CASE REPORT
Permanent direct His bundle pacing: initial report showing technical feasibility of an
alternative pacing therapy J.H. Geertnan, P.P. Delnoy, H.A Oude Luttikhuis
To prevent deterioration ofleft ventricular function during right ventricular apical pacing, permanent direct His bundle simulation can be considered in selected patients with low left ventricular ejection fraction and a normal His-ventricle conduction time. We describe our first short-term experiences with penmanent direct His bundle pacing in three patients. In two patients His bundle stimulation was still effective at six weeks' follow-up. In one patient loss of capture was registered, after which conventional RV apical pacing was performed. (Neti HeartJ2002;10:79-82.)
Keywords: His bundle, left ventricular function
Since the initial asynchronous right ventricular pacing, enormous progress has been made in optimising the modality of cardiac pacing leading to the physiological dual chamber rate-responsive pacing modes of today. Recent studies show a negative effect on haemodynamics in some patients with right ventricular (RV) apical pacing.1 RV apical pacing causes abnormal and prolonged contraction of the left ventricle2 and results in a negative inotropic effect,3 due to deleterious effects on ventricular synchrony. In addition, sustained RV apical pacing has been associated with structural, histological changes in myocardium.4 In a study of 557 patients with dilated heart failure, the presence of a permanent pacemaker with RV apical pacing was associated with a high risk ofdeath from progressive pump failure.5 His-Purkinje activation of ventricular myocardium causes synchronous activation and contraction ofthe ventricles and preserves left ventricular function. J.H. Geertman. P.P. Delnoy. H.A. Oude Luttlikhuls. Department of Cardiology, Isala Clinics Zwolle, Department of Cardiology, Groot Wezenland 20, 8011 JWZwolle. Address for correspondence: H.A. Oude Luttikhuis. E-mail:
[email protected]
Netherlands Heart Journal, Volume 10, Number 2, February 2002
Therefore, it seems logical to look for a more physiological pacing site in selected patients. Theoretically, in patients with narrow QRS complexes and intact His-ventricle conduction, permanent direct His bundle pacing is the optimal pacing site. Disadvantages are difficulties in positioning, stabilising and fixation of the pacing electrode for permanent pacing. Case 1. An 86-year-old man was admitted to our hospital because of collapses. The patient had no previous cardiac history. He was not on any medication and there was no evidence of myocardial ischaemia. On clinical examination he had a normal blood pressure at 150/70 mmHg, with an irregular pulse of65 bpm. On cardiac auscultation, there was a systolic 3/6 murmur over the aortic valve. No pulmonary crackles were heard. Basic neurological examination showed no abnormalities. Laboratory tests revealed: Hb 8.6 mmol/L, glucose 6.0 mmol/L and potassium 4.4 mmol/L. The ECG showed atrial fibrillation with a slowventricular rate of 50 bpm, QRS width of 110Ims, left axis and premature ventricular depolarisations. On echocardiography, the function of the left ventricle was moderately reduced: there were no signs of dilatation and the left ventricular end-diastolic diameter (LVEDD) was 52 mm. The aortic valve was sclerotic but no stenosis was found. A mitral valve regurgitation grade 1 was seen and a left atrial width of 70 mm was measured in the apical view. We decided to implant a permanent cardiac pacemaker because long RRintervals with atrial fibrillation were the suspected cause of the collapses. A pacing electrode was positioned in the His bundle region in order to preserve a normal ventricular activation.
ImplantatIon procedure Via femoral vein puncture, an EP-mapping catheter was positioned in the His bundle region. Subsequent mapping and localisation of the His bundle was performed in the right anterior oblique projection for an optimal visualisation of the tricuspid annulus. A His bundle electrogram was recorded, showing a Hisventricle conduction time of 60 milliseconds. Success79
Permanent direct His bundle pacing: initial report showing technical feasibility of an altemative pacing therapy
Figure 2. 12-lead ECG during His bundle stimulation.
Figure 1. 12-lead ECG before pacemaker implantation.
fil His bundle capture was defined as His-Purkinje mediated cardiac activation and depolarisation, demonstrated by ECG concordance of QRS and T wave complexes and a His-ventricle interval almost identical to the pace-ventricular interval, without widening of the QRS complexes as a sign of bundle branch conduction. After registration and validation ofthe His bundle by pacing (stimulation voltage twice threshold), the catheter was left in position in order to function as fluoroscopic landmark ofthe His bundle. Under local anaesthesia, the incision was made in the left subclavian region. A bipolar, retractable screw lead (Biotronic Elox 60-BP) was inserted via subclavian puncture, and during fluoroscopy positioned in the His bundle region. A 'J' shaped stylet was used to place
Figure 3a. X-ray in two directions afterpacemaker implantation. 80
the screw lead in the optimal position identified by the mapping catheter. After finding the optimal pacing site and carrying out control registration and unipolar stimulation, the screw was fixated. In this patient the pacing threshold was 1.3 Volt at a pulse width of 0.5 ms and 310 Ohm impedance. The lead was connected to a VVIR generator (Guidant Discovery II SR). After the procedure, a 12-lead surface ECG was taken and QRS complexes were of similar morphology to ECG before pacemaker implant (figures 1 and 2). Six weeks later, a check-up was performed in the outpatient clinic. Stimulation threshold measurement was 1.8 Volt with a pulse width of 1.0 ms and 360 Ohm lead impedance. Fluoroscopic control showed an unchanged and stable lead position (figure 3).
Figure 3b. Netherlands Heart Journal, Volume 10, Number 2, February 2002
Permanent direct His bundle pacing: initial report showing technical feasibility of an alternative pacing therapy
Case 2 An 83-year-old man was admitted to our hospital because of collapses. There was no relevant cardiac history except diabetes and hypertension. At time of admission, the patient was not on antiarrhythmic drugs. Clinical investigation was unremarkable. The ECG showed atrial fibrillation with a ventricular rate of 61 bpm, QRS width of 80 ms and QS complexes in leads II, III and aVF, suggesting prior inferior wall myocardial infarction. During monitoring, the patient collapsed again and at that moment long RR intervals of 26 seconds were registered. A temporary transvenous pacing wire was inserted. After a few days, a permanent pacemaker was inserted. In a procedure as described above, a retractable screw lead (Pacesetter 1388T) was fixated in the His bundle region. The His-ventricle conduction time was 60 ms. Stimulation threshold measurement was 0.7 Volt with 0.5 ms pulse width and 330 Ohm lead impedance. Two days later intermittent loss of capture was registered. We decided to remove the electrode from the His bundle region and convert to conventional RV apical pacing. Case 3 A 75-year-old man was admitted to our hospital because ofdizziness and collapses. He had an extensive cardiac history with an anteroseptal myocardial infarction eight years previously, recurring periods of congestive heart failure, and coronary bypass surgery with aneurysmectomy three years before. During the past two years he had had chronic atrial fibrillation. Medical therapy consisted of digitalis 0.125 mg pd, diuretics, oral nitroglycerin and acenocoumarol, and had not changed during the last weeks before
adcmission. The ECG showed atrial fibrillation with a ventricular rate of 55 bpm, with prolonged QRS duration (130 ms) and LBBB configuration. Echocardiography revealed a poor systolic left ventricular function: the ventricle was moderately dilated with an LVEDD of 68 mm. A grade 2-3/4 mitral valve regurgitation with left atrial enlargement (82x52 mm) was found. In this patient left ventricular pacing was combined with permanent direct His bundle stimulation. During implantation, the left ventricular electrode was positioned in the posterolateral cardiac vein. Implantation ofthe His bundle electrode was performed as described in case 1. His-ventricle conduction time was 57 ms. A retractable screw lead (Pacesetter 1388T) was positioned in the His bundle region. After implantation, the stimulation threshold was 1.2 Volt with 0.5 ms pulse width, and lead impedance of 400 Ohm. At six weeks' follow-up in the outpatients clinic, we measured a threshold of 0.6 Volt with a pulse width 0.4 ms from the His bundle electrode. On fluoroscopy, both leads proved to be in an unchanged position. Netherlands Heart Joumal, Volume 10, Number 2, February 2002
Discussion Transvenous His bundle stimulation was first described in humans in 1970.6 Catheter stability during contraction was of major technical concern. From a theoretical point ofview, permanent direct His bundle pacing is the most physiological method ofventricular stimulation in patients with narrow QRS complexes (
