Joep L.R.M. Smeets

Configuration of Unipolar Atrial Electrograms During Electrically Induced Atrial Fibrillation in Humans

BACKGROUND During atrial fibrillation (AF), the atrium is activated by multiple wavelets that continuously change in size and direction. The aim of this study was to correlate the temporal variation in AF electrogram configuration with the varying spatial patterns of activation. METHODS AND RESULTS In a group of 25 Wolff-Parkinson-White patients undergoing cardiac surgery, the free wall of the right atrium was mapped (244 points) during electrically induced AF. The unipolar electrograms recorded during 4 seconds of AF were classified into four categories: (1) single deflections, (2) short-double potentials, (3) long-double potentials, and (4) fragmented potentials. The proportion of these four types of electrograms during AF was as follows: singles, 77 +/- 12%; short-doubles, 7 +/- 3%; long-doubles, 10 +/- 7%; and fragmented, 6 +/- 4%. Electrogram morphology was an indicator for rapid uniform conduction (single potentials; positive predictive value [PPV] of 0.96), collision (short-double potentials; PPV of 0.33), conduction block (long-double potentials; PPV of 0.84), and pivoting points or slow conduction (fragmented potentials; PPV of 0.87). In type I, II, and III AF, the proportion of long-double potentials was 4 +/- 2%, 12 +/- 3%, and 18 +/- 7% (P < .05); the proportion of fragmented complexes was 2 +/- 2%, 6 +/- 3%, and 10 +/- 4% (P < .05), respectively. During electrically induced and self-terminating episodes of AF, no preferential anatomic sites for double or fragmented potentials were found in the right atrium. CONCLUSIONS The morphology of single unipolar electrograms during AF reflects the occurrence of various specific patterns of conduction. This might be used to differentiate between different types of AF and to identify regions with structural conduction disturbances involved in perpetuation of chronic AF.

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.

Comparison of procainamide and lidocaine in terminating sustained monomorphic ventricular tachycardia

Efficacy of procainamide and lidocaine in terminating spontaneous monomorphic ventricular tachycardia (VT) was assessed in a randomized parallel study. Patients with acute myocardial infarction and those with poor hemodynamic tolerance of VT were excluded. Procainamide 10 mg/kg was given intravenously with an injection speed of 100 mg/min, and lidocaine was administered at an intravenous dose of 1.5 mg/kg in 2 minutes. Fourteen patients were randomized to lidocaine and 15 to procainamide. Termination occurred in 3 of 14 patients after lidocaine and in 12 of 15 patients after procainamide (p <0.01). Procainamide stopped 8 of 11 VTs not responding to lidocaine, and lidocaine stopped 1 of 1 not responding to procainamde. Of a total of 41 VT episodes, 4 of 15 responded to lidocaine and 20 of 26 to procainamide (p <0.01). Because of VT recurrences, 16 patients could be studied repeatedly with drugs given in the reversed order. This resulted in a total of 55 trials of 79 drug injections. Lidocaine terminated 6 of 31 VTs and procainamide 38 of 48 (p <0.001). The protocol was stopped in 4 cases because of adverse effects. A comparison of the QRS width and QT interval before and at the end of the injection revealed significant lengthening of these values after procainamide but no change after lidocaine. In conclusion, procainamide is superior to lidocaine in terminating spontaneously occurring monomorphic VT.

Transvenous Cold Mapping and Cryoablation of the AV Node in Dogs: Observations of Chronic Lesions and Comparison to Those Obtained Using Radiofrequency Ablation

Cryoablation of the Proximal AV Node. Introduction: Radiofrequency (RF) is the most commonly used energy source for the treatment of cardiac arrhythmias. Surgical experience has shown that cryoablation also is effective for ablating arrhythmias. The aims of this study were to (I) investigate the feasibility of inducing permanent complete AV block (CAVB). (2) investigate the value of cold mapping to select the cryoablation site to produce permanent CAVB, (3) study the macro‐ and microscopic lesion characteristics 6 weeks later, and (4) compare them to those produced with RF energy.

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.

Isoprenaline and inducibility of atrioventricular nodal re-entrant tachycardia

Objectives To examine the effect of isoprenaline on slow and fast pathway properties and tachycardia initiation. Design Consecutive patients, prospective study. Setting Referral centre for cardiology, academic hospital. Patients 24 patients suffering from common type atrioventricular nodal re-entrant tachycardia (AVNRT). Interventions Programmed electrical stimulation and radiofrequency catheter ablation of the slow pathway. Measurements and main results AVNRT was induced before and after the administration of isoprenaline in nine patients (group 1), before isoprenaline only in five (group 2), and after isoprenaline only in 10 (group 3). The anterograde effective refractory period of the fast pathway was prolonged significantly during isoprenaline administration in group 1 (405 (31) v335 (34) ms, p < 0.001) and shortened in group 2 (308 (57)v 324 (52) ms, p = 0.005). There was also significant shortening in group 3 (346 (85) v 395 (76) ms, p < 0.001). Isoprenaline administration did not result in a significant change of the anterograde effective refractory period of the slow pathway in groups 1 and 3, but eliminated slow pathway conduction in group 2. Isoprenaline significantly shortened the minimal and maximal atrial to His bundle conduction interval recording in response to each extrastimulus of the slow pathway (210 (24)v 267 (25) ms, p < 0.001 and 275 (25) v328 (25) ms, p < 0.001, respectively) in group 1 and significantly prolonged these intervals (331 (34) v 274 (34) ms and 407 (33) v 351 (33) ms, respectively) in group 3. In all groups only minimal changes in the refractory period of the atrium occurred after isoprenaline administration. The effect of isoprenaline was also measured on the ventricular effective refractory period and on the minimal and maximal length of the ventriculoatrial (V2–A2) interval during ventricular pacing. Isoprenaline did not result in a significant change of the ventricular effective refractory period in groups 1 and 2 nor of the shortest and longest V2–A2 interval. In group 3, however, the ventricular effective refractory period and the shortest and longest V2–A2 interval shortened significantly after isoprenaline administration. Conclusions In group 1 isoprenaline did not affect inducibility of AVNRT because it prolonged the fast pathway refractory period without affecting slow pathway conduction. In group 2 isoprenaline shortened the fast pathway refractory period and appeared to abolish slow pathway conduction. Consequencely, isoprenaline prevented induction of AVNRT. In group 3 isoprenaline facilitated induction of AVNRT. This effect seemed primarily to be the result of shortening of retrograde refractoriness of the fast pathway with prolongation of slow pathway anterograde conduction and refractory period.

Beat-to-beat behavior of QT interval during conducted supraventricular rhythm in the normal heart.

To assess beat‐to‐beat behavior of QT interval under different conditions, high resolution recordings and computerized beat‐to‐beat analysis of the electrocardiogram were performed at rest, during recovery after short exercise, and during atrial pacing. Beat‐to‐beat variations of QT interval during sinus rhythm at rest and after short exercise were measured in ten healthy men. In an additional three patients with supraventricular tachycardia, beat‐to‐beat QT changes were studied after abrupt sustained acceleration and deceleration of heart rate by atrial pacing. Beat‐to‐beat changes in RH interval at rest are followed by minimal changes of the QT interval. The measured proportional change of the QT interval compared with the change in HR interval (Δ QT/A BR) was 0.02. This value represents 10% of the value expected for QT changes from Bazetts formula. Following short exercise QT interval did not change for 15 seconds and reached a maximal value 30 seconds later as compared to the RR interval (192 vs 115 sees, P < 0.001). The steady state of the QT interval during sustained atrial pacing was achieved after 132, 135, and 133 seconds for pacing intervals of 600, 500, and 600 msec, respectively. Our data indicate a relatively slow adaptation of the QT interval to changes in heart rate.