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At least 19 recordsLinked to original sources
PubMed1999

Tachycardia induced tachycardia: case report of right ventricular outflow tract tachycardia and AV nodal reentrant tachycardia.

Tachycardia induced tachycardia, or so called double tachycardia, is rare. A 34 year old woman is described who had a history of syncope, frequent extrasystoles, and episodes of non-sustained ventricular tachycardia, perceived as palpitation, without syncope. At electrophysiological study, during infusion of isoprenaline, an episode of non-sustained ventricular tachycardia arising from the right ventricular outflow tract initiated sustained atrioventricular nodal reentrant tachycardia, thought to be the cause of the patient's syncope. Ablation of the right ventricular outflow tract focus abolished the ventricular ectopy; the slow AV nodal pathway was also ablated. The patient no longer has either syncope or palpitation.

Adult↗
PubMed1996

Comparison of the ages of tachycardia onset in patients with atrioventricular nodal reentrant tachycardia and accessory pathway-mediated tachycardia.

Atrioventricular nodal reentrant tachycardia and accessory pathway-mediated tachycardia may have different ages of tachycardia onset. Symptom onset data were obtained in 519 patients (atrioventricular nodal reentrant tachycardia, 231, accessory pathway-mediated tachycardia, 288). The mean age of the patients at the time of evaluation was 47 +/- 17 years (atrioventricular nodal reentrant tachycardia) and 37 +/- 15 years (accessory pathway-mediated tachycardia). The mean age of symptom onset was 32 +/- 18 years for atrioventricular nodal reentrant tachycardia and 23 +/- 14 years for accessory pathway-mediated tachycardia. A significantly greater proportion of patients with atrioventricular nodal reentrant tachycardia had the initial onset of symptoms after the age of 20 years (atrioventricular nodal reentrant tachycardia, 67% vs accessory pathway-mediated tachycardia, 41%, p < 0.001). In summary, there is a different mean age of symptom onset for patients with atrioventricular nodal reentrant tachycardia and accessory pathway-mediated tachycardia.

Adult↗
PubMed1983

Maximal rate of tachycardia development: sinus tachycardia with sudden exercise vs. spontaneous ventricular tachycardia.

In addition to providing basic physiologic information, knowledge of the maximal rate of sinus tachycardia development may be helpful in developing algorithms permitting new generations of antitachycardia pacemakers to distinguish accurately between sinus and ventricular tachycardia. To determine the maximal rate of sinus tachycardia development, 50 normal subjects rushed up 100 stairs as rapidly as possible, with continuous electrocardiographic monitoring. During the first second of exercise, the mean cardiac cycle length shortened from 709 to 570 ms, equivalent to an increase in heart rate from 85 to 105 beats per minute, or 20 beats per minute per second. Thereafter, a more gradual decrease in cycle length occurred. Differences between men and women, smokers and non-smokers, and sedentary compared to active subjects were all insignificant. Analysis of 50 spontaneous episodes of ventricular tachycardia also revealed a sequential but more abrupt decrease in the cycle length during the first second from 757 to 360 ms, equivalent to a rate increase from 79 to 167 beats per minute, or 88 beats per minute per second. After approximately 1 1/4 seconds, the ventricular tachycardia cycle length remained virtually constant. Baseline cycle lengths were similar in the sinus and ventricular tachycardia groups, but differed in all subsequent beats, although overlap for individual subjects did occur.

Adolescent↗
PubMed1982

Drug conversion of nonsustained ventricular tachycardia to sustained ventricular tachycardia during serial electrophysiologic studies: identification of drugs that exacerbate tachycardia and potential mechanisms.

Eleven of 83 patients who had ventricular tachycardia (VT) and underwent serial electrophysiologic study (EPS) had a more severe VT induced while receiving a particular antiarrhythmic drug as compared to control study. For all patients only nonsustained VT was initiated during control study, while sustained VT occurred during drug testing with disopyramide (2 patients), quinidine (2 patients), amiodarone (4 patients), and encainide (7 patients), although spontaneous arrhythmias appeared well-controlled prior to repeat testing. Pacing techniques used to induce sustained VT were the same as those used in the control study in eight patients and "less aggressive" in three patients. Almost all episodes of sustained VT resulted in substantial hypotension, especially in patients who were taking encainide. Drugs associated with sustained VT increased the median tachycardia cycle length by 112 msec (p less than 0.005) but increased the median ventricular effective refractory period by only 30 msec (p less than 0.02). Assuming re-entry was responsible for VT, we postulate that drugs facilitated initiation of sustained VT by prolonging activation time but only minimally increasing refractoriness of the tachycardia circuit.

Adult↗
PubMed1990

[Induction of supraventricular tachycardia (paroxysmal junctional tachycardia and atrial tachycardia) by esophageal stimulation].

Transesophageal stimulation is tending to replace endocavitary electrophysiological studies in the investigation and treatment of supraventricular tachyarrhythmias. The aim of this study was to determine the sensitivity of this technique in the evaluation of paroxysmal junctional tachycardia (PJT) and atrial tachycardia (AT). Fifty-eight patients with these arrhythmias (PJT, n = 23; AT, n = 35) were investigated under basal conditions and then during Isoproterenol infusions with a protocol using incremental atrial stimulation and programmed atrial stimulation delivering one and two extra-stimuli on two paced rhythms (400-600 ms). It was possible to induce the arrhythmia in the 23 patients with PJT either under basal conditions (n = 16) or during Isoproterenol (n = 7). A reentrant mechanism was suggested in 22 patients by the following findings: position of the auriculogramme with respect to the ventriculogramme, presence or absence of a delaying branch block, situation and morphology of the P wave in lead V1 compared with atrial activation recorded by the esophageal catheter. Atrial tachycardia was induced in 26 patients (74 per cent), 19 under basal conditions, 6 with Isoproterenol and once after carotid sinus massage. As a conclusion, we can say that the sensitivity of transesophageal stimulation is the same as for endocavitary stimulation.

Adolescent↗
PubMed2003

Radiofrequency ablation of probable atrioventricular nodal reentrant tachycardia in children with documented supraventricular tachycardia without inducible tachycardia.

The reproducible induction of supraventricular tachycardia (SVT) during electrophysiological study is critical for the diagnosis of atrioventricular nodal reentry tachycardia (AVNRT), and for determining a therapeutic endpoint for catheter ablation. In the sedated state, there are patients with reentry SVT due to AVNRT who are not inducible at electrophysiological study. This article reports on the empiric slow pathway modification for AVNRT in six pediatric patients (age 6-17, mean 13.3 years) with documented, recurrent, paroxysmal SVT in the setting of a structurally normal heart who were not inducible at electrophysiological study. Atrial and ventricular burst and extrastimulus pacing at multiple drive cycle lengths were performed in the baseline state, during an isuprel infusion, and during isuprel elimination. Single AV nodal (AVN) echo beats were present in all patients, while classic dual AVN physiology was present in three of six patients. Radiofrequency energy was administered in the right posteroseptal AV groove resulting in accelerated junctional rhythm in five of six patients. Postablation testing demonstrated the elimination of echo beats in four patients, while dual AVN physiology and echo beats persisted in two patients. At follow-up (22-49 months, mean 29.5 months), all patients are asymptomatic without recurrence of SVT and are not taking any antiarrhythmic medication. In selected patients, empiric slow pathway modification may be offered as a potential cure in children with recurrent paroxysmal SVT who are not inducible at electrophysiological study. Elimination of slow pathway conduction may serve as a surrogate endpoint, though is not necessary for long-term success.

Adolescent↗
PubMed1981

Observations on mechanisms of circus movement tachycardia in the Wolff-Parkinson-White syndrome. Role of different tachycardia circuits and sites of block in maintenance of tachycardia.

Different mechanisms of block of impulse propagation in several re-entrant circuits resulted in a major discordance between the "echo-zone" and the "tachycardia-zone" in a patient with intermittent Wolff-Parkinson-White syndrome, dual atrioventricular nodal pathways, and bundle branch re-entry. This case illustrates the delicate balance in electrophysiological properties required between the tissues incorporated in a re-entrant circuit to initiate and sustain the arrhythmia. It also shows how the presence of several reentrant pathways can lead to refractoriness in the circuit responsible for the circus movement tachycardia.

Atrioventricular Node↗
PubMed1995

Evaluation of new self-learning techniques for the generation of criteria for differentiation of wide-QRS tachycardia in supraventricular tachycardia and ventricular tachycardia.

This study presents a comparison of three different methods for differentiating between supraventricular and ventricular tachycardias with wide-QRS complex. One set of criteria, derived using classical statistical techniques, was compared with two new self-learning computer techniques: the artificial neural networks and the induction algorithm approach. By analyzing the results obtained in an independent test set, using these new techniques, the criteria defined by the classical method could be improved.

Algorithms↗
PubMed1999

Prevalence, therapeutic response, and outcome of ventricular tachycardia in the out-of-hospital setting: a comparison of monomorphic ventricular tachycardia, polymorphic ventricular tachycardia, and torsades de pointes.

OBJECTIVE: To investigate out-of-hospital ventricular tachycardia (VT) cardiac arrest patients, comparing the prevalences and outcomes of the following VT subtypes among this population: monomorphic VT (MVT), polymorphic VT (PVT), and torsades de pointes (TdP, PVT with a prolonged QT interval). METHODS: This was a retrospective review from a fire department-based paramedic system of nontraumatic VT cardiac arrest patients (January 1991 to December 1994) with a supraventricular perfusing rhythm (SVPR) at some time during out-of-hospital care, with a measurable QT interval. QT interval was measured from an SVPR, and corrected QT interval (QTc) was calculated and considered prolonged if > 0.45 sec. VT was classified as polymorphic or monomorphic. TdP was defined as PVT with a prolonged QT interval. RESULTS: 196 patients were identified; six were excluded due to incomplete medical records, leaving 190 who met inclusion criteria and were used for data analysis. 117 (62%) patients had MVT, while 73 (38%) patients had PVT; of the 73 patients with PVT, 37 (51%) had normal QTc (non-TdP PVT) and 36 (49%) had prolonged QTc (TdP PVT). 97 (51%) patients had prolonged QTc (PQTc). Regardless of VT type (i.e., MVT vs PVT), 97 (51%) patients had prolonged QTc, with a mean QTc of 0.476+/-0.15 seconds prearrest and 0.464+/-12 seconds postarrest. Patients with PQTc were not more likely to have PVT (70 [37%] vs 76 [40%]; p = 0.705). No significant difference with respect to paramedic-witnessed arrests in each VT morphology group and each QT group was found. The overall hospital discharge rate was 28.4%. Regardless of VT type, patients had similar rates of out-of-hospital return of spontaneous circulation (ROSC) and hospital discharge; patients with PQTc were less likely to be discharged from the hospital (19.6% vs 37.6%; p = 0.01). 27.8% of TdP and 26.8% of non-TdP patients were discharged (p = 0.912). CONCLUSIONS: In this population of out-of-hospital VT arrest patients, MVT is the most common form of VT encountered; PVT and the subtype TdP are also seen in this population with approximately equal frequencies. All three rhythm types demonstrate similar responses to standard Advanced Cardiac Life Support therapy with equal rates of out-of-hospital ROSC and hospital discharge. PQTc may be a marker of poor clinical outcome in patients with out-of-hospital VT arrest.

Aged↗
PubMed1993

The response of paroxysmal supraventricular tachycardia to overdrive atrial and ventricular pacing: can it help determine the tachycardia mechanism?

INTRODUCTION: Standard electrophysiologic techniques generally allow discrimination among mechanisms of paroxysmal supraventricular tachycardia. The purpose of this study was to determine whether the response of paroxysmal supraventricular tachycardia to atrial and ventricular overdrive pacing can help determine the tachycardia mechanism. METHODS AND RESULTS: Fifty-three patients with paroxysmal supraventricular tachycardia were studied. Twenty-two patients had the typical form of atrioventricular (AV) junctional (nodal) reentry, 18 patients had orthodromic AV reentrant tachycardia, 10 patients had atrial tachycardia, and 3 patients had the atypical form of AV nodal reentrant tachycardia. After paroxysmal supraventricular tachycardia was induced, 15-beat trains were introduced in the high right atrium and right ventricular apex sequentially with cycle lengths beginning 10 msec shorter than the spontaneous tachycardia cycle length. The pacing cycle length was shortened in successive trains until a cycle of 200 msec was reached or until tachycardia was terminated. Several responses of paroxysmal supraventricular tachycardia to overdrive pacing were useful in distinguishing atrial tachycardia from other mechanisms of paroxysmal supraventricular tachycardia. During decremental atrial overdrive pacing, the curve relating the pacing cycle length to the VA interval on the first beat following the cessation of atrial pacing was flat or upsloping in patients with AV junctional reentry or AV reentrant tachycardia, but variable in patients with atrial tachycardia. AV reentry and AV junctional reentry could always be terminated by overdrive ventricular pacing whereas atrial tachycardia was terminated in only one of ten patients (P < 0.001). The curve relating the ventricular pacing cycle length to the VA interval on the first postpacing beat was flat or upsloping in patients with AV junctional reentry and AV reentry, but variable in patients with atrial tachycardia. The typical form of AV junctional reentry could occasionally be distinguished from other forms of paroxysmal supraventricular tachycardia by the shortening of the AH interval following tachycardia termination during constant rate atrial pacing. CONCLUSIONS: Atrial and ventricular overdrive pacing can rapidly and reliably distinguish atrial tachycardia from other mechanisms of paroxysmal supraventricular tachycardia and occasionally assist in the diagnosis of other tachycardia mechanisms. In particular, the ability to exclude atrial tachycardia as a potential mechanism for paroxysmal supraventricular tachycardia has important implications for the use of catheter ablation techniques to cure paroxysmal supraventricular tachycardia.

Adult↗
PubMed2001

Incidence and clinical significance of inducible atrial tachycardia in patients with atrioventricular nodal reentrant tachycardia.

INTRODUCTION: The purpose of this prospective study was to determine the prevalence and clinical significance of inducible atrial tachycardia in patients undergoing slow pathway ablation for AV nodal reentrant tachycardia who did not have clinically documented episodes of atrial tachycardia. METHODS AND RESULTS: Twenty-seven (15%) of 176 consecutive patients who underwent slow pathway ablation for AV nodal reentrant tachycardia were found to have inducible atrial tachycardia with a mean cycle length of 351+/-95 msec. The atrial tachycardia was sustained in 7 (26%) of 27 patients and was isoproterenol dependent in 20 patients (74%). The atrial tachycardia was not ablated or treated with medications, and the patients were followed for 9.7+/-5.8 months. Six (22%) of the 27 patients experienced recurrent palpitations during follow-up. In one patient each, the palpitations were found to be due to sustained atrial tachycardia, nonsustained atrial tachycardia, recurrence of AV nodal reentrant tachycardia, paroxysmal atrial fibrillation, sinus tachycardia, and frequent atrial premature depolarizations. Thus, only 2 (7%) of 27 patients with inducible atrial tachycardia later developed symptoms attributable to atrial tachycardia. CONCLUSION: Atrial tachycardia may be induced by atrial pacing in 15% of patients with AV nodal reentrant tachycardia. Because the vast majority of patients do not experience symptomatic atrial tachycardia during follow-up, treatment for atrial tachycardia should be deferred and limited to the occasional patient who later develops symptomatic atrial tachycardia.

Adult↗
PubMed1997

Successful radiofrequency ablation of idiopathic left ventricular tachycardia at a site away from the tachycardia exit.

OBJECTIVES: This study sought to assess the possibility of ablating verapamil-responsive idiopathic left ventricular tachycardia at a site distant from the tachycardia exit and thus to define the tachycardia circuit. BACKGROUND: The nature of the reentry circuit in idiopathic left ventricular tachycardia is unclear. If the circuit is of considerable size, then it should be possible to ablate the tachycardia at a site distant from the exit site. METHODS: Electrophysiologic studies and radiofrequency ablation were performed in 27 consecutive patients with verapamil-responsive idiopathic left ventricular tachycardia. In all 27 patients, the tachycardia exit site was defined as the site where the earliest Purkinje potential was recorded > or = 25 ms before the onset of the QRS complex during the tachycardia and where the pace map QRS complex resembled that during the tachycardia. A potential ablation site other than the exit site was then sought around the midseptum, proximal to the exit site. At such sites the tachycardia could be terminated transiently by pressure applied to the catheter tip, without induction of ventricular ectopic beats. RESULTS: The potential ablation site, other than the tachycardia exit site, was identified in seven male patients (mean [+/-SD] age 31 +/- 12 years, range 13 to 52). Application of the radiofrequency current at this site resulted in termination of the tachycardia within 1 to 5 s (mean 2.9 +/- 1.6), and successful ablation of the tachycardia was achieved in all seven patients (success rate 100%, 95% exact confidence interval 0.5898 to 1). The mean distance between the ablation site and the tachycardia exit site was 3.1 +/- 0.7 cm (range 2.0 to 4.0). A presystolic Purkinje spike was recorded 14 +/- 5 ms (range 8 to 20) before the onset of the QRS complex during the tachycardia. During the follow-up period of 24 +/- 11 months (range 12 to 39), there was no recurrence of tachycardia in these seven patients. CONCLUSIONS: Successful ablation of idiopathic left ventricular tachycardia can be achieved at sites away from the tachycardia exit site in some patients. This finding suggests that the reentry circuit is likely to be of considerable size, encompassing the middle, inferior and lower aspects of the left interventricular septum.

Action Potentials↗
PubMed1996

Value of analysis of ST segment changes during tachycardia in determining type of narrow QRS complex tachycardia.

OBJECTIVES: Repolarization changes during narrow QRS complex tachycardia were analyzed to differentiate the tachycardia mechanism and to guide the preliminary location of the accessory pathway. BACKGROUND: Noninvasive determination of the mechanism of tachycardia is becoming increasingly important in view of the role of catheter ablation techniques for the cure of supraventricular tachycardia. METHODS: We analyzed 159 12-lead electrocardiograms during narrow QRS complex tachycardia to evaluate 1) the tachycardia cycle; and 2) ST segment depression or T wave inversion, or both. Each patient underwent a complete electrophysiologic evaluation. RESULTS: There were 13 atrial tachycardias, 57 atrioventricular (AV) node reentrant tachycardias and 89 AV reciprocating tachycardias. The mean RR cycle did not differ among types of tachycardia. ST segment depression >2 mm or T wave inversion, or both, was present more often in AV reciprocating tachycardia (57%) than in AV node tachycardia (25%). The magnitude of ST segment depression was greater in AV reciprocating tachycardia than in AV node tachycardia (mean +/- SD 1.3 +/- 1.6 vs. 0.7 +/- 0.8 mm, p < 0.005). In AV reciprocating tachycardia distinct patterns of repolarization changes and P wave configuration were associated with different sites of the accessory pathway. CONCLUSIONS: The presence of ST segment depression >2 mm or T wave inversion, or both, during narrow QRS complex tachycardia suggests that AV reentry using an accessory pathway is the mechanism of the tachycardia. The phenomenon may be the consequence of a distinct pattern of retrograde atrial activation. Analysis of repolarization changes can guide preliminary localization of the accessory pathway even in the absence of ventricular preexcitation.

Adolescent↗
PubMed1997

Effects of almokalant, a class III antiarrhythmic agent, on supraventricular, reentrant tachycardias. Almokalant Paroxysmal Supraventricular Tachycardia Study Group.

The aim of the present study was to investigate the effects of almokalant on sustained reentrant supraventricular tachycardias. Reentrant tachycardias were induced, using transesophageal atrial stimulation, in 82 patients with atrioventricular reentrant tachycardia (n = 54) or AV nodal reentrant tachycardia (n = 28). After a baseline procedure during which the tachycardia was induced and overdrive terminated, the tachycardia was reinduced and studied during 12 minutes of infusion of either placebo or almokalant, aiming at plasma concentrations of 20, 50, 100, and 150 nmol/l. Each patient was studied at two dose levels during the same procedure. There was an increase in the RR interval during tachycardia of 6% at 100 nmol/l (p = 0.001 vs. baseline tachycardia). The QT interval during tachycardia increased by 5% (p = 0.001) at 50 nmol/l and by 10% (p = 0.001) at 100 nmol/l. Bundle branch block during tachycardia developed in 13% during almokalant infusion, aiming at 20 nmol/l, in 25% at 50 nmol/l, in 50% at 100 nmol/l, and in 33% at 150 nmol/l. Rapid baseline tachycardia, increasing almokalant dose, and an increasing number of induced tachycardias correlated with the appearance of bundle branch block. In six patients with AV nodal reentrant tachycardia, 2:1 AV block occurred, in all cases preceded by bundle branch block. The QT prolongation during sustained tachycardia was larger in patients who were noninducible at the same plasma concentration level than in the inducible patients. Almokalant caused bundle branch block and 2:1 AV block during sustained supraventricular tachycardia. These findings emphasize the importance of studying drug effects at rates in the range of clinical tachycardias that expose the conduction system to the limits of its refractoriness.

Adult↗
PubMed1995

Comparison of atrial-His intervals during tachycardia and atrial pacing in patients with long RP tachycardia.

INTRODUCTION: The purpose of this study is to describe a simple and reliable diagnostic maneuver that allows for the rapid differentiation of atypical AV nodal reentrant tachycardia (AVNRT) from other causes of long RP tachycardia. Long RP tachycardias may be caused by atypical AVNRT, orthodromic reciprocating tachycardia (ORT) involving a slowly conducting retrograde accessory pathway, or atrial tachycardia. The differentiation of atypical AVNRT from ORT or atrial tachycardia may be difficult, especially when the differential diagnosis includes a posteroseptal accessory pathway or an atrial tachycardia arising in the posteroseptal right atrium. METHODS AND RESULTS: Twelve patients with atypical AVNRT, 21 with ORT, and 12 with an atrial tachycardia diagnosed using conventional criteria were enrolled in this study. The atrial-His (AH) interval was measured at the His-bundle position during the tachycardia and during atrial pacing from the high right atrium at the tachycardia cycle length in the setting of sinus rhythm. In patients with atypical AVNRT, the mean AH interval was 69 69 msec +/- 50 msec (+/- SD) longer during high right atrial pacing than during the tachycardia (P < 0.001). In 10 of 12 patients with atypical AVNRT, the AH interval during atrial pacing was more than 40 msec longer than the AH interval measured during the tachycardia. In contrast, in patients with ORT or atrial tachycardia, the differences in AH interval between atrial pacing and tachycardia were never more than 20 and 10 msec, respectively. CONCLUSION: The difference in the AH interval between atrial pacing and the tachycardia allows a simple and rapid means of differentiating atypical AVNRT from other types of long RP tachycardias.

Adult↗
PubMed1992

Syncope associated with supraventricular tachycardia. An expression of tachycardia rate or vasomotor response?

BACKGROUND: Syncope in patients with supraventricular tachycardia has been suggested to be an ominous finding, predictive of rapid rates during tachycardia. METHODS AND RESULTS: To explore the mechanism of syncope during supraventricular tachycardia, tachycardia was induced in the supine position and after passive head-up tilting to 60 degrees in 13 patients with atrioventricular (AV) node reentry, eight patients with AV reentry, and one patient with atrial tachycardia. Tilt testing was also performed in sinus rhythm for 30 minutes (the last 15 minutes with isoproterenol infusion). Mean +/- SEM age was 38 +/- 3 years, and 11 patients had a history of syncope (median number of syncopal episodes, three; range, one to 30). The cycle length of tachycardia when upright was shorter than when supine (297 +/- 9 compared with 357 +/- 10 msec, p less than 0.001), and mean blood pressure fell to a greater extent after the onset of tachycardia (fall in mean blood pressure, 53 +/- 6 compared with 24 +/- 3 mm Hg, p less than 0.001). Mean blood pressure correlated significantly with tachycardia cycle length when supine (r = 0.58, p = 0.005) but not when tilted upright (r = 0.18, p = 0.45). Syncope occurred in seven patients during upright tachycardia. These seven patients had a greater fall in mean blood pressure with upright tachycardia than the 15 patients without syncope (fall in mean blood pressure, 70 +/- 4 compared with 45 +/- 5 mm Hg, p = 0.01), but there was no difference in the tachycardia cycle length (311 +/- 10 compared with 290 +/- 11 msec, p = 0.29). Six of the seven patients with tachycardia-induced syncope also had syncope with tilt testing in sinus rhythm compared with four of the 15 patients without tachycardia-induced syncope (p = 0.02). CONCLUSIONS: These data support the view that syncope during supraventricular tachycardia is related to vasomotor factors and does not predict a more rapid tachycardia rate.

Adult↗
PubMed1994

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 (> or = 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.

Coronary Disease↗