Biomedical subjects
Publications and source records attributed to R Sutton.
A patient dependent on a pacemaker and with a rate responsive unit presented with symptomatic ventricular tachycardia despite drug treatment. He was managed with a third generation implantable cardioverter defibrillator, while rate responsive pacing was maintained.
OBJECTIVE: To evaluate the effect of permanent pacing in cardioinhibitory malignant vasovagal syndrome. PATIENTS AND METHODS: 37 patients with permanent pacemakers for cardioinhibitory malignant vasovagal syndrome. All presented with syncope (median six episodes, median frequency two episodes a year) and after conventional investigation and invasive electrophysiological assessment they remained undiagnosed, and without a generally accepted indication for pacemaker implantation. In all vasovagal syncope with cardioinhibition (heart rate at syncope < 60 beats/min) developed during tilt tests performed according to the Westminster protocol (head up tilt at 60 degrees with a footplate support for 45 minutes or until syncope intervenes). Dual chamber pacemakers were implanted in 35 (95%) and VVI pacemakers in the remaining two (5%). RESULTS: Over a mean (SD) follow up since implantation of 50.2 (23.9) months symptomatic improvement occurred in 89%: 62% remained free of syncope and 27% were completely symptom free. The collective syncopal burden of these 37 patients was reduced from 136 to 11 episodes each year. During follow up three patients died from unrelated causes. Patients who become asystolic during the tilt test (sinus pause of at least four seconds) experienced no greater benefit from pacing than those with less extreme cardioinhibition. Patients who remained free of syncope since implantation were younger than those who continued to experience syncope. Patients who remained completely symptom free after implantation were younger, more likely to be male, and had had fewer syncopal episodes before implantation than those who continued to experience syncope or presyncope. No other demographic, clinical, investigative, or pacing variable suggested a more favourable outcome after implant. CONCLUSIONS: This retrospective and uncontrolled experience suggests a possible role for permanent pacing in selected patients with cardioinhibitory malignant vasovagal syndrome. Improved acquisition of tilt test data may enable better selection of patients who are suitable for permanent pacing. A randomised prospective study to compare permanent pacing with no treatment or with medical treatment in cardioinhibitory malignant vasovagal syndrome is indicated.
Operative cases where there is a potential for massive blood loss necessitates a system to rapidly warm and transfuse large volumes of blood over short periods of time. An in-house system in which both crystalloid solutions and blood products can be quickly added, warmed and available for infusion was developed to meet this need. The purpose of this study was to evaluate how blood products are affected when warmed and recirculated for an extended period of time. A recirculating rapid infusion system was assembled utilizing two filtered cardiotomy reservoirs, a centrifugal pump, a stainless steel blood heat exchanger, and 1/4 inch tubing, and applied in six adult orthotopic liver transplantations. The system was primed with 2 to 4 units each of fresh frozen plasma and packed red blood cells. The prime was recirculated and warmed to 37 degrees C. Samples for blood gases, oxygen saturation, hematocrit, plasma free hemoglobin, sodium and potassium levels were drawn after initial priming and then every 30 minutes until additional blood products were added. Results show no significant change in pH (6.57 +/- 0.21), pO2 (56 mmHg +/- 23 mmHg), pCO2 (173 mmHg +/- 138 mmHg), hematocrit (27% +/- 8.7%) and plasma free hemoglobin values (125 mg/dl +/- 9.4 mg/dl), following 3 hours of recirculation. However, potassium levels significantly decreased from 11.6 meq/L +/- 2.6 meq/L to 10.0 meq/L +/- 2.3 meq/L (p < 0.05), sodium levels significantly increased from 144 meq/L +/- 5.9 meq/L to 147 meq/L +/- 5.3 meq/L (p < 0.05) and oxygen saturations significantly increased from 59% +/- 9.1% to 70% +/- 16% (p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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OBJECTIVES: This study evaluated the ability of patients to manifest vasovagal reactions after orthotopic heart transplantation. BACKGROUND: Paradoxic stimulation of left ventricular baroreceptors may be the afferent limb of the vasovagal reflex in humans. Orthotopic heart transplantation causes surgical denervation of these receptors and would therefore be expected to abolish the vasovagal reflex. METHODS: To attempt to confirm this hypothesis, 10 patients with orthotopic heart transplantation underwent both head-up tilt testing while resting on a saddle support and testing for parasympathetic innervation of the donor heart before and after atropine infusion. Native and donor heart sinus rates were monitored by using an esophageal pill electrode throughout tilting and during parasympathetic testing. RESULTS: Unexpectedly, seven patients had vasovagal responses at saddle support tilt testing, during which native heart rate decreased by 25 +/- 7 beats/min and mean arterial blood pressure decreased by 55 +/- 9 mm Hg. In three of these patients, there was also a decrease in donor heart rate of 23 +/- 26 beats/min. Parasympathetic testing showed possible evidence of donor heart vagal reinnervation in these patients with donor heart bradycardia during tilt but not in those with vasovagal reactions to tilt without slowing of the donor heart rate. CONCLUSIONS: Vagal efferent reinnervation can occur after orthotopic heart transplantation in humans. However, the absence of such reinnervation in some patients with vasovagal responses to tilt calls into question the role of left ventricular receptors in inducing the vasovagal reaction.
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The symptom most frequently requiring investigation and consideration for cardiac pacing is syncope. This symptom is now receiving more attention than ever, mainly because of the advent of tilt table testing--a simple noninvasive procedure that has substantially reduced the number of syncopal patients remaining undiagnosed. The first part of this review addresses developments in the understanding of syncope, and the latter part covers developments in the understanding and therapy of atrioventricular block and sinus node disease, the management of carotid sinus syndrome, and two possible new indications for pacemaker therapy.
Twenty-three adult patients with a columnar lined (Barrett's) oesophagus are being treated with long-term omeprazole, 40 mg daily. Twelve had never undergone anti-reflux surgery (Group 1), the other eleven having previously had insertion of an Angelchik anti-reflux prosthesis (Group 2). Endoscopy was carried out six months before, immediately before and six months, one year and two years into treatment. Multiple and standardized biopsies were taken at each endoscopy. Results from the two groups were similar. During the 6-month run-in period there was a statistically non-significant increase in the linear extent of the columnar mucosa, but this showed a progressive, statistically significant decrease during the two years of treatment. Other evidence for regression of the Barrett's mucosa includes the emergence of large numbers of macroscopic squamous islands within the abnormal mucosa, an increase in the number of microscopic squamous islands, and microscopic squamous encroachment of the abnormal mucosa at the squamo-columnar junction. Histological assessment showed a reduction in the proportion of sulphomucin-rich intestinal metaplasia, but this only achieved statistical significance in Group 1. The results substantiate the importance of acid in the pathogenesis of Barrett's oesophagus. Omeprazole may have a therapeutic role in bringing about regression of the metaplastic epithelium.
A new generic code, patterned after and compatible with the NASPE/BPEG Generic Pacemaker Code (NBG Code) was adopted by the NASPE Board of Trustees on January 23, 1993. It was developed by the NASPE Mode Code Committee, including members of the North American Society of Pacing and Electrophysiology (NASPE) and the British Pacing and Electrophysiology Group (BPEG). It is abbreviated as the NBD (for NASPE/BPEG Defibrillator) Code. It is intended for describing the capabilities and operation of implanted cardioverter defibrillators (ICDs) in conversation, record keeping, and device labeling, and incorporates four positions designating: (1) shock location; (2) antitachycardia pacing location; (3) means of tachycardia detection; and (4) antibradycardia pacing location. An additional Short Form, intended only for use in conversation, was defined as a concise means of distinguishing devices capable of shock alone, shock plus antibradycardia pacing, and shock plus antitachycardia and antibradycardia pacing.
AIMS: To develop and validate an analytical procedure for the quantitation of pepsins and gastricsin in human gastric juice and to assess its potential in a controlled gastric secretory study. METHODS: High performance ion-exchange chromatography was used to separate human pepsin 1, 3a, 3b, 3c and gastricsin from gastric juice. Computed chromatographic areas for each enzyme were quantified by relation to a known amount of a secondary standard porcine pepsin. The assay procedure was validated by recovery and analytical precision studies. Gastric secretions after pentagastrin and insulin stimulation from 10 patients with portal hypertension were used to assess the potential of the analytical procedure. RESULTS: The assay precision varied from 1.5 to 9.0% within batch and 7.5 to 18.1% between batch, with about 100% recoveries of porcine pepsin A from human gastric juice over the assay range 0.025-0.5 mg/ml. A fourfold increase in combined pepsin and gastricsin concentration was observed following pentagastrin and insulin stimulation. The mean percentage content of pepsins 3a, 3b, 3c, and 1 in non-stimulated gastric juice were 4%, 72%, 12% and 1.4%, respectively, and did not change significantly after gastric stimulation. An approximate doubling of the percentage of gastricsin (10% to 20%) relative to the pepsins was observed, however, after both insulin and pentagastrin stimulation. CONCLUSIONS: This procedure for quantifying individual human pepsins and gastricsin in gastric juice is simple and reliable. It may be of considerable importance in determining the mechanisms involved in the control and secretion of these digestive enzymes in man, including the effect of anti-ulcer drugs and our understanding of the pathophysiology of peptic ulcer disease.
Disorders of the autonomic nervous control mechanisms of heart rate and vascular tone may cause syncope. Notably these are carotid sinus and vasovagal syndromes. Knowledge of their aetiology is limited. Each presents cardioinhibition and vasodepression. Pacing offers benefit in cardioinhibition and the mode required is usually dual chamber (DDI) with rate hysteresis. Pacing is unable to control vasodepression. A wide variety of drugs has been proposed to combat the vasodepressor components of these syndromes but none is wholly successful.
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OBJECTIVE: The aim was to determine the exact sequence of hormone changes during the progression of fluid retention in a canine model of "congestive cardiac failure" induced by rapid right ventricular pacing, and during recovery when pacing is stopped. METHODS: Rapid ventricular pacing at a rate of 250 pulses.min-1 was used in six mongrel dogs with implanted right ventricular pacemakers. Right heart haemodynamics were measured by means of Swan Ganz catheterisation, allowing flow measurement by thermodilution and pressure measurement by external manometry. Plasma renin activity, arginine vasopressin, and atrial natriuretic factor were assayed on venous blood samples by radioimmunoassay. Noradrenaline was assayed by high pressure liquid chromatography. RESULTS: The onset of rapid pacing was accompanied by a fall in cardiac output and a rise in pulmonary arterial, pulmonary capillary wedge, and right atrial pressures. Noradrenaline and atrial natriuretic factor rose. Plasma renin activity showed an initial fall followed by a rise, and arginine vasopressin was unchanged in the first 8 h. When rapid pacing was continued for a further 35 d, clinical signs of fluid retention appeared by day 28, by which time cardiac output had fallen, and central pressures risen further. Atrial natriuretic factor peaked at around 14 d whereas plasma renin activity, arginine vasopressin, and noradrenaline tended to reach a plateau at about d 20 and then to show further increases as clinical signs of fluid retention appeared; this was most marked with plasma renin activity. Cessation of pacing at d 35 caused a rapid reversal (increase) of cardiac output but a more gradual reversal (decrease) of right heart pressures over 5 d; only wedge pressure returned to base line. Arginine vasopressin and plasma renin activity fell rapidly to around 40% of the final pacing levels and reached basal values after 8 h and 48 h respectively. Noradrenaline fell after 8 h and reached basal levels in 5 d. Atrial natriuretic factor fell quickly by 60% after 8 h but remained above basal levels for 5 d. At the end of pacing, body weight fell rapidly in conjunction with a large diuresis. CONCLUSIONS: These findings are compatible with a major role of one or more of renin, vasopressin, and noradrenaline in the pathophysiology of the fluid retention of heart failure; the manifestations are not counteracted by the rise in atrial natriuretic factor.