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R van Mechelen

Publications and source records attributed to R van Mechelen.

17 recordsLinked to original sources
PubMed1992

Apparent P wave undersensing in a DDD pacemaker post exercise.

Wenckebach behavior of DDD pacemakers occurring when the P-P interval varies between the programmed upper rate interval and the total atrial refractory period is symmetrical in a sense that the pacemaker response during atrial rate acceleration is similar to the pacemaker response during atrial rate deceleration. This phenomenon can be observed in all patients with persistent AV block in whom a DDD pacemaker is implanted, during exercise testing when the spontaneous atrial rate exceeds the selected upper rate, i.e., the programmed upper rate interval. However, this phenomenon will not be observed in all patients with intermittent intact AV conduction during exercise. In this case report we describe a patient who showed an asymmetrical response during a bicycle exercise test. There was 1:1 atrial sensing ventricular pacing until the atrial rate exceeded the upper rate of 140 ppm, while atrial sensing was restored during recovery when the conducted sinus rhythm had decreased to 105 beats/min.

Aged↗
PubMed1992

Adaptive rate pacing controlled by the right ventricular preejection interval: clinical experience with a physiological pacing system.

In the Precept pacing system, the right ventricular intracardiac impedance waveform is used to evaluate either of two indicators of metabolic demand relative right ventricular stroke volume and preejection interval (PEI). PEI is known to reliably parallel contractility changes, which is reflective of physical and emotional stress. The stability and dynamic behavior of PEI were tested in ten patients with a Precept pacing system under various forms of exercise and during postural changes. Although significant patient-to-patient variability of the sensor values was observed, reflecting individual physiological differences, the chronic stability of PEI was excellent in the total device experience of 147 months. In all patients, PEI shortened significantly during bicycle ergometry from a mean value of 137.7 +/- 17.8 (range 96-162) to a mean value of 103.0 +/- 21.6 (range 92-109) (P less than 0.05). Low level bicycle exercise of short duration resulted in a prompt decrease in PEI and increase in pacing rate in all patients. There were no uniform postural responses overall, although some posture related rate changes were observed in two patients. We conclude that the first generation of a PEI based pacing system holds promise for adaptive rate pacing.

Aged↗
PubMed1990

The A-R interval as exercise indicator: a new option for rate adaptation in single and dual chamber pacing.

We investigated the possibility to use the interval from an atrial stimulus to the ventricular R wave (A-R interval) as an indicator of physical stress, in 16 patients with pacemakers implanted for severe atrial bradycardia but with intact AV conduction. The A-R interval was studied during incremental atrial pacing at rest and during exercise with a constant workload. In addition, the atrial pacing rate was kept constant just above spontaneous sinus rate and the dynamics of the A-R interval were studied during exercise with a low constant workload and during a maximal exercise test with increasing workload. Incremental atrial pacing prolonged the A-R interval and this response was blunted during exercise (P less than 0.003). Atrial pacing at a constant rate and during a constant workload resulted in an almost direct shortening of the A-R interval. When the workload was increased but the atrial rate kept constant, a pronounced shortening of the A-R interval was noted (P less than 0.0001). It is concluded that changes of the A-R interval during different kinds of exercise were prompt and predictable in patients with sinus node dysfunction but intact AV conduction. In these patients the shortening of the A-R interval during exercise may be a suitable indicator for rate adaptive atrial pacing.

Adult↗
PubMed1989

Hemodynamic effects of pimobendan given orally in congestive heart failure secondary to ischemic or idiopathic dilated cardiomyopathy.

Pimobendan (UD-CG 115 BS) was administered orally to 23 patients with congestive heart failure (functional class IV) caused by coronary artery disease (11 patients) or idiopathic dilated cardiomyopathy (12). All patients received maintenance doses of digoxin, furosemide and warfarin. Baseline data, collected during 15 hours, stayed within a 10% range. A 10-mg oral dose of pimobendan increased the heart rate from 95 +/- 20 to 109 +/- 24 beats/min (p less than 0.003). The pulmonary artery wedge pressure decreased from 23.0 +/- 5.9 to 10.1 +/- 5.2 mm Hg (p less than 0.0001), the cardiac index increased from 1.9 +/- 0.4 to 3.3 +/- 0.7 liters/min/m2 (p less than 0.0001) and the left ventricular stroke work index increased from 2,005 +/- 927 to 3,065 +/- 1,161 ml/mm Hg/m2 (p less than 0.0001). Statistically significant improvements in hemodynamic variables were still present 10 hours after the administration of pimobendan. Most patients felt better and reported no angina or other side effect, the incidence of ventricular arrhythmias was unchanged and no electrocardiographic changes suggesting ischemia were observed. Patients with severe congestive heart failure experienced a prolonged improvement of their cardiovascular condition after a single dose of pimobendan.

Administration, Oral↗
PubMed1988

Differential bipolar sensing of a dual chamber pacemaker.

Differential bipolar sensing was evaluated in 10 consecutive patients with symptomatic heart block managed with dual chamber pacing. During pacemaker implantation atrial and ventricular electrograms were recorded using unipolar (UP) and differential bipolar (DBP) sensing amplifiers. The mean peak-to-peak amplitudes of the UP and DBP atrial electrograms were 3.3 +/- 1.2 mV and 4.2 +/- 1.2 mV, respectively. The difference was statistically significant (p less than 0.05). The mean peak-to-peak amplitudes of the ventricular electrograms were, respectively, 6.8 +/- 1.5 mV and 7.5 +/- 1.4 mV (p less than 0.01). Within 6 weeks after pacemaker implantation, patients visited the outpatient clinic. Isometric exercise tests were performed during UP and DBP sensing of the pacing system. Myopotential sensing in the ventricle occurred in nine patients during UP sensing and in none of the patients during DBP sensing (p less than 0.01) at a sensitivity setting of 0.5 mV. In addition, chest wall stimulation was performed to assess the effects of far-field signals on the ventricular sensing circuit of the pulse generator. Chest wall stimuli inhibited ventricular output during UP sensing in all 10 patients, whereas during DBP sensing inhibition of the ventricular channel occurred in three patients and then only at high output (greater than 8 V) settings. The susceptibility of the pacing system to crosstalk was also determined. However, neither during UP sensing nor during DBP sensing could cross-stimulation or cross-inhibition be demonstrated. In conclusion, DBP sensing is superior to UP sensing in terms of myopotential and far-field sensing.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1986

Prevalence of retrograde conduction in heart block after DDD pacemaker implantation.

Electrophysiologic studies were performed before DDD pacemaker implantation in 50 patients with symptomatic heart block. The patients were separated into 2 groups. Group I consisted of patients with intact retrograde conduction and group II consisted of patients with blocked retrograde conduction. After pacemaker implantation, postventricular atrial refractory periods in patients in group I were programmed at 50 to 100 ms, in excess of the retrograde conduction times measured during electrophysiologic studies. In group II patients, postventricular atrial refractory periods were routinely programmed at 300 ms. During follow-up, patients visited the outpatient clinic at 3-month intervals for noninvasive assessment of the prevalence of retrograde conduction, and to test the inducibility of pacemaker-mediated tachycardias. The mean follow-up of group I (15 patients) was 27 +/- 10 months, whereas the mean follow-up of group II (35 patients) was 19 +/- 9 months. The mean number of noninvasive tests performed during follow-up was 8 +/- 3 per patient for group I and 5 +/- 3 per patient for group II. In group I, retrograde conduction remained intact in 12 patients (p less than 0.01). In 29 of 31 patients in group II, retrograde conduction remained absent (p less than 0.01). In 4 patients in group II, chronic atrial fibrillation occurred during follow-up. Chronic atrial fibrillation did not occur in any patient in group I. During serial electrophysiologic testing, no pacemaker-mediated tachycardias could be induced in any patient in group I or II.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1986

Atrial capture and dual chamber pacing.

During dual chamber pacing it is sometimes impossible to assess atrial capture even on the 12-lead ECG. We developed a strategy to identify atrial capture when it is not possible to do so by ECG, and when the ECG shows no evidence of spontaneous or paced atrial activity.

Atrial Fibrillation↗
PubMed1986

Failure to sense P waves during DDD pacing.

ECG tracings of three patients in whom AV universal (DDD) pacemakers were implanted intermittently demonstrated dropped P waves. In one patient, true atrial undersensing was present; in the others, sensing of the atrial electrode was appropriate, but sensing of sinus P waves was intermittently blocked by normal pacemaker operation. In this report we discuss the electrocardiographic diagnosis of atrial undersensing in order to avoid unnecessary reinterventions.

Aged↗
PubMed1986

Reflex cardiac asystole.

In this report we present the case of a patient with recurrent syncopal episodes. During one of the attacks the patient was monitored by telemetry and the ECG lead showed asystole for more than 7 seconds. As in cases of the cardioinhibitory type of hypersensitive carotid sinus syndrome (HCSS), asystole may represent suppression of the sinus node or suppression of both sinus and atrioventricular (AV) node. Unfortunately, in contrast to HCSS, there is no maneuver that can reproducibly induce episodes of asystole. Consequently, very little is known about the occurrence of AV block in the presence of sinus arrest. In the patient described in this report, we were able to demonstrate that suppression of sinus and AV nodes occurred simultaneously. It is interesting to note that in this type of syncope data from noninvasive and invasive techniques in assessing sinus nodal and AV nodal conduction may not be conclusive. In the group of patients with this type of syncope, permanent atrial demand pacing is contraindicated.

Arrhythmias, Cardiac↗
PubMed1985

Pacemaker electrocardiography of rate smoothing during DDD pacing.

A rate smoothing option is available in a new bipolar AV universal (DDD) pacemaker. In three patients, two with intact retrograde conduction and one with retrograde block, rate smoothing values of 3% and 6% were programmed. Irregular pacemaker-mediated tachycardia occurred in one patient and AV synchrony was temporarily lost in the other two patients. In this report, we describe the pacemaker electrocardiography of rate smoothing during DDD pacing.

Aged↗
PubMed1984

Serial electrophysiologic studies after single chamber atrial pacemaker implantation in patients with symptomatic sinus node dysfunction.

After single chamber atrial pacemaker implantation, serial electrophysiologic studies were performed noninvasively at intervals of 3 months over a total period of 3 years in 24 patients with symptomatic sinus node dysfunction. All patients underwent invasive electrophysiologic studies before pacemaker implantation and demonstrated intact anterograde AV conduction. Patients were divided into 2 groups: group I did not require antiarrhythmic drugs during follow-up whereas group 2 received antiarrhythmic drugs. In group I (11 patients) the atrial paced heart rate producing AV Wenckebach phenomenon (AVWHR) remained stable during a mean follow-up of 22 +/- 10 months; with a variability not exceeding 10 beats min-1 with respect to the initial AVWHR obtained during preoperative electrophysiologic study. In group 2 (13 patients) with a mean follow-up of 15 +/- 8 months a mean decrease of AVWHR of 19.2 +/- 17.5 beats min-1 was present between AVWHR before and 3 months after initiation of oral antiarrhythmic drugs (P less than 0.01). During chronic (greater than 3 months) antiarrhythmic drug therapy the variability of the AVWHR never exceeded 10 beats min-1 with respect to the AVWHR obtained 3 months after the initiation of oral drug therapy. Deterioration of anterograde AV conduction during long-term follow-up of patients with symptomatic sinus node dysfunction and intact anterograde AV conduction at the time of pacemaker implantation is a consequence of orally taken antiarrhythmic drugs, rather than a consequence of degeneration of the AV conducting system.

Aged↗
PubMed1984

Responses of an AV universal (DDD) pulse generator (Cordis 233D) to programmed single ventricular extrastimuli.

To evaluate factors playing a role in initiation and perpetuation of pacemaker-mediated tachycardias (PMTs), 22 consecutive patients with symptomatic conduction disorders were studied after implantation of an AV universal (DDD) pulse generator (Cordis 233D). Patients were divided into two groups, depending upon the presence or absence of ventriculo-atrial (VA) conduction during electrophysiological study (EPS) performed before pacemaker implantation. PMTs could be initiated in six of eight patients of Group I and in none of 14 patients of Group II. Initiation and perpetuation of PMTs during DDD pacing were dependent upon the capacity of the patient to conduct ventricular premature beats (VPBs) and subsequent paced ventricular beats retrogradely to the atria, and upon three programmable parameters of the pulse generator (AV delay period, upper rate limit, tachycardia response). Programmed single ventricular extrastimulation demonstrated that: (1) merely the presence of VA conduction during EPS, although necessary, was not sufficient to induce PMTs after DDD pacemaker implantation; (2) VPBs introduced late rather than early in the cardiac cycle initiated PMTs in a different way; (3) the initiation of PMTs could be prevented during study by adjusting the programmable parameters (AV delay period, upper rate limit, tachycardia response); (4) one of the two available tachycardia responses of the pulse generator (gradual fall-back response) was able to terminate and initiate PMTs consistently. These observations helped in understanding the responses of the Cordis 233D pulse generator to ventricular premature beats. They indicate that additional refinement of the pulse generator is necessary to solve the problem of PMT.

Aged↗
PubMed1983

Atrioventricular and ventriculo-atrial conduction in patients with symptomatic sinus node dysfunction.

In 14 patients with symptomatic sinus node dysfunction--sinus bradycardia, sino-atrial exit block, or sinus arrest--electrophysiological studies were performed before implantation of a pacemaker. In 8 patients incremental high right atrial pacing showed AV-nodal Wenckebach at pacing rates equal to or above 130/min (group I); in 6 patients AV-nodal Wenckebach was reached at pacing rates less than 130/min (group II). During ventricular pacing at a rate 10-15% faster than the existing sinus rate, ventriculo-atrial (VA) conduction was present in all patients of group I, while VA conduction was present in only 2 patients of group II (p less than 0.05). Patients with symptomatic sinus node dysfunction but with intact AV conduction frequently show VA conduction during ventricular pacing and thus are particularly at risk for developing a pacemaker syndrome when a ventricular demand (VVI) pacemaker is implanted. This complication can be avoided by atrial demand (AAI) pacing or AV sequential (DVI) pacing. When adequate experience has been gathered with AV universal (DDD) pacemakers, the indications for selection of a pacemaker in patients with symptomatic sinus node dysfunction will probably change.

Adult↗
PubMed1982

Benefits from adding nifedipine to the treatment of unstable angina when beta-blockade and isosorbide dinitrate have proved inadequate.

Nifedipine (10 mg orally six times daily) was given to patients with unstable angina persisting despite adequate beta-blockade (group I, 35 patients) or despite the association of adequate beta-blockade and sublingual isosorbide dinitrate (group II, 47 patients). Stabilization of anginal symptoms was achieved in 31/35 patients of group I and in 39/47 patients of group II. Aorto-coronary bypass grafting was carried out in 19 patients because of persisting unstable angina (five patients) or because of the severity of residual angina (14 patients). Tolerance to these drug combinations was excellent, with side-effects consisting mainly of transient headache (eight patients) and noncardiac ankle edema (eight patients). Nifedipine was found to be valuable in stabilizing unstable angina persisting despite beta-blockade and nitrates.

Aged↗
PubMed1978

Non-invasive diagnosis of pseudoaneurysm of left ventricle.

A patient free of symptoms, with a pseudoaneurysm of the left ventricle after inferoposterolateral myocardial infarction, is reported. The diagnosis was established by nuclear cardiography and echocardiography of the left ventricle.

Echocardiography↗
PubMedDate not supplied

[Hemodynamic effects of intravenous perfusion of amrinone in increasing doses in 12 patients with severe heart decompensation].

Twelve patients with severe heart failure were given amrinone by intravenous infusion in doses rising from 1 to 2, 3 and 4 mg X min-1, the interval between each dose being 30 min. The total cumulative dose was 300 mg over 120 min. Haemodynamic measurements were started the day before treatment to take into account nycthemeral fluctuations in haemodynamics and the possible effects of maintenance treatments and meals, all factors which might influence the baseline values. When given at a rate of more than 2 mg X min-1, amrinone significantly improved cardiac function (p less than 0.001). The mean pulmonary capillary pressure fell from 24.1 +/- 5.3 to 13.7 +/- 8.6 mmHg, and the cardiac index rose from 1.75 +/- 0.40 to 2.51 +/- 0.32 1 X min-1 X m-2. Heart rate and blood pressure were not significantly modified. No adverse reaction was observed during the infusion and the following 24 hours. Thus, intravenous amrinone proved effective in patients with severe heart failure, with maximal effects being obtained in doses of 3 mg X min-1.

Aged↗