Wide complex tachycardias. Differential diagnosis and management.

The majority of wide complex tachycardias are secondary to VT. The differential diagnosis of wide complex tachycardia also includes SVT with aberrancy or underlying bundle branch block and antegrade SVT conduction over an accessory pathway (antidromic SVT). VT is usually the result of reentry and most commonly arises in an area of diseased myocardium in the setting of previous myocardial infarction or cardiomyopathy. VT, however, can also occur in patients with structurally normal hearts. Criteria useful in diagnosis of wide complex tachycardia include clinical criteria (presence of structural heart disease or a history of previous myocardial infarction) and electrocardiographic criteria (the presence of capture or fusion beats, relation of atrial or ventricular activity, QRS duration and axis, and morphology). The acute management of wide complex tachycardia includes cardioversion and intravenous pharmacologic therapy. Almost all patients with VT require chronic therapy, although in rare patients treatment of acute precipitating factors may be sufficient. While pharmacologic therapy has been the mainstay of treatment for these patients, there have been many exciting advances using surgical, device, and ablative therapies.     

Supraventrikuläre Tachykardien

Supraventricular tachycardias (SVT) are paroxysmal tachycardias as are sinus tachycardia, atrial tachycardia, AV nodal reentry tachycardia, and tachycardia due to accessory pathways. All SVT are characterized by a ventricular heart rate >100/min and small QRS complexes (QRS width <120 ms) during tachycardia. It is essential to evaluate the arrhythmia history, to perform a good physical examination, and to accurately analyze the 12-lead electrocardiogram. An exact SVT diagnosis is then possible in >90% of SVT patients. For acute therapy, vagal maneuvers, adenosine, class I antiarrhythmic drugs, beta blocking agents, and calcium antagonists (verapamil type) are necessary, whereas drug therapy is not the method of choice for long-term treatment. Catheter ablation is an excellent therapeutic approach for patients with SVT with success rates >95%. Therefore, this approach is the treatment of choice for these patients.     

Herzrhythmusstörungen bei der Schwangeren und beim Fetus

For the acute treatment of supraventricular (SVT) and ventricular tachycardias (VT) in pregnant women, electrical cardioversion with 50-100 J is indicated in all unstable patients. In stable SVT the initial therapy includes vagal maneuvers or intravenous adenosine. For long-term therapy, beta-blocking agents with beta(1)-selectivity are first-line drugs or specific anti-arrhythmic drugs. An implantable cardioverter-defibrillator is another approach. In patients with symptomatic bradycardia, a pacemaker can be implanted using echocardiography at any stage of pregnancy. Evaluation of fetal arrhythmias in clinical practice is based on assessment of the chronological relationship between atrial and ventricular contraction (M-mode and Doppler ultrasound or magnetocardiography). Most forms of SVT can be treated with transplacental administration of anti-arrhythmic drugs. Atrioventricular (AV) block in fetuses with structural heart disease is frequently associated with hydrops fetalis and intrauterine death. Administration of corticoids and beta-mimetic drugs is used to treat antibody-mediated AV block and cardiomyopathy.     

ECG in the diagnosis of supraventricular tachyarrhythmias

The development of catheter ablation techniques during the last decade provided new data about the mechanism of supraventricular tachyarrhythmias and at the same time, set new requirements for their classification. An accurate diagnosis of individual SVT can usually be made during an electrophysiologic study that precedes catheter ablation. Nevertheless, clinically acceptable differential diagnosis of SVT can be based on analysis of a standard 12-lead electrocardiogram. This may prove useful especially when selecting optimum antiarrhythmic drug according to a suspected mechanism of arrhythmia. At the same time, electrocardiogram during SVT serves as a recording of clinical arrhythmia for catheter ablation. At present, SVTs are divided into 3 main categories: 1. atrial tachyarrhythmias confined solely to atrial tissue, 2. tachycardias involving the AV junction, and 3. AV reentrant tachycardias involving one or more accessory connections with an electric impulse travelling between atria and ventricles. The first category can be further subdivided into: a) macroreentrant atrial tachycardias related to the presence of macroscopic anatomical or functional barriers; b) focal atrial tachycardias arising from a focus of abnormal automaticity or microreentry in the atrium; c) the syndrome of inappropriate sinus tachycardia resulting most probably from hypersensitivity to adrenergic stimulation; d) atrial fibrillation based on the existence of multiple wandering wavelets in the atria. Electrocardiographic differential diagnosis is predominantly based on an analysis of the standard 12-lead ECG. Principal diagnostic features include the presence and timing of the P waves in relation to the QRS complex. Additional criteria comprise the presence or absence of AV block during the tachycardia, an axis orientation of the P waves and their morphology, the appearance of QRS alternans or frequency of tachycardia.     

Clinical management of patients with atrioventricular nodal reentrant tachycardia

A broad array of therapeutic options is currently available for the management of patients with AV nodal reentrant tachycardia. While acute termination of tachycardias is readily achieved, either by vagal maneuvers or intravenous medication, the decision to embark on a long-term therapeutic plan to prevent recurrences must be clinically individualized. When a chronic pharmacologic approach is desired, electrophysiologic testing is invaluable for confirming the diagnosis and selecting appropriate medication. However, the growing awareness of potential proarrhythmic effects and the inconvenience and expense of lifelong drug therapy, coupled with other advances in the field, have made nonpharmacologic approaches more attractive. This is especially so for symptomatic younger patients. The definitive cure rates achievable with surgery are now being approached by transcatheter AV nodal modification procedures that ablate AV nodal reentrant tachycardia while preserving anterograde AV nodal conduction. Over the next decade, it is likely that the latter technique will become widely used for the long-term management of symptomatic AV nodal reentrant tachycardia.     

Differential electrophysiologic properties of decremental retrograde pathways in long RP' tachycardia

Long RP' supraventricular tachycardias (SVT) often demonstrate both slow and decremental conduction properties in the retrograde pathway of the reentrant circuit. The electrophysiologic properties of these pathways are poorly understood. We studied 10 patients with long RP' SVT (RP'/RR, 0.52 to 0.71); five had the unusual form of atrioventricular nodal reentry (fast-slow) and five patients had accessory AV pathways with slow, decremental retrograde conduction properties. During SVT, the effects of intravenous adenosine (37.5 to 150 micrograms/kg), which increases potassium current (iK) in supraventricular tissue and hyperpolarizes membrane potential toward Ek (-90 mV), and the response to slow-inward channel blockade with verapamil (0.10 to 0.20 mg/kg iv) were evaluated. Adenosine and verapamil has similar effects in the presence of fast-slow AV nodal reentry since both agents terminated SVT by producing block in the retrograde slow AV nodal pathway. In contrast, adenosine and verapamil had differential effects on retrograde conduction in decremental accessory pathways. Adenosine terminated all episodes of SVT in the retrograde decremental pathway, whereas verapamil had a direct effect on this tissue in only two of five patients. Decremental retrograde accessory pathways can therefore demonstrate at least two types of electrophysiologic responses. Pathways that respond only to adenosine-induced hyperpolarizing K+ current likely comprise depressed fast-Na+ channel tissue, i.e., partially depolarized (greater than -60 to -70 mV) atrial tissue. In contrast, decremental accessory pathways that respond to both modulation of the slow-inward calcium current and K+ conductance have pharmacologic properties similar to those of the AV node and may represent more completely depolarized atrial fibers with resting membrane potentials of -60 mV or less.     

A new algorithm in the differential diagnosis of wide complex tachycardia.

A correct electrocardiographic diagnosis of the mechanism ofa wide complex tachycardia (WCT) is important when institutingemergent therapy and for long-term prognostic and therapeuticconsiderations. While any algorithm has the risk of oversimplifyinga complex problem, it is absolutely essential to have an initialstrategy for the acute evaluation of an arrhythmia. Causes of wide QRS tachycardia include (1) supraventriculartachycardia (SVT) with pre-existing or functional bundle branchblock, including sinus tachycardia, atrial tachycardia, atrialflutter, atrial fibrillation (AF) and AV nodal re-entry tachycardia,(2) orthodromic circus movement tachycardia with pre-existingor functional bundle branch block, (3) SVT with conduction overan accessory pathway, (4) Antidromic circus movement tachycardiausing an accessory pathway in the anterograde direction andAV     

Rhythmusstörungen bei Schwangeren

Atrial premature beats are frequently diagnosed during pregnancy (PR) and supraventricular tachycardia (SVT) (atrial tachycardia, AV nodal reentrant tachycardia, circus movement tachycardia) less frequently. For acute therapy, electrical cardioversion with 50–100 J is indicated in all unstable patients. In stable SVT the initial therapy includes vagal maneuvers to terminate breakthrough tachycardias. For short-term management, when vagal maneuvers fail, intravenous adenosine is the first choice drug and may safely terminate the arrhythmia. For long-term therapy, ß-blocking agents with β₁ selectivity are first-line drugs; class Ic agents or the class III drug sotalol (sot) are effective and therapeutic alternatives. Ventricular premature beats are also frequently present during PR and benign in most of the patients; however, malignant ventricular tachyarrhythmias [sustained ventricular tachycardia (VT), ventricular flutter (VFlut), ventricular fibrillation (VF)] were observed less frequently. Electrical cardioversion is necessary in all patients with hemodynamically unstable situation and life-threatening ventricular tachyarrhythmias; in hemodynamically stable patients, initial therapy with ajmaline, procainamide or lidocaine is indicated. If prophylactic therapy is needed, ß-blocking agents with ß₁ selectivity are considered as first choice drugs. If this therapy is ineffective, class Ic agents or sot can be considered. In patients with syncopal VT, VF, VFlut or aborted sudden death an implantable cardioverter-defibrillator is indicated. In patients with symptomatic bradycardia, a pacemaker can be implanted using echocardiography at any stage of PR. The treatment of the pregnant patient with cardiac arrhythmias requires important modification of the standard practice of arrhythmia management. The goal of therapy is to protect the patient and fetus through delivery, after which chronic or definitive therapy can be administered. In addition, antiarrhythmic therapy is also possible during breastfeeding.     

Dual chamber arrhythmia detection in the implantable cardioverter defibrillator

INTRODUCTION: Dual chamber implantable cardioverter defibrillator (ICD) technology extended ICD therapy to more than termination of hemodynamically unstable ventricular tachyarrhythmias. It created the basis for dual chamber arrhythmia management in which dependable detection is important for treatment and prevention of both ventricular and atrial arrhythmias. METHODS AND RESULTS: Dual chamber detection algorithms were investigated in two Medtronic dual chamber ICDs: the 7250 Jewel AF (33 patients) and the 7271 Gem DR (31 patients). Both ICDs use the same PR Logic algorithm to interpret tachycardia as ventricular tachycardia (VT), supraventricular tachycardia (SVT), or dual (VT+ SVT). The accuracy of dual chamber detection was studied in 310 of 1,367 spontaneously occurring tachycardias in which rate criterion only was not sufficient for arrhythmia diagnosis. In 78 episodes there was a double tachycardia, in 223 episodes SVT was detected in the VT or ventricular fibrillation zone, and in 9 episodes arrhythmia was detected outside the boundaries of the PR Logic functioning. In 100% of double tachycardias the VT was correctly diagnosed and received priority treatment. SVT was seen in 59 (19%) episodes diagnosed as VT. The causes of inappropriate detection were (1) algorithm failure (inability to fulfill the PR相似文献   

12-Kanal-Elektrokardiogramm

The surface electrocardiogram (ECG) is an important diagnostic tool for the diagnosis of arrhythmias and acute coronary syndrome. Supraventricular tachycardias (SVT) are paroxysmal tachycardias as are sinus tachycardia, atrial tachycardia, AV nodal reentry tachycardia, and tachycardia due to accessory pathways. All SVT are characterized by a ventricular heart rate >100/min and small QRS complexes (QRS width <0.12 s) during tachycardia. It is important to analyze the relation between P wave and QRS complex to look for an electrical alternans as a leading finding for an accessory pathway. Wide QRS complex tachycardias (QRS width ≥ 0.12 s) occur in SVT with aberrant conduction and SVT with bundle branch block or ventricular tachycardia (VT). In broad complex tachycardias, AV dissociation, negative or positive concordant pattern in V₁–V₆, a notch in V₁ and QR complexes in V₆ in tachycardias with left bundle branch block morphologies are findings indicating VT. In addition, an R/S relation <1 in V₆ favors VT when right bundle branch block tachycardia morphologies are present. By analyzing the surface ECG in the right way with a systematic approach, the specificity and sensitivity of correctly identifying a SVT or VT can be raised by >95%. The 12-lead surface ECG allows the coronary culprit lesion to be located in 97% due to determination of the 12-lead ST segment deviation score.     

H?ufigkeit, Diagnostik und Therapie von Herzrhythmusst?rungen in der Schwangerschaft

Atrial premature beats are frequently diagnosed during pregnancy (PR), supraventricular tachycardia (SVT) less frequently. For acute therapy, electrical DC-cardioversion with 50–100 J is indicated in all unstable patients (pts). In stable SVT, the initial therapy includes vagal maneuvers to terminate breakthrough tachycardias. For short-term management, when vagal maneuvers fail, intravenous adenosine is the drug of first choice and may safely terminate the arrhythmia. Ventricular premature beats are also frequently present during PR and benign in most pts, while life-threatening ventricular tachyarrhythmias (sustained ventricular tachycardia (VT), ventricular flutter (VFlut), ventricular fibrillation (VF)) are observed less frequently. Electrical DC cardioversion is necessary in all pts with a hemodynamically unstable situation and life-threatening ventricular tachyarrhythmias; in hemodynamically stable pts, initial therapy with ajmaline, procainamide or lidocaine is indicated. In pts with syncopal VT, VF, VFlut or aborted sudden death, an implantable cardioverter-defibrillator is indicated. In pts with symptomatic bradycardia, a pacemaker can be implanted using echocardiography at any stage of PR.     

Paradoxical responses to pacing maneuvers differentiating atrioventricular node reentrant tachycardia and junctional tachycardia

A 40-year-old female presented at our hospital because of heart palpitations. During an electrophysiological study, atrioventricular (AV) conduction showed dual AV nodal physiology. Three types of supraventricular tachycardia (SVT) were induced. The initiation of SVT was reproducibility dependent on a critical A–H interval prolongation. An early premature atrial contraction during SVT repeatedly advanced the immediate His potential with termination of the tachycardia, indicating AV node reentrant tachycardia (AVNRT). However, after atrial overdrive pacing during SVT without termination of the tachycardia, the first return electrogram resulted in an AHHA response, consistent with junctional tachycardia. The mechanism of paradoxical responses to pacing maneuvers differentiating AVNRT and junctional tachycardia was discussed.     

Subcostal M-mode echocardiography of the right atrial wall in the diagnosis of cardiac arrhythmias

The M-mode echocardiogram of the right atrial (RA) wall can be easily recorded in each person from the subcostal location. In a normal RA wall motion pattern, atrial contraction is represented by a markedly prominent posterior motion. The presence or absence of atrial contractions in the subcostal RA wall echocardiogram, their amplitude, and their timing may help in the diagnosis of cardiac arrhythmias with the simultaneously recorded non-diagnostic electrocardiogram. Flat and hidden P waves can be accurately identified throughout the cardiac cycle. It is possible to distinguish between atrial, ventricular, and nodal premature beats and to recognize atrial fibrillation, atrial flutter, paroxysmal atrial tachycardia, paroxysmal atrial tachycardia with block, atrioventricular (AV) nodal tachycardia, and supraventricular tachycardias with aberrant ventricular conduction. The diagnosis of wandering pacemaker, AV dissociation, sinoatrial block, and AV block is facilitated. On the basis of study of 60 patients with various rhythm disturbances, it was concluded that analysis of the subcostal RA wall echocardiogram is a new, helpful noninvasive approach in the diagnosis of cardiac arrhythmias.     

A case of incessant junctional tachycardia in a female patient with aneurysm of the interauricular septum]

A permanent supraventricular tachycardia (SVT) was diagnosed in a 54-year-old hypertensive but cardiologically asymptomatic female patient, admitted to a surgery department for biliary lithiasis and hepatic echinococcosis. Heart rate was about 130 bpm and ECGs showed negative P waves in leads I, II, III, aVF, and precordial leads V2 to V6, being the RP' interval longer than P'R interval. Pharmacological intervention during Holter monitoring (20 hours) was instituted: following i.v. propranolol (4 mg), heart rate progressively decreased (to 112 bpm), mainly due to an increase in SVT RP' interval, and brief, spontaneous SVT interruptions occurred, preceded by P'R interval prolongation; SVT stopped after P' recording, and resumed after 2 sinus beats, (showing enlarged P waves and slightly prolonged PR interval), induced by cycle length shortening; later on, under i.v. amiodarone infusion (100 mg/hour) and coincident with the sleeping period, SVT cycle length progressively increased (to 600 msec), due to equivalent increases in P'R and R'P intervals. Two premature ventricular contractions (PVC) occurred during Holter monitoring at a coupling interval of 80-85% of SVT cycle length (480 msec): one PVC apparently originated in left ventricle lateral wall, captured the atria, which were activated 75 msec earlier than expected; the other PVC, apparently originated in left ventricle septoapical region, did not interfere with SVT cycle length. Before these data, a diagnosis of circus movement tachycardia, incorporating a concealed accessory pathway with slow retrograde conduction and ventricular insertion in the postoroseptal or left posterior paraseptal region, and showing minor impairment of antegrade AV nodal conduction, was made. Invasive electrophysiological study was then discarded. With combined oral antiarrhythmic therapy (amiodarone, 600 mg/d), plus propafenone, 450 mg/d), sinus rhythm was permanently restored, with evidence of intraatrial block, slightly prolonged PR interval and no preexcitation. Transesophageal echocardiography revealed a small atrial septal aneurysm associated with a small atrial septal defect; echocardiographic features were consistent with the hypothesis of incomplete regression of the atrial septal aneurysm after partial closure of the atrial septal defect. Abdominal surgery (cholecystectomy plus partial hepatic pericystectomy) was performed without any complications or SVT recurrences. During a 6-month follow-up period, maintaining amiodarone (200 mg/d) and propafenone (450 mg/d), the patient remained SVT-free, and Holter monitoring performed at 3 and 5 months showed permanent sinus rhythm and 1:1 AV conduction with slightly prolonged PR interval (less than 0.29 sec and shortening at faster heart rates). This case documents Holter monitoring capability for the evaluation of tachycardia mechanisms in patients with permanent SVT.     

Cardiac arrhythmias in pregnancy

Atrial premature beats are frequently diagnosed during pregnancy (PR), supraventricular tachycardia (SVT; atrial tachycardia, AV nodal reentrant tachycardia, circus movement tachycardia) less frequently. For acute therapy, electrical cardioversion with 50-100 J is indicated in all unstable patients (pts). In stable SVT the initial therapy includes the vagal maneuver to terminate breakthrough tachycardias. For short-term management, when the vagal maneuver fails, intravenous adenosine is the first-choice drug and may safely terminate the arrhythmia. For long-term therapy, beta-blocking agents with beta 1 selectivity are first-line drugs; class Ic agents or the class III drug sotalol (sot) are effective and therapeutic alternatives. Ventricular premature beats are also frequently present during PR and benign in most pts; however, malignant ventricular tachyarrhythmias (sustained ventricular tachycardia [VT], ventricular flutter [VFlut], ventricular fibrillation [VF]) were observed less frequently. Electrical cardioversion is necessary in all pts with a hemodynamically unstable situation and life-threatening ventricular tachyarrhythmias; in hemodynamically stable pts, initial therapy with ajmaline, procainamide or lidocaine is indicated. If prophylactic therapy is needed, beta-blocking agents with beta 1 selectivity are considered as first-choice drugs. If this therapy is ineffective, class Ic agents or sot can be considered. In pts with syncopal VT, VF, VFlut or aborted sudden death an implantable cardioverter-defibrillator is indicated. In pts with symptomatic bradycardia, a pacemaker can be implanted using echocardiography at any stage of PR. The treatment of the pregnant patient with cardiac arrhythmias requires important modification of the standard practice of arrhythmia management. The goal of therapy is to protect the patient and fetus through delivery, after which chronic or definitive therapy can be administered.     

Clinical and electrophysiologic effects of magnesium sulfate on paroxysmal supraventricular tachycardia and comparison with adenosine triphosphate.

Electrophysiologic studies have shown that intravenous magnesium sulfate prolongs atrioventricular (AV) nodal conduction and refractoriness and thus could play a role in the management of patients with paroxysmal AV reentrant supraventricular tachycardia (SVT). The present study evaluates the clinical and electrophysiologic effects of intravenous magnesium sulfate in patients with SVT and compares them with those of adenosine triphosphate (ATP), one of the most potent drugs in the treatment of this arrhythmia. Patients with inducible sustained SVT were treated with ATP (10 or 20 mg) and magnesium sulfate (2 g over 15 seconds) during electrophysiologic study. If the tachycardia failed to terminate by the sixth minute, an additional 2 g dose of magnesium was given. ATP (10 or 20 mg) was significantly better than magnesium for terminating induced tachycardias (14 of 14 vs 6 of 14, p less than 0.0001). Arrhythmia termination with ATP was due to anterograde AV nodal blockade in all but 1 patient who developed retrograde block over an accessory pathway with decremental conduction. Arrhythmia termination by magnesium was due to retrograde block over an accessory pathway in 3 patients (including the patient with accessory pathway exhibiting decremental conduction), anterograde AV nodal conduction block in 2 patients and premature ventricular complexes in 1 patient. During induced tachycardias, only AH intervals were prolonged by ATP, whereas magnesium significantly prolonged AH and QRS intervals. Short-lasting side effects (chest pain, flushing, nausea) occurred after both drugs were administered but were more severe after magnesium.(ABSTRACT TRUNCATED AT 250 WORDS)     

Usefulness of superficial electrocardiogram in the diagnosis of narrow QRS tachycardias: correlation with intracavitary electrocardiograms

INTRODUCTION AND OBJECTIVES: The electrocardiogram is an important tool to diagnose tachycardias. The sequence of analysis of the superficial electrocardiogram was evaluated for the diagnosis of supraventricular tachycardias with narrow QRS complexes (<= 110 ms) establishing correlation with intracavitary electrograms. PATIENTS AND METHODS: Between November 1996-October 1998, 674 electrophysiological studies were revised. 173 cases were selected, during which supraventricular tachycardias were inducted. In each study, the superficial electrocardiographic leads were correlated with the intracavitary electrograms during tachyarrhythmias. The P waves were located with respect to the R waves, the R-T or T-R' intervals, and the T waves, and relations between atrioventricular and ventriculoatrial intervals were established with the P-R' and R-P intervals, respectively, in the electrocardiogram. RESULTS: 107 patients were female. Upon locating the P waves in the electrocardiogram, in each supraventricular tachycardia we observed: a) P waves coincided with the R waves: 30 typical nodal reentries; b) P waves between R and T waves: 95 orthodromic atrioventricular reentries, 27 nodal reentries, 1 atrial tachycardia; c) P waves between T and R' waves: 4 nodal reentries, 5 orthodromic atrioventricular reentries, 7 atrial tachycardias, and 相似文献   

Usefulness of intravenous diltiazem in predicting subsequent electrophysiologic and clinical responses to oral diltiazem

Diltiazem, 0.25 mg/kg, was given intravenously during induced tachycardias in 6 patients with atrioventricular (AV) nodal reentrant tachycardia (group I) and in 24 patients with AV reentrant tachycardia incorporating a retrogradely conducting accessory pathway (group II). In all 6 group I and in 15 of 24 group II patients, tachycardias terminated within 1 minute after diltiazem administration, with a weak link in the anterograde direction. In 3 other patients in group II, tachycardias were terminated by a premature ventricular complex within 1 minute. In the remaining 6 patients in group II, in whom tachycardias failed to terminate, rates of tachycardias decreased as a result of suppression of anterograde AV nodal conduction by diltiazem. Electrophysiologic studies were performed subsequently 2 hours after the third dose of 90 mg of diltiazem, which was given orally at 8-hour intervals. In 18 responders to intravenous diltiazem who were subjected to oral diltiazem testing, sustained supraventricular tachycardia (SVT) could be induced in only 2. Of the 6 nonresponders, sustained tachycardias could not be induced in 3. Twelve patients, including 11 responders and 1 nonresponder to intravenous diltiazem who responded to oral diltiazem testing, were discharged with oral diltiazem therapy, 90 mg every 8 hours, with follow-up periods of 2 to 13 months (mean 7 +/- 4 [+/- standard deviation]). The frequency of recurrent SVT decreased significantly; 8 patients were free of tachycardias and 4 had occasional recurrences of SVT that required no hospital visit. In conclusion, intravenous diltiazem is effective in terminating SVT. Termination of SVT by intravenous diltiazem predicts subsequent electrophysiologic and clinical responses to oral diltiazem.     

Functional properties of accessory atrioventricular pathways in Wolff-Parkinson-White syndrome: Clinical implications

The Wolff-Parkinson-White syndrome is an uncommon cardiac disorder due to the presence of an accessory atrioventricular pathway resulting in ventricular pre-excitation and supraventricular tachycardias. The recognition of the Wolff-Parkinson-White syndrome is important because of the potential for the development of extremely rapid ventricular rates during atrial fibrillation that may lead to ventricular fibrillation and sudden death. The diagnosis of the Wolff-Parkinson-White syndrome is obvious when classic delta waves and short P-R intervals are present, but the electrocardiographic manifestations of the syndrome may be subtle and vary considerably from patient to patient. Certain commonly used antiarrhythmic medications may be useful for the treatment of reciprocating tachycardia in these patients and yet prove to be ineffective—or even deleterious—in preventing excessively rapid conduction to the ventricles during atrial fibrillation. An appreciation of the functional properties of the accessory pathways in the Wolff-Parkinson-White syndrome and how they are affected by pharmacologic agents should result in improved recognition of this entity and more effective medical management of patients with a risk of sudden death.     

Summary of efficacy and safety of flecainide for supraventricular arrhythmias

This report provides an overview of the safety and efficacy of flecainide for supraventricular tachyarrhythmias (SVT) based on a review of the world literature. This review provided 107 entries, but 5 were review articles and 22 were articles not translated into English. The remaining 80 articles or published abstracts form the basis for this report. A total of 1,371 courses of therapy with intravenous or oral flecainide, or both, were represented. Efficacy was defined by each investigator. Intravenous flecainide was successful in terminating ongoing tachycardias in 81% of reported cases of atrioventricular (AV) nodal reentrant tachycardias, 88% of AV reentrant tachycardias and 100% of atrial tachycardias. Atrial fibrillation or flutter was terminated by intravenous flecainide in 62% of cases and arrhythmias associated with Wolff-Parkinson-White syndrome in 73%. Oral flecainide was successful in longer-term management of arrhythmia in 74 and 81% of patients with AV nodal and AV reentrant tachycardia, respectively, and in 83% with atrial tachycardia. Atrial flutter or fibrillation responded to oral drug in 61% of cases and arrhythmias related to Wolff-Parkinson-White syndrome in 61%. Adverse experiences were reported in studies totaling 695 patients (designated "at-risk patients"). They were not commented on in studies with the remaining 594 patients. Overall, a total of 6.9% of at-risk patients (3.7% of total patients) reported cardiac adverse experiences; 19% of at-risk patients (10% of total patients) reported at least 1 noncardiac adverse effect. Cardiac adverse events included worsened arrhythmias in 28, conduction disturbances in 15 and congestive heart failure in 5. The most frequent noncardiac adverse experiences were paresthesia and visual disturbance.(ABSTRACT TRUNCATED AT 250 WORDS)