Pedro Brugada

A new approach to the differential diagnosis of a regular tachycardia with a wide QRS complex.

BackgroundIn the differential diagnosis of a tachycardia with a wide QRS complex (.0.12 second) diagnostic mistakes are frequent. Therefore, we investigated the reasons for failure of presently available criteria, and we identified new, simpler criteria and incorporated them in a stepwise approach that provides better sensitivity and specificity for making a correct diagnosis. Methods and ResultsA prospective analysis revealed that current criteria had a poor specificity for the differential diagnosis. The value of four new criteria incorporated in a stepwise approach was prospectively analyzed in a total of 554 tachycardias with a widened QRS complex (384 ventricular and 170 supraventricular). The sensitivity of the four consecutive steps was 0.987, and the specificity was 0.965. ConclusionsCurrent criteria for the differential diagnosis between supraventricular tachycardia with aberrant conduction and ventricular tachycardia are frequently absent or suggest the wrong diagnosis. The absence of an RS complex in all precordial leads is easily recognizable and highly specific for the diagnosis of ventricular tachycardia. When an RS complex is present in one or more precordial leads, an RS interval of more than 100 msec is highly specific for ventricular tachycardia. This new stepwise approach may prevent diagnostic mistakes.

Transcoronary chemical ablation of ventricular tachycardia.

After identification of the artery supplying blood to the arrhythmogenic area, transcoronary chemical ablation of ventricular tachycardia was undertaken in three patients with incessant tachycardia in whom the other therapeutic options had failed. Sterile ethanol (96%) was given at a dose of 1.5 ml in two patients and a total of 6 ml in the third. The arrhythmia was cured in two patients and suppressed during a 1-month period in the third until new collateral blood supply to the arrhythmogenic area developed and ventricular tachycardia recurred. The procedure was then repeated successfully. After administration of ethanol in the high interventricular septum, one patient developed temporary complete atrioventricular block and a pacemaker was implanted. No other complications occurred. We observed that in patients with ventricular tachycardia after myocardial infarction, it is possible to identify and catheterize small coronary arteries responsible for blood supply to the site of origin or pathway of ventricular tachycardia. After careful transcoronary mapping with saline, chemical ablation can prevent further episodes of the arrhythmia in selected patients.

Mechanisms of supraventricular tachycardia

Programmed electrical stimulation of the heart in combination with intracardiac recordings has contributed a wealth of new information on the mechanisms and pathways of supraventricular tachycardia in humans. This knowledge has resulted in better treatment approaches to these patients. Questions still remain, however, about the mechanisms of atrial flutter and fibrillation and of some types of atrial tachycardia. The location of the circuit in paroxysmal atrioventricular nodal tachycardia also continues to puzzle investigators. The use of refined mapping techniques during cardiac surgery should provide answers to these questions in the near future.

Clinical and electrophysiologic characteristics of exercise-related idiopathic ventricular tachycardia

In 37 (70%) of 53 patients with idiopathic ventricular tachycardia (VT), episodes were mainly related to exercise (group 1). These patients were younger (33 +/- 14 vs 44 +/- 18 years, p = 0.015) and more often had dizziness during VT (71 vs 40%, p = 0.003) than the 16 patients in whom VT was not exercise-related (group 2). Patients in group 1 needed cardioversion less often to terminate the arrhythmia (4 (11%) vs 6 (40%), group 2 [p = 0.04]). VT was initiated during exercise testing in 62% of patients in group 1 but in only 1 patient in group 2 (p = 0.0004). Induction of clinical VT during programmed stimulation was observed in a similar percentage in group 1 (49%) and group 2 (50%) patients. Isoproterenol infusion facilitated the induction of VT in 9 of 20 (45%) group 1 and in 2 of 8 (25%) group 2 patients (p = not significant). After a mean follow-up of 2.9 +/- 2.5 years, 8 (22%) group 1 patients and 5 (31%) group 2 had at least 1 episode of symptomatic VT. Only 1 patient died suddenly. Class III drugs were the most useful in preventing recurrences. Beta-blocking agents were of little value in both groups. Patients with VT and a structurally normal heart have a good prognosis despite recurrences of their arrhythmia. The relation of the arrhythmia to exercise has no prognostic implications.

Pacemaker Syndrome with AAI Rate Variable Pacing: Importance of Atrioventricular Conduction Properties, Medication, and Pacemaker Programmability

A patient who received an AAI Activitrax rate variable pacemaker for treatment of symptomatic sinus bradycardia is described, disopyramide prolonged the anterograde effective refractory period of the fast conducting atrioventricular (AV) nodal pathway to such an extent, that conduction switched to the slow AV nodal pathway at low atrial pacing rates. This gave rise to symptoms of the pacemaker syndrome during moderate exercise because the paced atrial event was conducted with a long, spike to Q interval with occurrence of the paced atrial event just after the preceding QRS complex. A change of medication solved this problem. Programming a bipolar electrode configuration avoided sensing of far‐field QRS signals with the associated problems of resetting the basic pacing interval as well as the upper rate interval. AAI rate variable pacing requires careful evaluation of AV conduction properties, AV conduction intervals as well as the influence of medication to be given. The use of multiprogrammable pacemakers with marker channel capability will significantly facilitate the understanding and resolution of anomalous behavior.

The electrocardiographic, clinical, and electrophysiologic spectrum of idiopathic monomorphic ventricular tachycardia

Clinical, ECG, and electrophysiologic data from 47 patients who had episodes of sustained or nonsustained monomorphic VT with no evidence of structural heart disease were reviewed. According to the QRS configuration during tachycardia, four groups were distinguished. Nine patients had a right bundle branch block configuration and superior frontal plane QRS axis (group 1). Nine patients had a right bundle branch block configuration but an intermediate or right QRS axis (group 2). Group 3 consisted of five patients with a left bundle branch block configuration and a left axis deviation, and in group 4 there were 24 patients who had a left bundle branch block configuration with an intermediate or right frontal axis. Patients in group 1 had dizziness during tachycardia less frequently, but they needed cardioversion to terminate their arrhythmias more often. They experienced tachycardia during exercise less often, and tachycardia was not initiated during exercise testing. They had fewer ventricular premature beats according to the Holter recording. During the electrophysiologic study, VT was induced and terminated by pacing more often in this group. Patients with idiopathic VT with a right bundle branch block configuration and a superior axis seem to be a unique group of patients with idiopathic VT, and reentry seems to be the most likely arrhythmia mechanism in this group. The other ECG configurations share the same clinical and electrophysiologic characteristics, which suggest that the underlying arrhythmia mechanism is the same.

On the mechanisms of ventricular tachycardia acceleration during programmed electrical stimulation.

BackgroundThe pathophysiological mechanisms leading to acceleration of ventricular tachycardia (VT) are still unclear. Methods and ResultsHigh-resolution epicardial mapping was used to study the mechanisms of VT acceleration by programmed electrical stimulation (PES) in a model of sustained reentrant VT in Langendorff-perfused rabbit hearts (n =40). Three different mechanisms responsible for acceleration of VT were identified: 1) induction of double-wave reentry (n =6), defined as the occurrence of two successive activation waves circulating in the same direction in the same circuit; 2) change to a functionally determined circuit (n =4), defined as reentry of the impulse around a functional line of block without involvement of a fixed obstacle; and 3) change of the reentrant circuit to reentry within a different, faster anatomic pathway (n =3). Analysis of 81 episodes of sustained monomorphic VT induced by PES in 74 patients with clinically documented sustained VT in the setting of chronic coronary artery disease showed that in 22 episodes VT was suddenly accelerated by PES (mean cycle length, from 345±73 to 277±71 msec, p<0.01). ConclusionsWith the observations made in the experimental model, the following tentative classification of the mechanisms of VT acceleration of the 22 episodes was made: 1) induction of double-wave reentry in two, 2) change to a functionally determined circuit in four, and 3) change to reentry within a faster anatomic circuit in 16. Simple criteria suggest that these mechanisms may apply in the clinical situation.

The activitrax rate responsive pacemaker system

Bipolar Medtronic Activitrax rate responsive pacemakers were implanted in 31 patients for ventricular (28) or atrial (3) pacing. Mean follow-up was 16 months (range 10 to 26). Twenty pacemakers were implanted after catheter ablation of the His bundle, 7 for sick sinus syndrome. 1 for atrioventricular block and 3 for sick sinus syndrome with atrioventricular block. A rate response value was selected that gave a pacing rate of about 100 pulses/min during walking. Of the 31 patients, all had 24-hour ambulatory electrocardiographic monitoring with diary, 11 walked a 20-minute circuit, including a flight of stairs, and 20 had a treadmill exercise test. In 9 patients the pacing rate could be compared with the underlying sinus rate during exercise and was seen to match it very closely. In 12 patients the pacing rate during car driving was found to be similar to the sinus rate of 5 volunteers under similar conditions (mean minimum and maximum rate was 80 and 99 pulses/min, respectively). No pacing-induced arrhythmias were seen during ambulatory electrocardiographic monitoring. At high pacing rates slightly irregular pacing intervals were sometimes observed, which was due to polarization sensing. Sporadically, 1 pacing interval shortened to the upper rate value, because of a known and now resolved timing anomaly. Neither anomaly was of clinical consequence and the first could be resolved by reprogramming.(ABSTRACT TRUNCATED AT 250 WORDS)

Electrophysiology, Mechanisms, Diagnosis, and Treatment of Paroxysmal Recurrent Atrioventricular Nodal Reentrant Tachycardia

In 1967 the technique of programmed electrical stimulation of the heart was introduced in clinical cardiology by the groups of Durrer et al [133D] and Coumel et al [174C]. Using this technique, tachycardias can be initiated in most patients suffering from paroxysmal recurrent supraventricular rachycardia [98W]. In a portion of patients with paroxysmal supraventricular tachycardia, the arrhythmia originates in the atrioventricular (AV) node, and reentry is thought to be the mechanism. This chapter reviews the electrophysiologic characteristics, the diagnosis, and the mechanisms of intranodal rachycardia, based upon knowledge derived from observations made during programmed electrical stimulation of the heart. Using this information, therapeutic consequences will be discussed.

The Role of Triggered Activity in Clinical Arrhythmias

Recent observations in the experimental laboratory have shown that rhythmic activity based upon after-depolarizations reaching threshold can be initiated by pacing techniques. From these observations criteria have been advanced to diagnose arrhythmias based upon this mechanism. To evaluate the value of these criteria for diagnosing triggered activity in patients suffering from tachycardias we looked for their presence in patients with well- proven anatomically determined re-entry. Criteria considered as suggestive for triggered activity could also be observed in patients having a circus- movement using an accessory atrioventricular pathway. It is concluded that they are not reliable to distinguish between triggered activity and re-entry as a mechanism for tachycardias in the intact human heart. If an inverse relation between the prematurity of the tachycardia initiating beat and the interval between this beat to the first tachycardia complex is accepted as an argument against triggered activity, re-entry was the mechanism of tachycardia in 417 out of 425 patients in whom the arrhythmia could reproducibly be induced during programmed stimulation of the heart.