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Biomedical subjects

J M McComb

Publications and source records attributed to J M McComb.

At least 19 recordsLinked to original sources
PubMed1996

Vasopressin release during orthostatic hypotension after cardiac transplantation.

At the time of cardiac transplantation all nerves from the donor ventricles are cut. These nerves may regrow, but there is no method of measuring any regrowth. Arginine vasopressin (AVP) release was studied during hypotension induced by head-up tilt and lower body negative pressure (LBNP) in transplant recipients and in normal controls. Subjects were tilted to 60 degrees for up to 60 min or until symptomatic. Lower body negative pressure (40 mmHg) was applied for 10 min after 30 min rest. Seven of 17 transplant recipients and 11 of 12 controls became symptomatic during tilt testing, and 9 of 12 controls and 9 of 17 transplant recipients became symptomatic after 10 min of LBNP. Symptoms during tilt did not predict symptoms during LBNP. Resting AVP levels were similar but osmolality was greater in transplant recipients. Resting haematocrit was reduced, and atrial natriuretic peptide increased in transplant recipients, suggesting increased plasma volume. In symptomatic subjects, changes in humoral concentrations were similar when compared between transplant recipients and normals, except that the rise in AVP at the time of symptoms was reduced in transplant recipients, with a comparable drop in blood pressure consistent with persistent cardiac afferent denervation in a subset of transplant recipients.

Adult↗
PubMed1996

Reproducibility of electrophysiological measurements in cardiac transplant recipients.

The clinical usefulness of certain electrophysiological measurements, particularly those of sinus node function, is limited by variation in autonomic tone resulting in poor reproducibility. The denervated transplanted heart is not susceptible to direct autonomic control and, therefore, electrophysiological measurements may be more reproducible in this group. To our knowledge, this hypothesis has not previously been systematically evaluated. Ten adult recipients underwent serial electrophysiological studies between 10-18 days after cardiac transplantation. Five studies were performed at 2-hour intervals during a single day, between 9:00 a.m. and 5:00 p.m. Spontaneous cycle length (SCL) was recorded. Sinus node recovery time (SNRT), sinoatrial conduction time (SACT), and atrioventricular (AV) Wenckebach cycle length were measured using standard techniques. The effective refractory periods of the complete AV conducting system (AVERP), atrium (AERP), and ventricle (VERP) were measured. Corrected maximal SNRT was normal in all subjects. Mean coefficients of variation (Cv) for SCL, corrected maximal SNRT, and SACT were 2.8%, 7.4%, and 3.5%, respectively. AVERP was less than AERP in seven subjects, limiting further analysis. The mean Cv for AV Wenckebach cycle length was 2.1%. The mean coefficients of variation for AERP were 3.6% and 3.7%, and for VERP 3% and 3.3%, at 600- and 400-ms drive cycle lengths, respectively. Previous studies report much greater variation in innervated subjects particularly of indices of sinus node function. Thus, the reproducibility of electrophysiological measurements of sinus and AV node function in the transplanted heart is better than in normal subjects. This may have important implications for the reliability of electrophysiological testing in transplant recipients.

Atrioventricular Node↗
PubMed1996

Exercise response after cardiac transplantation: correlation with sympathetic reinnervation.

OBJECTIVE: To investigate the relation between sympathetic efferent reinnervation and chronotropic competence during exercise testing after cardiac transplantation. PATIENTS: Twenty five long-term cardiac transplant recipients and 11 normal controls. SETTING: Regional cardiothoracic centre. METHODS: Intracoronary tyramine was given to the transplant recipients and the per cent heart rate change measured. Exercise tests were performed in patients and controls according to the chronotropic assessment exercise protocol, and the per cent heart rate reserve measured at peak exercise and 6 min afterwards to estimate the recovery rate. RESULTS: The mean (SD) percentage heart rate change after intracoronary tyramine was 15.7 (15.4). Heart rate reserve achieved at peak exercise was 68.3 (20.6)% compared with 102.7 (9.3)% in the controls (P < 0.001). Heart rate recovery at 6 min was 41.7 (20.1)% compared with 79.5 (9.0)% in the controls (P < 0.001). Total workload was 69.0 (33.0) METS.min compared with 117.2 (41.9) METS.min in the controls (P < 0.01). There was a positive correlation between heart rate reserve achieved at peak exercise and response to tyramine (r = 0.66, P < 0.01), between heart rate recovery and response to tyramine (r = 0.69, P < 0.001), and between total workload and response to tyramine (r = 0.63, P = 0.04). CONCLUSION: Functional sympathetic efferent reinnervation of the sinus node occurred in some patients after transplantation, and was associated with improved heart rate response during and recovery after exercise, as well as with increased total workload.

Adult↗
PubMed1996

Permanent pacemaker use after cardiac transplantation: completing the audit cycle.

OBJECTIVE: To determine the effects of delaying permanent pacemaker implantation in cardiac transplant recipients from less than tree weeks to three weeks or more post transplantation-a change prompted by an earlier audit. DESIGN: Retrospective review of resting 12 lead electrocardiograms and prospective 24 hour ambulatory electrocardiograms. Comparison of pacemaker usage before (period 1) and after (period 2) the policy change in November 1990. SETTING: Outpatient department, supra-regional cardiopulmonary transplant unit. PATIENTS: All 30 consecutive orthotopic cardiac transplant recipients who received a permanent pacemaker within one month of transplantation between May 1985 and August 1995. MAIN OUTCOME MEASURES: Presence of pacing on the 12 lead electrocardiogram and during 24 hour ambulatory electro-cardiogram monitoring (pacemaker programmed to 50 beats per minute). RESULTS: 16/152 (10.5%) cardiac transplant recipients received permanent pacemakers in period 1 compared with 14/180 (7.8%) in period 2 (P = NS). Evidence of pacing was seen on 12 lead electrocardiograms at three months in 37.5% recipients in period 1 compared with 78.6% in period 2 (P = 0.03). At six months pacemaker usage had declined to 18.8% in period 1 and 35.7% in period 2 and at three years to 13.3% in period 1 and 40% in period 2 (P = NS for both). 21% patients in period 1 paced on ambulatory 24 hour monitoring compared with 38.5% in period 2 (P = NS). CONCLUSIONS: Delaying permanent pacemaker implantation to three weeks or more after cardiac transplantation reduced the proportion of permanent pacemaker implantations, slightly but not significantly. There was a significant increase in permanent pacemaker usage at three months post transplantation with trends towards increased usage at later times, suggesting more appropriate selection of patients for permanent pacing.

Clinical Protocols↗
PubMed1996

Permanent pacemaker implantation after cardiac transplantation: extra cost of a conservative policy.

OBJECTIVE: To determine the costs of a change in permanent pacemaker implantation policy to later implantation (day 21+) after cardiac transplantation. DESIGN: Retrospective review of patient records including duration of temporary pacing, timed of permanent pacemaker implantation, and length of hospital stay for every patient surviving > or = 14 days from November 1990 to August 1995 (period 2) and for all patients in whom permanent pacemakers were implanted between May 1985 and November 1990 (period 1). SETTING: Supra-regional cardiopulmonary transplant unit. PATIENTS: 335 consecutive adult cardiac transplant recipients at Freeman Hospital between May 1985 and August 1995. MAIN OUTCOME MEASURES: The cost of the policy change was calculated by subtraction of the overall saving in pacemaker implantations from the overall cost of the extra inpatient stay in period 2 due to delayed implantation. RESULTS: Mean inpatient stay per patient following cardiac transplantation of permanent pacemaker recipients in period 1 was 13.8 days compared with 23.9 days in period 2 (P < 0.001). The cost of this extended hospital stay is 60,095 pounds. Had the implantation policy not been changed, a further seven patients would have received a permanent pacemaker in period 2. A saving in pacemaker hardware of 16,275 pounds was made. Overall, however, the new permanent pacemaker implantation policy increased expenditure by 43,820 pounds, assuming that permanent pacemaker implantation was the only reason for the extended hospital stay. CONCLUSION: The change in policy from early to later permanent pacemaker implantation has markedly increased expenditure.

Clinical Protocols↗
PubMed1995

Evolution of the chronotropic response to exercise after cardiac transplantation.

The chronotropic response to exercise is abnormal in cardiac transplant recipients as a result of autonomic denervation. Differences in the response between recent transplant recipients and longer-term survivors have been described in previous cross-sectional studies. These changes have not been assessed directly using serial studies. The effect of sinus node dysfunction on the chronotropic response has not previously been determined. Thirty-one transplant recipients underwent serial treadmill exercise tests using the chronotropic exercise assessment protocol 3 and 6 weeks and 3 and 6 months after transplantation. Sinus node function was assessed using standard electrophysiologic techniques. The chronotropic response increased between 3 and 6 weeks after transplantation in all subjects. Six months after transplantation, there was a further marked increase in the response in a subgroup of 5 subjects. These subjects also had a dramatic decrease in heart rate on cessation of exercise. Three subjects had abnormal sinus node function. Although heart rates and chronotropic response were below average in these subjects, 2 other subjects with normal sinus node function on electrophysiologic testing had lower heart rates and worse chronotropic responses. Thus, the chronotropic response to exercise evolves over the first 6 weeks after cardiac transplantation in all subjects. In a number of recipients (16%), there is a marked increase in chronotropic response between 3 and 6 months, which suggests efferent sympathetic reinnervation. There was no clear difference in chronotropic response between subjects with and without evidence of sinus node dysfunction.

Adult↗
PubMed1994

Sinus node function after cardiac transplantation.

OBJECTIVES: This study aimed to examine changes over time in sinus mode function after cardiac transplantation; to determine the incidence, natural history and etiology of sinus node dysfunction in transplant recipients; and to identify any early predictors of long-term sinus node function. BACKGROUND: Bradyarrhythmias caused by sinus node dysfunction are common immediately after cardiac transplantation. Existing electrophysiologic studies have been limited by small numbers and have reported an unexpectedly high incidence of sinus node dysfunction (approximately 50%) compared with the incidence of bradyarrhythmias in other studies. There have been no previous studies reporting serial electrophysiologic data. Thus, the natural history of sinus node dysfunction after transplantation has not been adequately described. METHODS: Serial electrophysiologic studies of sinus node function and 24-h ambulatory electrocardiographic recordings were performed at 1, 2, 3 and 6 weeks and 3 and 6 months after transplantation in 40 adult recipients. RESULTS: The overall incidence of sinus node dysfunction was 17.5% (7 of 40). Six patients (15%) had sinus node dysfunction from week 1; one developed sinus node dysfunction at 3 months. Sinus node recovery time returned to normal by 6 weeks in all six patients with early sinus node dysfunction, but abnormalities of sinoatrial conduction persisted in two. Two patients who required pacing during ambulatory monitoring at 2 weeks after transplantation (temporary pacemaker 50 beats/min, demand) received a permanent pacemaker. One patient required pacing at 3 weeks and continued to require pacing 6 months after transplantation. CONCLUSIONS: The incidence of sinus node dysfunction after cardiac transplantation is lower than has been previously reported in electrophysiologic studies. Sinus node automaticity improves with time, although abnormalities of sinoatrial conduction may persist. The best predictor of permanent pacing requirements is the temporary pacing requirements during 24-h Holter monitoring 2 and 3 weeks after transplantation, with temporary pacing set at 50 beats/min on demand.

Arrhythmia, Sinus↗
PubMed1994

Vasodepressor reactions after orthotopic cardiac transplantation: relationship to reinnervation status.

Ventricular vagal nerve endings are thought to trigger vasodepressor syncope. Reports of vasodepressor reactions associated with donor bradycardia after cardiac transplantation have led to speculation that vagal reinnervation occurs. We assessed reinnervation status in seven patients 23-36 months (median 24 months) post-transplantation. Heart rate responses to vagal manoeuvres (respiration, Valsalva) and sympathetic stimuli (exercise and injection of tyramine into the coronary artery supplying the sinus node) were measured. All patients underwent 60 min of 60 degrees head-up tilt with foot plate support. During tilt four of the seven had vasodepressor reactions with a fall in mean arterial pressure of 20-90 mmHg. During vasodepression two patients had falls in donor heart rate of 13 and 40% relative to peak heart rate during tilt. These two patients had evidence of functional sympathetic reinnervation. By contrast the two patients without donor bradycardia during vasodepression had only limited or no evidence of sympathetic reinnervation. No patient had consistent evidence of parasympathetic reinnervation as judged by the heart rate response to vagal manoeuvres. Head-up tilt can thus produce vasodepressor reactions with donor bradycardia after cardiac transplantation in the absence of consistent evidence of vagal reinnervation. Left ventricular nerve endings may not be the only mediators of tilt-induced vasodepressor reactions in man. Donor bradycardia during vasodepression may reflect sympathetic withdrawal and not vagal reinnervation.

Blood Pressure↗
PubMed1994

Radiofrequency ablation of a Mahaim fiber following localization of Mahaim pathway potentials.

We report radiofrequency ablation of a Mahaim fiber in a patient with wide complex supraventricular tachycardia. Pathway potentials from the lateral aspect of the right AV groove were recorded, which were distinct from the His potential. During atrial pacing, decremental properties of the fiber were demonstrated, which resulted in prolongation of the interval between the atrial electrogram and the Mahaim pathway potential. The pathway potentials, preexcitation, and tachycardia disappeared after a single application of radiofrequency energy, after which the patient has remained free of palpitations. Mapping of a Mahaim fiber by identifying pathway potentials thus allowed accurate localization and successful ablation with minimal energy. We therefore suggest that, where possible, recording of such Mahaim potentials may be the optimal technique for Mahaim fiber localization.

Adult↗
PubMed1994

Cardiovascular and respiratory effects of adenosine in humans after pulmonary denervation.

Adenosine infusion causes tachycardia in normal subjects. A proposed mechanism is secondary pulmonary stretch receptor activation due to hyperventilation, induced by direct stimulation of carotid body chemoreceptors by adenosine. We examined responses to adenosine (incremental doses given by intravenous infusion, 5 min each rate) in six normal volunteers and six lung-transplant recipients with pulmonary denervation. Adenosine caused chemoreceptor stimulation in both groups with minute ventilation increasing from 5.8 +/- 0.4 to 10.7 +/- 1.3 l/min (P < 0.05) in the volunteers and from 4.8 +/- 0.4 to 9.2 +/- 0.8 l/min (P < 0.001) in the lung-transplant recipients. There was no difference in the magnitude of the ventilatory increase between the two groups (P = NS at all infusion rates). Adenosine produced tachycardia in both groups, with heart rate increasing from 66 +/- 5 to 84 +/- 3 beats/min (P < 0.01) in the volunteers and from 82 +/- 6 to 110 +/- 6 beats/min (P < 0.05) in the lung-transplant recipients. There was no difference in the magnitude of the heart rate response between the two groups (P = NS at all infusion rates). These data suggest, contrary to previous thinking, that pulmonary stretch receptor activation does not contribute to adenosine-induced tachycardia in humans.

Adenosine↗