Incessant nonreentrant tachycardia due to simultaneous conduction over dual atrioventricular nodal pathways mimicking atrial fibrillation in patients referred for pulmonary vein isolation

It has been reported that conduction over the fast and slow pathways of the AV node can occur simultaneously, leading to a double ventricular response from each atrial beat. We report the cases of two patients referred to us for evaluation of symptomatic, incessant, and irregular narrow-complex tachycardia, misdiagnosed as atrial fibrillation, for consideration of pulmonary vein isolation. At presentation, careful evaluation of the electrograms revealed the presence of two ventricular activations for each atrial beat. At electrophysiologic study, both patients were found to have nonreentrant tachycardias arising from simultaneous conduction over the fast and slow pathways of the AV node. In one patient, the tachycardia had resulted in cardiomyopathy. Slow AV nodal pathway ablation performed in both patients resulted in cure of their tachycardias and recovery of ventricular function in the patient with cardiomyopathy.     

Subcostal M-mode echocardiography of the right atrial wall for differentiation of supraventricular tachyarrhythmias with aberration from ventricular tachycardia

Atrial contractions can be reliably detected by subcostal M-mode echocardiography of the right atrial wall. Recognition of various rhythm disturbances, especially tachyarrhythmias, is facilitated in the simultaneously recorded nondiagnostic ECG. Differentiation between supraventricular tachycardias with aberration and ventricular tachycardia with atrioventricular dissociation is alleviated. However, this technique is of limited value in the diagnosis of ventricular tachycardia with retroconduction and is not useful in differentiating supraventricular tachycardias with wide QRS from ventricular tachycardia when atrial fibrillation coexists.     

Determinants of QRS alternans during narrow QRS tachycardia

This study was designed to prospectively determine the incidence of QRS alternans during various types of narrow QRS tachycardia and to clarify the determinants of QRS alternans. An electrophysiologic study was performed in 28 consecutive patients with a narrow QRS tachycardia. Persistent QRS alternans was observed in 6 (43%) of 14 patients during orthodromic reciprocating tachycardia, 5 (71%) of 7 patients during atrial tachycardia and 3 (43%) of 7 patients during atrioventricular (AV) node reentrant tachycardia. Incremental atrial pacing during sinus rhythm resulted in QRS alternans in patients who had QRS alternans during tachycardia, unless the shortest pacing cycle length associated with 1:1 AV conduction exceeded the tachycardia cycle length. In patients without QRS alternans during narrow QRS tachycardia, incremental atrial pacing during sinus rhythm resulted in persistent QRS alternans in five patients in whom the shortest pacing cycle length associated with 1:1 AV conduction was 60 to 180 ms less than the tachycardia cycle length. In an additional 20 patients without a narrow QRS tachycardia, persistent QRS alternans was observed during incremental atrial pacing in 11 (55%) of the patients. In six of six patients who had QRS alternans during abrupt rapid atrial pacing, QRS alternans was not observed when the same pacing rates were achieved gradually. Among the patients with narrow QRS tachycardia, the mean tachycardia cycle length in those who had QRS alternans (mean +/- SD 288 +/- 44 ms) was significantly shorter than in those who did not (369 +/- 52 ms, p less than 0.001). The presence of QRS alternans was not related to the tachycardia mechanism, relative or functional refractory period of the His-Purkinje system (at a drive cycle length of 500 ms), age, presence of structural heart disease, direction of input into the AV node or concealed retrograde conduction in the His-Purkinje system. In conclusion, QRS alternans during narrow QRS tachycardias is a rate-related phenomenon that depends on an abrupt increase to a critical rate and is independent of the tachycardia mechanism.     

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.     

Regular Wide QRS Complex Tachycardia During Atrial Fibrillation in a Patient with Preexcitation Syndrome: A Case Report

AV Conduction in WPW. We report an unusual case of a relatively regular wide QRS complex tachycardia alternating with periods of an irregular narrow QRS complex tachycardia during atrial fibrillation in a patient with Wolff-Parkinson-White syndrome. Both tachycardias resulted from atrial fibrillation, the wide QRS complex tachycardia being due to 2:1 AV conduction of a type I atrial fibrillation across a posteroseptal accessory AV connection.     

An electrocardiographic criterion to detect AV dissociation in wide QRS tachyarrhythmias

A study was carried out on 12 patients with wide QRS tachycardia, 8 of whom presented with atrioventricular (AV) dissociation (Group A) and 4 with 1:1 AV association (Group B). This investigation aimed at assessing whether significant variations occurred in the QRS amplitude between the two groups. Group A showed more marked variations in QRS amplitude (31.7 +/- 13%) compared to Group B patients (6.2 +/- 1.2%) (p less than 0.001). The amplitude changes observed in Group A patients are probably related to variations in telediastolic volume resulting from the occasional contribution of the atrial systole. The findings suggest that variability in QRS amplitude during wide QRS tachyarrhythmias is a reliable sign of the presence of an AV dissociation. The possibility of diagnosing an AV dissociation on a surface ECG without visible P waves is an important finding, which though not pathognomonic of ventricular tachycardia, is a valid ECG criterion for assessing the ventricular origin of arrhythmias. This ECG criterion can be usefully applied in clinical practice along with others already used for the differential diagnosis of wide QRS tachyarrhythmias.     

Transient entrainment and interruption of atrioventricular node tachycardia

The possibility of transiently entraining and interrupting the common type of atrioventricular (AV) node tachycardia (anterograde slow, retrograde fast AV node pathway) was studied using atrial and ventricular pacing in 18 patients with paroxysmal AV node tachycardia. Transient entrainment occurred in all patients. During atrial pacing, localized block in the AV node for one beat followed by anterograde conduction over the fast pathway was observed in three patients. During ventricular pacing, localized block for one beat followed by retrograde conduction over the slow pathway was not observed in any patient. Neither atrial nor ventricular fusion beats were observed during entrainment. These observations indicate in a way not previously shown that reentry involving two functionally dissociated pathways in the AV node is the underlying mechanism of paroxysmal AV node tachycardia. The inability to demonstrate atrial or ventricular fusion beats during entrainment suggests a true intranodal location of the reentrant circuit. Finally, the ability to transiently entrain intranodal tachycardia demonstrates that this electrophysiologic phenomenon is not exclusively limited to macroreentrant circuits.     

Incidence and determinants of multiple morphologically distinct sustained ventricular tachycardias

The incidence and determinants of multiple morphologically distinct ventricular tachycardias were examined prospectively in 71 consecutive patients with at least one documented spontaneous episode of sustained monomorphic ventricular tachycardia. Mean frontal and horizontal QRS axes were determined from the 12 lead electrocardiograms (ECGs) of 190 spontaneous and 352 induced tachycardias. Two or more morphologically distinct spontaneous tachycardias were observed in 19 (43%) of 44 patients who had at least two documented spontaneous episodes. In 43 (61%) of the 71 patients, multiple morphologically distinct tachycardias were induced by programmed ventricular stimulation. Overall, 57 (80%) of the 71 patients had at least two morphologically distinct tachycardias. Predictors of multiple tachycardia configurations were selected by multivariate analysis from clinical and angiographic variables and were similar for both spontaneous and induced ventricular tachycardia: presence of multiple previous myocardial infarctions (p = 0.032 spontaneous, p = 0.005 induced) and number of different antiarrhythmic drug treatments during which ventricular tachycardia was documented (p = 0.0089 spontaneous, p less than 0.0001 induced). These data demonstrate that a large majority of patients with sustained monomorphic ventricular tachycardia exhibit more than one distinct QRS configuration when adequate ECG documentation of multiple episodes is obtained during different antiarrhythmic drug treatments. In individual patients, caution should be used in attributing clinical significance to a single unique QRS configuration.     

The differential diagnosis on the electrocardiogram between ventricular tachycardia and preexcited tachycardia

The 12-lead surface electrocardiogram is a simple and useful tool for the differential diagnosis of regular wide QRS complex tachycardia. However, criteria do not as yet exist to discriminate between ventricular tachycardia and supraventricular tachycardia with anterograde conduction over an accessory pathway (preexcited tachycardia). Therefore, we designed a new stepwise approach with three criteria for the electrocardiographic differential diagnosis between ventricular tachycardia and preexcited tachycardia and prospectively studied 267 regular tachycardias with electrophysiologically proven mechanism and a wide QRS complex (≥ 0.12 s): 149 consecutive ventricular tachycardias and 118 consecutive preexcited regular tachycardias. Underlying heart disease was old myocardial infarction in 133 of 149 (89%) ventricular tachycardias. The patients presenting with preexcited tachycardia had no additional structural heart disease. Atrial fibrillation with preexcited QRS complex was not included. The criteria favoring ventricular tachycardia were: (1) presence of predominantly negative QRS complexes in the precordial leads V₄ to V₆, (2) presence of a QR complex in one or more of the precordial leads V₂ to V₆, and (3) AV relation different from 1:1 (more QRS complexes than P waves). The final sensitivity and specificity of these three consecutive steps to diagnose ventricular tachycardia were 0.75 and 1.00, respectively. This new stepwise approach is sensitive and highly specific for the differential diagnosis between ventricular tachycardia in coronary artery disease and preexcited regular tachycardia.     

TRANSESOPHAGEAL ELECTROCARDIOGRAPHY AND ATRIAL PACING IN ACUTE CARDIAC CARE: DIAGNOSTIC AND THERAPEUTIC VALUE

The utility of transesophageal electrocardiography using a bipolar 'pill electrode' was assessed in 17 consecutive patients with tachycardia presenting to our casualty department. Standard 12-lead electrocardiography showed regular narrow QRS tachycardia in 12 patients, and five patients had wide QRS tachycardia. Esophageal atrial electrogram recordings were obtained in 14 patients (82%), and these were helpful in determining the mechanism of tachycardia in 11 patients (78%). Of these 11, seven patients fulfilled criteria for atrioventricular junctional (AVJ) tachycardia based on measurement of the minimum interval between the onset of ventricular depolarisation and earliest atrial (esophageal) activity. One of these patients had presented with a wide QRS tachycardia. The other four patients were diagnosed as having ventricular tachycardia (VT) following diagnosis of AV dissociation. Atrial overdrive pacing, via the pill electrode, successfully reverted four of the nine patients (44%) with narrow QRS tachycardia but no patient with VT. Esophageal recording during tachycardia is a simple, relatively non-invasive technique which is helpful in suggesting the mechanism of tachycardia both in patients with narrow and wide QRS tachycardia, and may have a therapeutic role in patients with AVJ tachycardia. (Aust NZ J Med 1989; 19: 11–15.)     

Re-entrant tachycardia using two bypass tracts and excluding AV node in short PR interval, normal QRS syndrome.

In patients with the short PR interval, normal QRS complex syndrome, paroxysmal tachycardias are usually the result of circus movement involving the AV node and a partial or complete AV nodal bypass. We report 2 patients with this syndrome who suffered distressing rapid paroxysms of tachycardia but in whom there was evidence of a concealed direct VA connection. In both patients, tachycardia was initiated with critical AV prolongation distal to the His bundle, in response to programmed atrial premature stimuli. The constancy of the timing of the atrial echo from the onset of the QRS complex in the presence of a varying HV interval is evidence for involvement of the ventricles in the re-entry pathway. In addition, in both patients the appearance of left bundle-branch block during tachycardia was associated with appropriate prolongation of tachycardia cycle length consistent with the presence of a direct VA connection. The short AH interval during tachycardia and the absence of critical AH prolongation suggests the participation of a rapidly conducting pathway in the anterograde limb of the tachycardia circuit.     

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   

Computer detection of premature ventricular complexes: A modified approach

The accuracy of a data reduction system for arrhythmia detection in identifying premature ventricular complexes was evaluated in continuous tape records of 30 patients in a coronary care unit. Computer analysis was performed with a Honeywell 316 digital computer. Threshold values for dominant complexes were automatically determined and recognition of premature ventricular complexes was based on differences in QRS configuration, timing and T wave configuration from the dominant complexes. Verification of the computer accuracy in detecting premature ventricular complexes was made with visual beat by beat inspection using a two channel strip chart recorder with simultaneous recording of the electrocardiogram and computer signal. This procedure allowed for exact beat to beat correlation and, thus, absolute determination of false positive and false negative identifications.From 0.5 to 6 continuous hours of monitoring per patient (average 3.5 hours) were analyzed for a total of 105 monitoring hours. The basic cardiac rhythms noted were normal sinus rhythm, sinus arrhythmia, sinus tachycardia, demand pacemaker rhythm, atrial fibrillation and atrioventricular (A-V) dissociation with junctional rhythm. Premature ventricular complexes were evident in 28 tapes (93 percent) including 12 (43 percent) with multifocal premature ventricular complexes and 3 (11 percent) with ventricular tachycardia. The visual count of premature ventricular complexes totaled 7,921. Of these, 7,542 (95 percent) were properly classified by the computer. The total computer count was 8,717, representing a 13 percent false positive and 5 percent false negative identification rate. The false positive identifications of premature ventricular complexes occurred during periods of 10 seconds or more of continuous noise artifact and in the presence of atrial premature complexes conducted aberrantly. When these sections of tape were excluded, the computer had a less than 2 percent false negative and 3 percent false positive rate of identification of premature ventricular complexes.     

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 transcardiac lead system for identification and termination of supraventricular and ventricular tachycardia

The value of a transcardiac lead system (coronary sinus to right ventricular apex) to record atrial and ventricular electrical activity and its pacing capabilities was assessed in 20 patients with a variety of tachycardias (atrial tachycardia in 3 patients, atrial flutter in 4, intranodal tachycardia in 6, circus movement tachycardia using an accessory pathway in 1 patient, and ventricular tachycardia in 9). The transcardiac lead invariably showed both atrial and ventricular electrical activity during sinus rhythm and tachycardias, allowing application of the same criteria as used when analyzing cardiac rhythm on the surface electrocardiogram. Atrial complexes had a mean amplitude of 4.2 mV during sinus rhythm and varied from 3.0 to 4.1 mV during the different types of tachycardia. Ventricular complexes had a mean amplitude of 9.8 mV during sinus rhythm, 13.8 mV during supraventricular tachycardia and 16.1 mV during ventricular tachycardia. The duration of the QRS complex on the transcardiac lead was equal to the duration of the QRS complex on the surface electrocardiogram during tachycardias with a small or wide QRS complex. By varying the intensity of current delivered through the transcardiac lead, only right ventricular pacing (mean current intensity 1.2 +/- 0.4 mA) or simultaneous atrioventricular pacing (mean current intensity 4.7 +/- 3.3 mA) could be achieved. Termination of all episodes of tachycardia was achieved with either ventricular pacing or simultaneous atrioventricular pacing. This transcardiac lead system allows clear identification of atrial and ventricular events, is suitable for tachycardia analysis using simple surface electrocardiographic algorithms and allows pacing termination of a variety of tachycardias.     

Intravenous adenosine triphosphate during wide QRS complex tachycardia: safety, therapeutic efficacy, and diagnostic utility

PURPOSE: Inappropriate administration of intravenous verapamil to patients with wide QRS complex tachycardia due to ventricular tachycardia or atrial fibrillation with Wolff-Parkinson-White syndrome occurs frequently because of misdiagnosis, and may precipitate a cardiac arrest. We evaluated the safety and the diagnostic and therapeutic utility of adenosine triphosphate administered to a consecutive series of 34 patients during wide QRS complex tachycardia due to a variety of mechanisms. PATIENTS AND METHODS: Patients who had a hemodynamically and electrically stable, monomorphic, wide (greater than 120 msec) QRS complex tachycardia induced during an invasive cardiac electrophysiologic test were studied. Hemodynamic stability was defined by a systolic blood pressure greater than 80 mm Hg and no clinical evidence of cerebral or myocardial ischemia. Adenosine triphosphate, 20 mg, was administered as a rapid intravenous bolus via a peripheral vein during wide QRS complex tachycardia. Five surface electrocardiogram leads, at least three intracardiac electrograms, and blood pressure were monitored. RESULTS: Ventricular tachycardia was present in 14 patients (mean age 50.6 +/- 19 years, cycle length 326 +/- 67 msec) and adenosine triphosphate terminated the arrhythmia in one case. Ventricular tachycardia cycle length did not change. Among 10 patients with supraventricular tachycardia with mechanisms not involving the AV node (average ventricular cycle length 346 +/- 82 msec), one case of ectopic atrial tachycardia was terminated. The ventricular rate was transiently increased in patients with Wolff-Parkinson-White syndrome and atrial fibrillation (average R-R interval 351 +/- 84 msec in control and 317 +/- 82 msec after adenosine triphosphate, p less than 0.001). Reentrant tachycardias involving the AV node (cycle length 302 +/- 52 msec) terminated in seven of 10 patients. The drug was well tolerated, and no patient developed hemodynamic compromise necessitating cardioversion as a result of adenosine triphosphate. CONCLUSION: In the setting of electrophysiology testing, adenosine triphosphate is a safe agent, even when administered inappropriately during arrhythmias for which it is relatively ineffective, such as ventricular tachycardia, and Wolff-Parkinson-White syndrome with atrial fibrillation. It is an effective agent in terminating supraventricular tachycardia involving the AV node. Tachycardia termination following adenosine triphosphate, when used as a diagnostic test to indicate obligatory participation of the AV node, had a sensitivity of 70%, specificity of 92%, and a positive predictive accuracy of 85%. Thus, adenosine triphosphate also has diagnostic utility, but should be used after the appropriate arrhythmia diagnosis has been made based on the clinical history and analysis of the 12-lead electrocardiogram.     

Akuttherapie lebensbedrohlicher tachykarder Rhythmusstörungen

Life-threatening supraventricular tachyarrhythmias include atrial fibrillation, atrial flutter, AV-nodal reentrant tachycardia with rapid ventricular response and preexcitation syndromes combined with atrial fibrillation. Ventricular tachyarrhythmias still remain one of the leading causes of death; these arrhythmias include monomorphic and polymorphic ventricular tachycardia, torsade de pointes tachycardia, ventricular fibrillation and ventricular flutter. In all patients with tachycardias, an attempt should be made to differentiate between narrow (QRS duration < 0.12 s) or wide QRS complex (QRS duration ≥ 0.12 s) tachycardias. In the assessment of patients (pts) with supraventricular/ventricular tachyarrhythmias, attention should be given to identify whether the tachycardia is associated with worsening angina or low cardiac output. In pts with narrow QRS complex tachycardias or pts with atrial fibrillation and preexcitation syndromes immediate synchronized cardioversion should be performed if signs or symptoms of instability (hypotension, evidence of end-organ dysfunction, worsening angina) exist. In pts with a stable hemodynamic situation, vagal maneuvers, adenosine or calcium channel blockers can be used. Management of atrial flutter usually centers on cardioversion or rapid atrial pacing to normal sinus rhythm. In the treatment of patients with deemed unstable ventricular tachycardia (VT), electrical cardioversion is the treatment of choice. In more stable patients, ajmaline is the preferred agent after myocardial infarction and lidocaine if myocardial ischemia is present. In pts with torsade de pointes tachycardias aggressive steps must be taken to prevent degeneration of this rhythm to ventricular fibrillation (VF). Magnesium sulfate has recently been demonstrated efficacious and is currently considered first-line drug therapy. Transcutaneous overdrive pacing should be attempted if magnesium is unsuccessful. The pt with pulseless VT or VF demands early electrical countershock.     

Precipitation of cardiac arrest by verapamil in patients with Wolff-Parkinson-White syndrome

After the administration of verapamil for rapid tachycardias, five patients developed ventricular fibrillation or required urgent cardioversion. All episodes occurred in hospital emergency rooms, and each patient was resuscitated. Examination of electrocardiograms confirmed the presence of the Wolff-Parkinson-White syndrome. In four patients, the presenting tachyarrhythmia was atrial fibrillation with preexcited ventricular complexes, and in one patient a narrow QRS complex tachycardia was initially recorded. Acceleration of atrioventricular conduction occurred within 10 minutes of administration of verapamil, 5 to 10 mg intravenously. Subsequently, intracardiac electrophysiologic studies confirmed the presence of accessory atrioventricular pathways capable of rapid antegrade conduction in each patient. Because of this potentially fatal adverse response, verapamil should not be used in patients with atrial fibrillation and preexcited ventricular complexes.     

Atrioventricular nodal re-entrant tachycardia with QRS voltage and cycle length alternation and aberrant conduction due to two distinct antegrade slow pathways.

QRS voltage and cycle length alternation can be seen during supraventricular re-entrant tachycardias, especially in atrioventricular (AV) re-entrant tachycardia. We present a case of a 20-year-old man, in which AV nodal re-entrant tachycardia (AVNRT) shows alternation of QRS voltage and cycle length, as well as right bundle branch block aberration due to a re-entrant circuit using two distinct, beat-to-beat alternating slow AV nodal pathways antegradely and a single fast pathway retrogradely. Although more than one antegrade slow pathway exists, creation of a single lesion at the right posterior atrial septum using the conventional right-sided approach successfully eliminated AVNRT.     

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.