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Biomedical subjects

D E Ward

Publications and source records attributed to D E Ward.

At least 19 recordsLinked to original sources
PubMed1992

Cost implications of the British Pacing and Electrophysiology Group's recommendations for pacing.

OBJECTIVE: To compare present pacing practice with the recommendations recently published by the British Pacing and Electrophysiology Group and to assess the increase in annual budget required to implement these recommendations in a regional cardiothoracic unit. DESIGN: Retrospective analysis of pacemaker implantation for 1991 with calculation of the costs required to implement the group's recommendations based on average 1991 costs of the types of pacing generators and electrode leads used. SETTING: Regional cardiothoracic unit for South West Thames Health Authority. PATIENTS: 433 consecutive patients receiving permanent pacemaker generators: 76 (18%) with sinus node disease; 270 (62%) with atrioventricular block; 25 (6%) with both sinus node disease and atrioventricular block; 59 (14%) with chronic atrial fibrillation and atrioventricular block; and 3 (1%) with carotid sinus or malignant vasovagal syndromes. RESULTS: Only 102 (24%) patients received pacemaker generators recommended by the British Pacing and Electrophysiology Group; however, 355 (82%) patients were older than 65 years, and 264 (61%) were aged 75 or over. The cost of hardware for pacing was 462,885 pounds. Using generators as recommended would have cost 810,525 pounds for "optimal" systems (an increase of 75%) and 710,750 pounds for "alternative" systems (an increase of 54%). These increases would have been considerably reduced by limiting the use of sophisticated pacing to younger patients (aged under 75). Further savings could be made by using the least expensive pacing models available. CONCLUSIONS: Implementing these recommendations should reduce morbidity related to bradyarrhythmia but will lead to major increases in pacing costs. Age and patients' expected activity may be used to select simple pacing systems and thus to contain cost. More research is needed to determine which patient groups will benefit most from complex pacing systems.

Adult↗
PubMed1992

Assessment of QT dispersion in symptomatic patients with congenital long QT syndromes.

It has been suggested that QT dispersion recorded on the surface electrocardiogram may be a predictor of arrhythmic events in patients with congenital QT prolongation. To evaluate this, 9 patients (6 female, mean age 17.6 years) with congenital long QT syndromes, all of whom had syncope and documented torsades de pointes, were studied. Patients were studied off treatment and during therapy with beta-blocking agents. Three patients were also studied after left stellate ganglionectomy. An age-matched control group was also studied. Good quality 12-lead electrocardiograms were recorded from all patients. For each lead, QT and RR intervals were measured, and QTc value was calculated. QT and QTc dispersions were calculated for each patient. Patients had a significantly longer mean QT interval compared with that of the control group (450 +/- 100 vs 359 +/- 63 ms; p = 0.015) at similar mean RR intervals (736 +/- 231 vs 783 +/- 289 ms), with a longer mean QTc value (0.53 +/- 0.08 vs 0.41 +/- 0.02 s1/2; p = 0.004). Patients also had longer QT and QTc dispersions compared with those of the control group (110 +/- 45 vs 43 +/- 12 ms [p = 0.004], and 0.108 +/- 0.03 vs 0.05 +/- 0.02 s1/2 [p = 0.002], respectively). QT and QTc dispersions on and off beta-blocking agents were not significantly different. Comparing patients with frequent and those with infrequent symptoms, there was no difference in QT or QTc dispersion either off treatment or during therapy with beta-blocking agents.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1992

Is hypomagnesemia arrhythmogenic?

An understanding of the role of magnesium in cardiac conduction is complicated by the multiplicity of intracellular events coordinated by the magnesium ion. Several reports have cited magnesium deficiency as the cause of a variety of ventricular and supraventricular arrhythmias. On further inspection, the circumstances of each report strongly suggest the coexistence of significant potassium depletion; isolated hypomagnesemia as a cause of arrhythmia is not reported. This discussion brings together new data from basic science with that of clinical research to refute the suggestion that isolated hypomagnesemia is arrhythmogenic. However, there is sufficient evidence to indicate that hypomagnesemia will significantly exacerbate the proarrhythmic effect of hypokalemia, particularly if occurring in the presence of digoxin toxicity. Potassium and magnesium depletion are commonly concomitant, and simultaneous repletion of both ions in the presence of hypokalemia-induced arrhythmia would be both logical and effective. The beneficial effects of intravenous magnesium in the acute control of ventricular tachyarrhythmia are concluded to occur as a result of a separate antiarrhythmic action, quite independent of underlying magnesium balance.

Arrhythmias, Cardiac↗
PubMed1992

A prospective study of the efficacy and safety of adjuvant metoprolol and xamoterol in combination with amiodarone for resistant ventricular tachycardia associated with impaired left ventricular function.

Combination antiarrhythmic drug therapy may be more effective than treatment with a single agent for control of refractory cases of sustained ventricular tachycardia (VT). In a prospective randomized crossover study of 20 patients with impaired left ventricular function (ejection fraction of 28% +/- 8%) and recurrent VT in spite of treatment with amiodarone, we compared the efficacy and safety of adjuvant therapy with metoprolol, 50 mg two times daily and xamoterol, 200 mg two times daily. Metoprolol caused hemodynamic deterioration in five patients, and only one also experienced intolerance to xamoterol. Sustained VT was inducible in all 20 patients who were receiving amiodarone alone but was suppressed or rendered nonsustained in 8 of 20 patients during treatment with amiodarone plus xamoterol and in 6 of 17 patients during treatment with amiodarone plus metoprolol. Addition of xamoterol restored sinus rhythm in four patients who presented with incessant VT, and metoprolol was effective for three of them. Neither beta-blocker significantly altered tachycardia cycle length or any electrophysiologic parameter other than the slowing of the sinus rate. Both beta-blockers suppressed exercise-induced VT in 3 of 4 patients, and addition of xamoterol significantly increased treadmill exercise duration (7.1 +/- 1.8 min) compared with administration of amiodarone alone (3.8 +/- 1.5 min; p < 0.01). Fourteen patients were discharged with prescriptions for amiodarone-beta-blocker combinations. During a mean follow-up period of 13 months (range, 2 to 24 months), there were three cases of recurrent VT (in all patients VT remained inducible) and no sudden deaths.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Effect of intravenous adenosine on human atrial and ventricular repolarisation.

OBJECTIVE: The aim was to assess the effects of therapeutic doses of intravenous adenosine on human atrial and ventricular repolarisation. METHODS: The effects of 6 mg and 12 mg bolus doses of adenosine on the atrial and ventricular monophasic action potentials were studied using the contact catheter technique in 19 patients undergoing routine diagnostic electrophysiology studies. The effect on atrial repolarisation was studied before and after beta blockade in a subgroup of patients. RESULTS: The duration of the monophasic action potential to 90% repolarisation (MAPD90) was measured in all cases. After 6 mg of adenosine the atrial MAPD90 shortened from 227(SD 29) ms to 188(25) ms (p < 0.005); after 12 mg it shortened from 221(31) ms to 168(32) ms (p < 0.001). The maximum shortening was unaltered by propranolol 0.15 mg.kg-1. The ventricular MAPD90 showed no significant change after 12 mg, at 240(32) ms v 234(33) ms. CONCLUSIONS: Therapeutic doses of adenosine shorten the atrial but not the ventricular monophasic action potential duration. The effect is dose dependent and not abolished by beta blockade.

Action Potentials↗
PubMed1992

Difficulties in the use of electrocardiographic criteria for the differential diagnosis of left bundle branch block pattern tachycardia in patients with a structurally normal heart.

In patients with left bundle branch block pattern tachycardia, electrocardiographic criteria, based on leads V1, V2 and V6, have been shown to be effective for the diagnosis of ventricular tachycardia in patients with a previous myocardial infarct. To test these criteria on a wider population, we studied 53 consecutive patients with left bundle branch block pattern tachycardia. Seventeen patients had supraventricular tachycardia and 36 had ventricular tachycardia, 18 with a previous myocardial infarction, two with cardiomyopathy, and 16 with a normal heart. The sensitivity for the diagnosis of ventricular tachycardia in patients with a previous myocardial infarct of the combined criteria was 100% but was only 50% for the other patients, which was not significantly different from the patients with supraventricular tachycardia (29%). Two other criteria, right axis shift in tachycardia and ventricular ectopics during sinus rhythm with the same morphology as the tachycardia, were only seen in patients with ventricular tachycardia, and combined with the other criteria allowed the correct identification of 35/36 patients with ventricular tachycardia. To conclude, the electrocardiographic criteria based on leads V1, V2 and V6 are not sensitive for the diagnosis of a ventricular origin of left bundle branch block pattern tachycardia in patients with a normal heart and additional criteria are required for the diagnosis in these patients.

Adult↗
PubMed1992

Comparison of verapamil and diltiazem in the suppression of idiopathic ventricular tachycardia.

This study examines the efficacy of verapamil and diltiazem in the suppression of idiopathic ventricular tachycardia (VT). Eight patients (mean age 29.8 +/- 12.3 years, two males and six females) with VT, without any underlying cardiac abnormality on clinical examination and noninvasive investigation, were studied. The inducibility of the clinical VT was examined by treadmill exercise testing and programmed ventricular stimulation (PVS). In six patients, VT was inducible by exercise testing and in the remaining two by PVS. Following baseline testing, verapamil (120-mg thrice daily) and diltiazem (60-mg thrice daily) were administered in random order, allowing 5 half-lives for the drug to load before evaluation. Two patients had complete suppression of the VT and the remaining six patients demonstrated a partial response to both calcium antagonists. In the patients with a partial response, the duration of the longest run of VT was reduced (baseline 96.0, 34.2 SEM); verapamil 19.2 (7.5); diltiazem 45.3 (21.4 beats), whereas, there was no change in the rate of VT (baseline 199.7 (8.0); verapamil 184.5 (11.4); diltiazem 201.0 (9.5 beats/min). No proarrhythmic effect was observed with either of the drugs in these patients. We conclude that idiopathic VT can be suppressed in some patients by calcium antagonists. In patients with a partial response, the length of run of the VT can be reduced, but the rate is unaffected. Verapamil and diltiazem do not differ in their ability to suppress VT in individual patients.

Adult↗
PubMed1992

Relationship between spectral measures of heart rate variability and ventricular ectopic activity in patients with idiopathic ventricular tachycardia.

This study examines the relationship of hourly spectral measures of heart rate variability (HRV) to the occurrence of ventricular ectopic (VE) activity in 20 patients with idiopathic ventricular tachycardia and frequent VE's. Spectral measures of HRV were obtained from 24-hour Holter recordings from the patients in a drug free state and included the total energies in the spectrum, the low frequency components (L) (0.04-0.15 Hz) representing predominantly sympathetic tone with some contribution from the parasympathetic and high frequency components (H) (0.15-0.4 Hz) representing mainly parasympathetic tone. A high H component (parasympathetic) was defined as area > 12 msec and high L components (sympathetic) as area > 30 msec. On an hourly analysis of spectral components in relation to VE activity, VE's occurred significantly more frequently during periods of low H and low L (F = 20.5, DF = 3, P < 0.0001). The number of VE's did not differ statistically in the other combinations of H and L components (low H, low L = 612.8 (50.1); high H, low L = 180.1 (36.8); low H, high L = 338.4 (58.9); high H, high L = 204.9 (17.7) VE's/hr (SEM). The results suggest that VE's are more frequent during periods of low H and low L and are diminished when either H or L are increased in patients with idiopathic ventricular tachycardia. The results would be consistent with the hypothesis that the parasympathetic nervous system has an electrophysiologically stabilizing effect on the myocardium.

Adult↗
PubMed1992

Transtelephonic interrogation of the implantable cardioverter defibrillator.

Third generation implantable cardioverter defibrillators (ICDs) have extensive memory capability to store data about the patient's arrhythmias and the effect of therapies delivered by the ICD. However, this data has so far been accessible only when the patient attends the pacing clinic. Two Medtronic 9421 PCD TeletraceR transmitters have been used to interrogate Medtronic 7216A and 7217B PCD S at distances of up to 300 miles from our hospital and transmit the data to a 9420 PCD TeletraceR receiver. Successful transmission of data has been obtained on 50 occasions with 100% data concordance with repeat transmission. The system can reduce the number of unscheduled clinic visits, reduce delay in making a diagnosis following unexpected delivery of a shock therapy, and reassure patients about to be discharged following ICD implantation. The benefits are magnified where patients reside far away from the implanting center.

Electric Countershock↗
PubMed1992

Catheter ablation by low energy DC shocks for successful management of atrial flutter.

OBJECTIVE: To assess the effects of low energy ablation of the substrate for atrial flutter. DESIGN: Initial retrospective analysis of patients undergoing low energy ablation of the atrioventricular node for refractory atrial flutter (group 1) was followed by a prospective assessment of low energy ablation in the posterio-inferior right atrium for the same condition (group 2). SETTING: Tertiary referral centre for management of cardiac arrhythmias. PATIENTS: Seven men (aged 50-67 years) with refractory atrial flutter. INTERVENTIONS: Multiple (3-10) low energy DC shocks with a cumulative energy of 100-245 J in the region of the atrioventricular node in group 1 and 12-15 low energy DC shocks (cumulative energy 110-235 J) guided by the anatomical landmarks of the triangle of Koch and applied directly to the atrial wall. MAIN OUTCOME MEASURE: Freedom from recurrence of atrial flutter. RESULTS: In group 1 despite initial complete atrioventricular block in three patients, atrioventricular conduction had resumed in all by one month. All four, however, were in sinus rhythm at follow up six to 13 months later. Two of the three patients in group 2 were free of atrial flutter at follow up three to four months after ablation. CONCLUSION: Ablation of the atrial flutter substrate with low energy DC shocks is feasible. Precise electrophysiological mapping is not necessary.

Aged↗
PubMed1992

Prognostic value of baroreflex sensitivity testing after acute myocardial infarction.

BACKGROUND: Disturbances of autonomic function are recognised in both the acute and convalescent phases of myocardial infarction. Recent studies have suggested that disordered autonomic function, particularly the loss of protective vagal reflexes, is associated with an increased incidence of arrhythmic deaths. The purpose of this study was to compare the value of differing prognostic indicators with measures of autonomic function and to assess the safety of arterial baroreflex testing early after infarction. METHODS: As part of a prospective trial of risk stratification in post-infarction patients arterial baroreflex sensitivity, heart rate variability, long term electrocardiographic recordings, exercise stress testing, and ejection fraction were recorded between days 7 and 10 in 122 patients with acute myocardial infarction. RESULTS: During a one year follow up period there were 10 arrhythmic events. Baroreflex sensitivity was appreciably reduced in these patients suffering arrhythmic events (1.73 SD (1.49) v 7.83 (4.5) ms/mm hg, 95% confidence interval (CI) 4.8 to 7.3, p = 0.0001). Significant correlations were noted with age (r = -0.68, p less than 0.001) but not left ventricular function. When baroreflex sensitivity was adjusted for the effects of age and ventricular function baroreflex sensitivity was still considerably reduced in the arrhythmic group (2.1 v 7.57 ms/mm Hg, p less than 0.0001). Depressed baroreflex sensitivity carried the highest relative risk for arrhythmic events (23.1, 95% CI 7.7 to 69.2) and was superior to other prognostic variables including left ventricular function (10.4, 95% CI 3.3 to 32.6) and heart rate variability (10.1, 95% CI 5.6 to 18.1). No major complications were noted with baroreflex testing and in particular no patients developed ischaemic or arrhythmic symptoms during the procedure. CONCLUSIONS: Disordered autonomic function as measured by depressed baroreflex sensitivity or reduced heart rate variability was associated with an increase incidence of arrhythmic events in post-infarction patients. Baroreflex testing can be safely performed in the immediate post-infarction period.

Adult↗
PubMed1992

Comparative electrophysiological effects of captopril or hydralazine combined with nitrate in patients with left ventricular dysfunction and inducible ventricular tachycardia.

OBJECTIVE: To assess the electrophysiological and antiarrhythmic effects of pharmacological load manipulation by an angiotensin converting enzyme (ACE) inhibitor (captopril) and a direct vasodilator (hydralazine plus isosorbide mononitrate) in patients with inducible ventricular tachycardia and impaired left ventricular function. DESIGN: Randomised open label cross-over comparison of three regimens. SETTING: Tertiary arrhythmia referral centre. SUBJECTS: Eight patients with reduced left ventricular function and sustained ventricular tachycardia inducible by programmed stimulation. INTERVENTIONS: Three treatment regimens each of 48 hours duration: captopril, hydralazine plus isosorbide mononitrate, and control (no vasodilator). MAIN OUTCOME MEASURES: Changes in central haemodynamics, electrophysiological parameters, and induction of ventricular tachycardia during treatment with captopril, or hydralazine combined with nitrate, compared with a control period. RESULTS: Both vasodilator treatments produced similar balanced reductions in peak systolic pressures and filling pressures compared with controls. Captopril had no effect on sinus cycle length, atrial refractoriness, or intraventricular conduction, but prolonged ventricular effective and functional refractory periods and QT interval during constant rate atrial pacing. Hydralazine combined with nitrate did not significantly alter any electrophysiological variable. Ventricular tachycardia was similarly inducible during all three periods. CONCLUSIONS: Load manipulation by captopril but not hydralazine combined with nitrate prolonged ventricular refractoriness and repolarisation, possibly reflecting a combination of mechano-electrical effect with the restraining influence of ACE inhibitors on reflex sympathetic stimulation.

Aged↗
PubMed1992

Efficacy of flecainide, sotalol, and verapamil in the treatment of right ventricular tachycardia in patients without overt cardiac abnormality.

OBJECTIVE: A comparison of the efficacy of verapamil, sotalol, and flecainide to suppress right ventricular tachycardia (VT) in patients with a clinically normal heart. DESIGN: Patients underwent treatment serially with verapamil (360 mg daily), sotalol (240 or 320 mg daily), and flecainide (200 or 300 mg daily), (the larger dose was for patients heavier than 80 kg) to suppress tachycardia. Each drug was given orally for five half lives before testing. PATIENTS: 23 patients with right VT associated with a clinically normal heart were studied. OUTCOME MEASURES: The effects of drug treatment were examined by the number of ventricular events on 24 hour Holter monitoring, and the ability of tachycardia to be induced by treadmill exercise testing (Bruce protocol) and programmed ventricular stimulation (Wellens protocol), compared with drug free baseline tests. SETTING: Patients were studied in a tertiary referral centre. RESULTS: All three drugs suppressed ventricular salvos (> 3, < 5 consecutive ventricular premature contractions) (p < 0.01) and VT (p < 0.05) on Holter monitoring and did not differ statistically in effect. Exercise induced VT was also suppressed by all three drugs (p < 0.01), and of these sotalol was the most effective although this was not statistically significant (14/23 inducible when drug free, 4/23 on flecainide, 2/23 on sotalol, 5/23 on verapamil). Sustained and non-sustained VT induced by programmed stimulation was also suppressed by the three drugs (p < 0.01) and again sotalol was the best of these though the differences did not achieve statistical significance (17/23 inducible when drug free, 4/17 on flecainide, 2/17 on sotalol, and 6/17 on verapamil). Proarrhythmic effects of drugs were found in a few patients. There was no difference in the efficacy of the drugs in patients with histological abnormalities of the myocardium when compared with those of normal histology. CONCLUSIONS: Ventricular tachycardia associated with a clinically normal heart can be suppressed by flecainide, sotalol, or verapamil. In individual patients sotalol was the most frequently effective drug (effective in > 89% of patients) and is a suitable choice for first line treatment.

Adult↗
PubMed1992

Intravascular ultrasound imaging of the coronary arteries: an in vitro evaluation of measurement of area of the lumen and atheroma characterisation.

OBJECTIVE: To assess the accuracy of measurement of area of the lumen, and sensitivity, and specificity of detection of atheroma in coronary arteries in vitro with a commercially available 20 MHz intravascular ultrasound system. SETTING: A teaching hospital department of cardiology with the support of the department of cardiovascular pathology. PROCEDURE: 10 segments of coronary artery were removed from cadaver hearts. Intravascular ultrasound imaging was performed at fixed levels and the vessels were then sectioned and photographed before histological preparation. An independent blinded observer measured luminal area and assessed the presence of atheroma on the intravascular ultrasound images of 76 vessel sections (304 quadrants). The sensitivity and specificity of detection of atheroma was assessed in comparison with the histologically prepared sections. Luminal areas from intravascular ultrasound, photographs of cross sections of the vessels and histological sections were compared with the technique of limits of agreement. RESULTS: Overall 36% of the 304 quadrants studied histologically had identifiable atheroma. Intravascular ultrasound sensitivity for atheroma was 0.593 and the specificity was 0.839. The positive predictive value was 0.674, and the relative risk 3.139. Values for area of the vessel lumen were on average 9.4 mm2 (confidence interval (CI) 8.6-10.2 mm2) larger than those measured from photographs and 10.7 (CI 9.8-11.6 mm2) larger than those measured from the histological sections. CONCLUSIONS: The intravascular ultrasound system assessed in this study significantly overestimated coronary vessel luminal area and had low sensitivity and specificity for detection of atheroma. Improvements in image resolution are required before this system can provide useful information on coronary artery size and morphology.

Coronary Artery Disease↗
PubMed1991

The electrophysiological effects of flosequinan.

We have evaluated the acute electrophysiological effects of flosequinan in 18 patients with normal ventricular function. Following intravenous infusion of flosequinan 100 mg over 1 h, mean (SD) systolic blood pressure fell from 131 +/- 19 to 120 +/- 22 mmHg (P less than 0.02) and there was significant shortening of sinus cycle length (732 +/- 151 to 575 +/- 93 ms, P less than 0.001), AH interval (110 +/- 45 to 71 +/- 19 ms, P less than 0.01), QRS duration (98 +/- 28 to 91 +/- 26 ms, P less than 0.02) and QT interval (373 +/- 47 to 337 +/- 35 ms, P less than 0.001), but no change in sinus node recovery time, intra-atrial conduction time, HV interval or the corrected QTc interval. There was a reduction in both anterograde atrioventricular Wenckebach cycle length (299 +/- 53 to 259 +/- 52 ms, P less than 0.01) and retrograde ventriculoatrial Wenckebach cycle length (375 +/- 77 to 300 +/- 56 ms, P less than 0.01). There was no change in atrial or ventricular effective refractory period (ERP) but atrial functional refractory period (FRP) shortened (233 +/- 31 to 212 +/- 24 ms, P = 0.07) as did ventricular FRP (249 +/- 24 to 234 +/- 21 ms, P less than 0.01). Patients received an oral dose of flosequinan 50 mg 12 h later. By 24 h, sinus cycle length, QRS duration and the QT interval had all returned towards baseline values, but ventricular ERP had lengthened (199 +/- 22 to 215 +/- 26 ms, P less than 0.06).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗