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Biomedical subjects

D E Ward

Publications and source records attributed to D E Ward.

At least 145 records · Page 8Linked to original sources
PubMed1989

Paediatric use of flecainide in supraventricular tachycardia: clinical efficacy and pharmacokinetics.

Twenty three children with recurrent supraventricular tachycardia were treated with flecainide. Twenty one of these received intravenous treatment during an attack (2 mg/kg over 10 minutes). The tachycardia was terminated in 17. After an intravenous bolus of flecainide, blood samples were drawn at regular intervals for analysis of flecainide concentration over 48 hours. Pharmacokinetic variables were calculated--median terminal half life 7.5 hours, median volume of distribution 6.2 l/kg, and median plasma clearance 7.2 ml/min/kg. There was a significant correlation between half life and age. Twenty of the children received long term treatment with an oral preparation of flecainide to prevent further attacks. Twelve had no further attacks and 16 were considered to have good control. Two children suffered potentially serious arrhythmogenic effects soon after the start of oral treatment and flecainide had to be stopped. During oral treatment regular blood samples were drawn and plasma concentrations were analysed to assess the therapeutic range. This did not differ substantially from that proposed in adults (400-800 micrograms/l). Eight children were electively withdrawn from oral flecainide to see whether they really needed it. Blood samples for measurement of flecainide concentration were drawn after their last oral dose. Pharmacokinetic variables were calculated: time to maximum concentration 2 hours, median terminal half life 7.9 hours. For the combined data from patients receiving intravenous and oral treatment there was a significant correlation between elimination half life and age. An intravenous dose of 2 mg/kg over at least 10 minutes and an initial oral dose of 6 mg/kg/day in three divided doses is recommended. Treatment should be started in hospital so that children in whom the drug may be arrhythmogenic can be identified and plasma concentrations measured to identify patients in whom lack of efficacy is caused by underdosage.

Administration, Oral↗
PubMed1989

Efficacy and safety of adenosine in the treatment of supraventricular tachycardia in infants and children.

One hundred and seventeen episodes of supraventricular tachycardia in 50 children, including 28 infants, were treated with intravenous adenosine. Adenosine was prepared in a sterile solution of 0.9% saline (1 mg/ml) and given in incremental doses of 0.05 mg/kg every two minutes to a maximum of 0.25 mg/kg. Ninety of the 117 episodes were terminated. This included 88 of the 102 episodes of junctional tachycardia (79 of the 92 episodes of atrioventricular reentry tachycardia, seven of the eight episodes of atrioventricular nodal reentry tachycardia, and both of the episodes of long R-P' tachycardia). Only one of four episodes of His bundle tachycardia and one of the eight episodes of ectopic atrial tachycardia were terminated. None of the three episodes of atrial flutter were terminated. Side effects were frequent but mild and included transient complete atrioventricular block (less than 6 s), sinus bradycardia (less than 40 s), ventricular extrasystoles, flushing, nausea, headache, and respiratory disturbance. Reinitiation (within 5 s) of supraventricular tachycardia occurred in 13 of the terminated episodes. Although reinitiation limited its clinical efficacy in some patients, intravenous adenosine offered a safe and efficient method of rapid termination of most episodes of supraventricular tachycardia and in some cases facilitated diagnosis of the mechanism.

Adenosine↗
PubMed1989

Single-chamber cardiac pacing with two forms of respiration-controlled rate-responsive pacemaker.

Ventilatory changes correlate with the heart rate response during exercise, and such changes have been used to determine an appropriate chronotropic response in the Biorate (RDP3 and MB-1) and Meta pacemakers, both of which use a thoracic impedance measurement principle. Ten patients with the Biorate and 11 patients with the Meta were studied. In both groups, significant rate response and improvement in exercise duration compared with fixed rate ventricular pacing were achieved during symptom-limited treadmill exercise tests, with good correlations between the pacing rate and estimated oxygen consumption. Motion artefacts affected the measured impedance of both pacemakers, with rate response occurring during arm movements in the absence of respiratory activity. This observation suggested that both pacemakers have the potential of activity sensing. The earlier version of the Biorate (RDP3) was limited by myopotential interference, and erosion of the auxiliary lead can be problematic in some patients.

Electrocardiography↗
PubMed1988

Relative efficacy of various physical manoeuvres in the termination of junctional tachycardia.

The ability of four vagotonic physical manoeuvres to terminate paroxysmal junctional tachycardias was tested in 35 patients with inducible and sustained arrhythmia. Each manoeuvre was used up to three times in an attempt to terminate an induced tachycardia and was judged to be effective if it terminated two out of the three induced episodes. The Valsalva manoeuvre in the supine position was effective in 19 (54%), right carotid sinus massage in 6 (17%), left carotid sinus massage in 2 (5%), and the diving reflex in 6 (17%) cases. 4 of the 6 patients who responded to right carotid sinus massage and all patients who responded to the diving reflex also responded to the Valsalva manoeuvre. The Valsalva manoeuvre while standing was effective in 9 (20%) patients only. Patients in whom the manoeuvres terminated the tachycardias were significantly younger than those who did not respond (median age: 30 vs 45 years, p less than 0.01). Physical manoeuvres were much more successful in terminating atrioventricular re-entry tachycardias (19/24) than atrioventricular nodal re-entry tachycardias (3/11, p less than 0.01). Efficacy of the manoeuvres was related to their bradycardic effect in sinus rhythm.

Adolescent↗
PubMed1988

Adenosine in the diagnosis of broad complex tachycardia.

Adenosine, in incremental bolus doses up to 0.25 mg/kg, was given during regular broad complex tachycardia in 26 patients examined in an electrophysiological laboratory. In 8 of 9 cases of broad complex supraventricular tachycardia (SVT) the arrhythmia was terminated, converted into a narrow complex SVT, or atrioventricular block was induced. In all 9 cases of narrow complex SVT, the arrhythmia was stopped, or atrioventricular block was induced. The arrhythmia was stopped in only 1 of 17 cases of ventricular tachycardia. 6 patients with atrial fibrillation and ventricular pre-excitation were given adenosine, with no effect on mean ventricular rate (averaged over 3 s), although a significant, but short-lived, reduction in minimum RR interval was observed (from 242 ms, SD 45, to 217 ms, SD 39). The mean dose of adenosine required to stop the arrhythmia or to induce atrioventricular block in broad complex SVT (0.14 mg/kg, SD 0.04) was higher than in narrow complex SVT (0.11 mg/kg, SD 0.04). No adverse haemodynamic effects were observed in any patient, and large doses were tolerated by the patients with ventricular tachycardia. The data show that adenosine has a useful role in the diagnosis and treatment of regular broad complex tachycardia.

Adenosine↗
PubMed1988

Rate-responsive pacing with a pacemaker that detects respiratory rate (Biorate): clinical advantages and complications.

The respiratory-dependent pacemaker (RDP3 or MB-1, Biorate, Biotec International, S.p.A., Bologna, Italy) detects the respiratory rate by measuring thoracic impedance using a subcutaneous auxiliary lead. The sensed respiratory rate is used to determine the pacing rate response. This pacemaker had been implanted in 9 patients with a mean age of 58 (range 42-69) years. During symptom-limited treadmill exercise, rate-modulated pacing resulted in a significant increase in pacing rate (mean +/- SD, 124 +/- 10 vs. 71 +/- 3 beats/min p less than 0.001) and exercise capacity (343 +/- 147 vs. 463 +/- 120 s, p less than 0.05) compared to those achieved with constant rate ventricular pacing. Brief treadmill exercise tests showed appropriate rate response to increased walking speed and gradient. However, rate response was modified by arm swinging-induced motion artefact which affected the measured "impedance." Complications observed on follow-up included perforation of the auxiliary lead in 2 patients and symptomatic myopotential interference in 3 patients with the RDP3 pacemaker, all of whom required unit replacement. It is concluded that although the respiratory-dependent pacemaker can confer physiological benefit in patients with bradycardia, myopotential interference (largely overcome by the new version MB-1 with programmable sensitivity) and the auxiliary lead can be problematic in some patients.

Adult↗
PubMed1988

A double-blind comparison of felodipine and hydrochlorothiazide added to metoprolol to control hypertension.

Seventy-six uncomplicated hypertensive patients treated in General Practice, whose seated diastolic blood pressure (Phase V) (dBP) remained greater than or equal to 95 mmHg after a minimum of 4 weeks treatment with metoprolol 50 mg b.i.d. as antihypertensive monotherapy, were randomized to receive the selective 'calcium antagonist' felodipine 5 mg b.i.d. or hydrochlorothiazide 12.5 mg b.i.d. in addition to metoprolol 50 mg b.i.d. The trial duration was 8 weeks, the dose of the felodipine or hydrochlorothiazide being doubled after 4 weeks if 'control' of BP (dBP less than 90 mmHg) was not achieved on the initial doses. Over the trial period of 8 weeks, felodipine reduced dBP from 102 to 85 mmHg and hydrochlorothiazide from 101 to 91 mmHg; the dBP reduction in the felodipine group was greater than that in the hydrochlorothiazide group (17 vs 9 mmHg) and the attained dBP lower in the felodipine group. About half of the patients in each group required the higher dose. Both regimes were effective and well tolerated. In the dosages used, felodipine was a slightly more effective antihypertensive drug than hydrochlorothiazide when added to metoprolol. There was no apparent difference in the tolerability of the two regimes.

Adult↗
PubMed1988

Clinical electrophysiologic effects of flecainide acetate.

Flecainide acetate depresses the rate of depolarization of action potential (Vmax), the so-called "membrane stabilizing action." In the intact heart it has a unique profile of substantial effect on conduction with modest effect on refractoriness. After intravenous administration, clinical electrophysiologic studies show that conduction through atrial myocardium, atrioventricular (AV) node, His-Purkinje system, and ventricular myocardium is depressed, the most prominent effect being on the His-Purkinje system. Refractorines of the normal atrial and AV nodal myocardium is not prolonged while that of the ventricular muscle is slightly increased. Atrial fibrillation (60% to 70%), atrial tachycardia (90% to 100%), and nodal and AV tachycardia (80% to 90%) are generally terminated, while flutter is usually slowed, but in a small proportion of patients (10% to 20%) might be terminated by the intravenous use of flecainide acetate. This drug has also been shown to be effective in terminating stable ventricular tachycardia (70%). However, it appears to be slightly less effective in suppressing inducibility of ventricular arrhythmias. Administered orally, flecainide is very effective in decreasing ventricular ectopic activity (80% to 95%) and nonsustained ventricular tachycardia. Thus, flecainide has a wide range of antiarrhythmic properties, making it a useful agent in the management of a variety of supraventricular and ventricular arrhythmias. In a small proportion of patients, however, its use can lead to apparent arrhythmogenic effects, the most dangerous being exacerbation of ventricular tachycardia.

Animals↗
PubMed1988

Hysteresis of the ventricular paced QT interval in response to abrupt changes in pacing rate.

The rate of QT adaptation to abrupt changes in pacing rate was studied in seven patients with newly diagnosed complete heart block with a ventricular escape rate of less than 40 beats.min-1. Their median age was 70 (range 36-84) years, and none was taking any cardioactive medication known to affect the QT interval. From a baseline pacing rate of 50 or 110 beats.min-1 the ventricular rate was increased or decreased to a new level. The time taken for the ventricular paced QT interval to complete 90% of the change secondary to the change in rate was found to be 136(16) s (mean(SEM] when the rate was increasing and 189(25) s when the rate was decreasing (p less than 0.01). This time interval was independent of the magnitude of the rate change and the baseline heart rate from which the change occurred. Furthermore, the time course of QT adaptation was found to be exponential and was characterised by a time constant of 49.1(2.2) s when the rate was increasing and 60.4(2.0) s when the rate was decreasing (p less than 0.01). It is concluded that QT measurements in response to a change in pacing rate should take into account the time dependent nature of QT changes.

Adult↗
PubMed1988

Prolongation of the QT interval as an indicator of risk of a cardiac event.

The thesis (stated or implied) that acquired QT interval (or QTc) prolongation reflects physiological disturbance similar to those found in the congential syndromes has been assumed to be of central importance in many studies of QT prolongation in the clinical setting. There is no evidence to support this assumption. It is suggested that the use of rate correction of the measured QT interval has obscured our understanding of repolarization abnormalities. Although a QT interval corrected for heart rate may reflect a relationship between the duration of repolarization and heart rate in a single value (e.g. QTc) the corrected value clearly embodies complex influences other than those directly due to rate and for which no 'correction' is, as yet, possible.

Arrhythmias, Cardiac↗
PubMed1988

Selective vibration sensing: a new concept for activity-sensing rate-responsive pacing.

A clinically available model of an activity-sensing, rate-responsive pacemaker (Activitrax, Medtronic) utilizes body vibration during exercise as an indicator of the need for a rate increase. Although having the advantage of rapid onset of rate response, this system lacks specificity and the rate response does not closely correlate with the level of exertion. In addition, this pacemaker is susceptible to the effects of extraneous vibration. In this study involving 20 normal subjects fitted with an external Activitrax pacemaker, the rate responses to a variety of exercises were studied and were compared with the corresponding sinus rates. The vibration generated at the level of the pacemaker was also measured by accelerometers in three axes. Only a fair correlation (r = 0.51) was achieved between the pacemaker rate and the sinus rate. The total root mean square value of acceleration in either the anteroposterior or the vertical axes was found to have a better correlation (r = 0.8). As the main accelerations during physical activities were in the lower frequency range (0.1-4 Hz), a low-pass filter was used to reduce the influence of extraneous vibration. Selective sensing of the acceleration level may be usefully implemented in an algorithm for activity pacing.

Adult↗
PubMed1988

Limitations of rate response of an activity-sensing rate-responsive pacemaker to different forms of activity.

The responses of an activity-sensing rate-responsive system (Activitrax) to various forms of physiological activity were assessed in 15 individuals who had this pacemaker. Nine were patients with complete heart block and atrial arrhythmias; their mean age was 60 years (range, 41-85 years). Six were age-matched healthy volunteers who were exercised with an external Activitrax system attached firmly to the chest wall. The pacemaker was programmed to achieve a pacing rate of about 100 bpm at the end of the first stage of the Bruce protocol (pacemaker settings: rate = 70-150 bpm; threshold = low to medium; response = 6-9). In the activity-sensing ventricular pacing mode, all patients achieved a significant increase in treadmill time compared to constant-rate ventricular pacing (mean +/- SD, 8.0 +/- 3.3 vs 5.4 +/- 2.3 minutes; p less than 0.01), with a mean maximum pacing rate of 123 +/- 18 bpm. Jogging in place produced a prompt increase in pacing rate, with the maximum achieved at the end of the exercise. However, physiological activities such as hand-grip, the Valsalva maneuver and standing resulted in only minimal rate response. Pacing rate after ascending 4 flights of stairs was the same as that achieved after descending the same stairs (100 +/- 8 vs 105 +/- 4 bpm; p = 0.1). All 15 subjects were exercised from resting heart rate for 3 minutes on a treadmill at 1.2 mph and 2.5 mph with four gradients at each speed. Although the pacing rate increased with a faster treadmill speed (p less than 0.005), it did not respond appropriately to a change in gradient compared to the sinus rate. We conclude that although activity-sensing rate-responsive pacing gives a prompt increase in pacing rate and improves maximum exercise tolerance, further refinement is necessary because: (1) physiological activities not associated with significant movement are not detected by this pacing system; (2) detection of vibrations as an indicator of activities does not correlate well with the level of exertion.

Adult↗
PubMed1988

Comparative evaluation of chronotropic responses of QT sensing and activity sensing rate responsive pacemakers.

The rate responses of activity sensing (ATS) and QT sensing (QTS) rate responsive pacemakers to different forms and durations of exercises were compared. Nine patients with ATS and five with QTS were studied. All had complete heart block and atrial arrhythmias. At the onset, the pacemakers were programmed to achieve a pacing rate of 100-110 bpm by the end of stage 1 of the Bruce protocol, and to a pacing rate range of 70-150 bpm. With progressive exercise, using a treadmill (Bruce protocol), the maximum pacing rates in the two groups were not significantly different (mean +/- SD: 123 +/- 18 vs 129 +/- 23 bpm, ATS vs QTS). The time taken to return to the baseline pacing rate during recovery was significantly longer with QTS (178 +/- 70 vs 264 +/- 68 s, p less than 0.05). Brief exercise tests on a treadmill were performed for 3 min each with different combinations of treadmill speeds (1.2 and 2.5 mph) and gradients (0, 5, 10 and 15%). In both groups of patients, faster walking speed was associated with a faster pacing rate at each gradient. However, with increasing gradients, at each speed, there was a rise in the maximum pacing rate only in patients with QTS. During brief exercise tests, the maximum rate was achieved by the end of exercise in patients with ATS, but was delayed by 33 +/- 20 s after exercise in patients with QTS.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Rate modulation by arm movements of the respiratory dependent rate responsive pacemaker.

The rate response to arm movements of the respiratory dependent rate responsive pacemaker (RDP3, Biotec) was assessed in four patients implanted with this pacemaker. The pacemaker was implanted in the left prepectoral region and the auxiliary impedance measuring electrode positioned subcutaneously over the right second intercostal space with its tip lateral to the mid-clavicular line. The lower rate of the pacemaker was programmed to 75 bpm. While holding the breath, swinging arm movements (30 times) resulted in rate acceleration. The peak rate was faster when the arm on the side of the auxiliary electrode was swung (mean +/- SEM, 117 +/- 8 compared to 130 +/- 5 bpm, P less than 0.5). The mean rate response of the subjects to brief treadmill exercise (Bruce stage I) performed with both hands holding the support rails, swinging the right arm only, swinging left arm only and swinging both arms were 108, 140, 135 and 128 bpm respectively. Impedance measurement confirmed the significant influence of arm movements on thoracic "impedance" changes, which was mainly caused by electrode motion artifacts affecting the two electrode measuring system. This effect was dependent on the relative positions of the impedance measuring electrodes (i.e., between the pacemaker casing the auxiliary lead). Subsequently the auxiliary lead of the respiratory pacemaker (MB-1, and Biorate) was implanted in the lower part of the chest on the right sternal edge in another patient. Rate acceleration was only observed when the arm on the side of the pacemaker was swung. As arm movements often accompany physical activities, pacing rate can be affected and should be considered when programming this pacemaker.

Arm↗