inducibility of atrial fibrillation in patients with WPW syndrome and atrioventricular re-entrant tachycardia

BACKGROUND: Atrial fibrillation (AF) in patients with Wolff-Parkinson-White syndrome (WPW) may induce complex ventricular arrhythmias resulting in sudden cardiac death. It is essential to find an effective non-invasive diagnostic method allowing to select patients at risk of life-threatening arrhythmias. Our objective was to examine Doppler predictors of AF in patients with WPW and atrioventricular re-entrant tachycardia (AVRT). MATERIAL AND METHODS: 65 patients with WPW and AVRT (33 men, mean age 39 +/- 11 y) were prospectively studied. In all patients TTE was performed with measurements of left ventricle (LV) diameters, volumes and parameters of systolic and diastolic function. TTE was followed by invasive electrophysiology study (EPS) and radiofrequency current ablation of accessory pathway.AF lasting at least 30 s was induced in 29 (44.6%) patients during EPS. Reduction of right upper pulmonary vein (RUPV) systolic velocity (P < 0.005) and systolic to diastolic velocity ratio (P < 0.005) and increase in atrial reversal velocity (P < 0.05) of RUPV flow and difference between duration of RUPV atrial reversal flow and A wave of mitral profile (P < 0.05) were associated with increased risk of AF in patients with WPW syndrome and AVRT. Systolic and atrial reversal velocities were identified as independent predictors of AF in those patients. CONCLUSIONS: Systolic and atrial reversal right upper pulmonary vein flow velocities have been shown to be independent predictors of AF inducibility in patients with Wolff-Parkinson-White syndrome and atrioventricular re-entrant tachycardia.     

The Management of Patients with Suspected Wolff-Parkinson-White Syndrome—A Four Year Review

Abstract: Thirty-six patients with the electrocardiographic pattern of Wolff-Parkinson-White (WPW) Syndrome had electrophysiological (EP) studies over a four year period. Thirty-two patients were symptomatic and supraventricular tachycardia (SVT) or atrial fibrillation (A Fib) had been demonstrated in 19 of these patients. Four patients were asymptomatic. The diagnosis of WPW was confirmed in 33 of the 36 patients at EP studies and in 24 of 33 the location of the accessory atrioventricular connection (AAVC) from the surface ECG was confirmed at EP studies. The effective refractory period of the AAVC in 30 patients ranged from 200–550 ms (m 284 ± 58 ms). A Fib could be induced in 20 of the 32 patients and SVT in 21 of the 33 patients. In 14 of 21 patients the SVT had narrow QRS complexes; in three patients the QRS was wide and in four patients both types were noted. In three patients the diagnosis of WPW was disproved at EP studies. On the basis of EP studies, drug therapy was recommended in 21 patients. In 12 of the 21 patients previous drug therapy was changed. Nine of these 12 patients showed symptomatic improvement. Of the remaining patients one required surgery because of failed medical treatment; the two other patients died and their deaths could be attributed to failure of medical therapy. In seven patients no change was made in drug therapy and in two, intermittent drug therapy was recommended. In six patients no drug therapy was prescribed. Two patients were treated with magnetactivated implantable pacemakers capable of delivering coupled, fixed-interval right ventricular extrastimuli. Neither of these was successful and thus surgery was recommended. Six patients have undergone surgical section of their AAVC with complete control of tachycardia; two patients are awaiting surgery. EP studies were helpful in the management of the majority of symptomatic patients with suspected WPW Syndrome. Surgery offers an attractive alternative to long term, and occasionally unsuccessful, drug therapy and should be considered in suitable patients.     

Intracorporeal cardiac pacemakers for refractory tachycardia (excluding atrial disease). Apropos of 18 cases]

The treatment of paroxysmal tachycardia by the use of permanent pacing to prevent or terminate attacks is discussed. The series comprises 18 patients with follow-up periods ranging from 1 to 12 years. In 6 cases the indication for pacing was atrial tachy-arrythmias favourised by bradycardia (5 of whom had vagally- induced atrial arrythmias). The atrial pacemaker successfully prevented attacks in 4 out of 6 cases. Three cases of chronic reciprocating tachycardia were successfully treated by simultaneous atrial and ventricular pacing or using sequential pacing with a very short P-R interval. Eight cases of paroxysmal orthodromic reciprocating tachycardia in the WPW syndrome were paced: in 5 cases pacing was employed to terminate attacks by atrial (3 cases) or ventricular (2 cases) stimulation, in the other 3 cases pacing was used to prevent the bradycardia which favourised the initiation of tachycardia. Good results were obtained in all 8 cases. Ventricular stimulation was used to terminate attacks in one patient with refractory ventricular tachycardia but the patient had a sudden death probably caused by the pacemaker. The place of these different pacing techniques with respect to medical treatment and specialised arrhythmia surgery is discussed.