P. F. H. M. van Dessel

Exercise capacity after His bundle ablation and rate response ventricular pacing for drug refractory chronic atrial fibrillation

OBJECTIVE: To evaluate exercise capacity of patients with chronic atrial fibrillation in whom His bundle ablation followed by ventricular rate response pacing (VVIR) was carried out because of drug refractoriness. DESIGN: Prospective study. PATIENTS: 25 consecutive patients, all with chronic symptomatic drug refractory atrial fibrillation, underwent His bundle ablation. Before this intervention all patients were on antiarrhythmic drugs to attain acceptable heart rate control and to relief symptoms. MAIN OUTCOME MEASURES: Exercise capacity, including measurements of VO2, was examined before and after a mean interval of seven months following His bundle ablation. RESULTS: Exercise capacity after His bundle ablation increased from a mean of 109 (SD 49) W to 118 (46) W (P < 0.002), but VO2 at peak exercise did not change significantly. Maximum exercise capacity was achieved with a significantly lower maximum driven heart rate than the spontaneous heart rate before ablation. CONCLUSIONS: Exercise capacity of patients who underwent His bundle ablation followed by VVIR pacing remained unchanged or improved during a mean follow up of seven months. Larger patient populations with longer follow up are necessary to examine determinants of improved exercise capacity.

Ten Year Follow‐Up After Radiofrequency Catheter Ablation for Atrioventricular Nodal Reentrant Tachycardia in the Early Days Forever Cured, or a Source for New Arrhythmias?

Background: Radiofrequency (RF) catheter ablation is highly effective with a low complication rate. However, lesions created by RF energy are irreversible, inhomogeneous, and therefore potentially proarrhythmic.

Towards a better risk stratification for sudden cardiac death in patients with structural heart disease.

With the introduction of the implantable cardioverter defibrillator (ICD), patients can be protected against sudden cardiac death (SCD) due to ventricular arrhythmia (VA). Guidelines have been drawn up for selecting patients for primary and secondary prophylaxis. However, most ICD recipients today who receive an ICD for primary prevention will not experience a life-threatening VA requiring antitachypacing or shock therapy. Better risk stratification is desirable with efficacy, costs and complication rate in mind. An overview is presented of widely accepted and potentially valuable risk markers and the role they may play in better identifying candidates for ICD therapy. (Neth Heart J 2009;17:101–6.)

Noninvasive detection of epicardial and endocardial activity of the heart

Determining electrical activation of the heart in a noninvasive way is one of the challenges in cardiac electrophysiology. The ECG provides some, but limited information about the electrical status of the heart. This article describes a method to determine both endocardial and epicardial activation of the heart of an individual patient from 64 electrograms recorded from the body surface. Information obtained in this way might be helpful for the treatment of arrhythmias, to assess the effect of drugs on conduction in the heart and to assess electrical stability of the heart.

Localization of late potentials using body surface mapping

Late potentials recorded at the body surface as defined by Simson [1] are assumed to reflect delayed activation in a myocardial substrate. However, in a substantial subset of patients with documented ventricular tachycardia (VT) no late potentials can be detected on the signal averaged ECG (SAECG). Also direct proof of the anatomic correlation between intracardial signals and the surface leads is still lacking. This study aimed to investigate the relation between simultaneously recorded late potentials at multiple sites on the body surface (SABSM) and late/diastolic activation within the heart utilizing a multi-lead endocardial electrode array. Several technical considerations should be accounted for when correlating intracardiac activity with late potentials detected with SABSM. First, it is required that the 3D positions of the electrodes in the heart are known in order to make the spatial correlation. Second, it should be noted that the amplitude of late potentials in averaged signals in any lead will not only be influenced by the size and orientation of the underlying electrical wave front but also by the distance of the source to the electrode. The amplitude of a signal generated by a dipole will diminish rapidly with the distance between source and recording electrode. This means that irrespective of the location of the substrate in the heart the maximum amplitude of late potentials will usually be recorded in the precordial region. To avoid underestimation of the significance of late potentials in other chest areas, a correction for the effect of electrode-source distance is needed. Since the potential measured at the surface is a result of the potential distribution at all points in the heart and a transfer matrix, this transfer matrix should be estimated. The transfer matrix could be computed from volume conductance theory and information derived from MR images. For practical purposes, however, a measure that can be derived from the data itself is preferable.

A nevv method for detecting late potentials using multichannel ECGs

We developed a procedure that is able to detect, quantify and localize late potentials that will also be applicable to patients with abnormally wide QRS complexes.

The use of simultaneous multichannel endocardial and surface electrocardiograms for verification of exit site localization using body surface mapping

Exit sites of monomorphic ventricular tachycardia and focal sites of ventricular extrasystoles can be localized using an endocardial catheter in conjunction with a multichannel surface ECG, in order to find a suitable site for ablation. For this procedure, as well as for the diagnosis of these types of arrhythmia it is desirable to know the relation between surface ECG and site of origin accurately. This knowledge can be provided by endocardial pacing on well-known sites and recording the resulting ECG, but this method is hampered by the low resolution of catheter localization techniques, breathing of the patient, and cardiac motion. By pacing on an endocardial basket catheter, that has 64 electrodes, and simultaneously recording of the endocardial and body-surface leads, we may obtain useful data to establish the relation between pacing site, endocardial activation spreading, and surface ECG. These data can be used to create and verify localization methods for ectopic and paced beats. In this paper, we investigate the stability of basket-paced beats and localization results.

Local Filtered QRS Duration during Sodium-channel Blockade in Brugada Syndrome Patients

The Brugada syndrome is associated with sodium channel dysfunction and the characteristic ST segment elevation is thought to arise from the right ventricle. We hypothesized that sodium channel blockade in Brugada syndrome patients cause more activation delay in leads overlying the right ventricle than in other leads. ECG data were recorded during infusion of a sodium channel blocker in 17 family members of Brugada syndrome patients. Signal averaged and filtered signals from a number of body surface leads were investigate for small potentials that are generated by myocardium close to the recording electrode. ST segment elevation in V1 during sodium channel blockade was accompanied by pronounced activation delay in V1 after the end of the QRS complex in lead II (32±18 ms), whereas activation in V6 was not later than end of QRS (12±13 ms). The latest activation in V1 was delayed to a greater extend than in control patients without ST elevation during sodium channel blockade (151±17 ms vs 128±10 ms, p<0.005). We conclude that the activation of the right ventricle in Brugada syndrome patients is more sensitive to sodium channel blockade compared to the left ventricle and compared to patients without ST segment elevation.