Biomedical subjects
Publications and source records attributed to N P Lewis.
Many florid physical signs of aortic regurgitation have been described. We describe a florid investigational finding of virtually monotonous intracardiac reverberation originating at the aortic valve leaflets.
The cardiorespiratory responses to maximal treadmill exercise were compared in matched groups of patients with chronic renal anaemia or treated chronic heart failure, and in normal controls. Exercise capacity was similarly reduced in both patient groups compared to normal controls, the raised respiratory exchange ratio at peak exercise implying anaerobic metabolism due to limited oxygen delivery in heart failure and limited oxygen carrying capacity in anaemia. Minute ventilation (VE) was related linearly to minute CO2 production (VCO2) in all subjects (each r > 0.92) from all three groups. The slope of the VE/VCO2 relationship was normal in anaemia but steeper in heart failure, reflecting ventilation/perfusion mismatching in chronic heart failure.
The cardiorespiratory responses to exercise and forced hyperventilation were measured in 17 unselected patients with syndrome X (angina, positive exercise test, normal coronary arteriogram, no other cardiovascular disease) and compared with those in 15 healthy subjects. Forced hyperventilation produced hypocapnia and metabolic alkalosis but no chest pain or electrocardiographic change. Patients with syndrome X showed reduced maximum oxygen consumption with an increased respiratory exchange ratio at peak exercise, confirming that exercise was limited by skeletal muscle perfusion--and thus that the increase in cardiac output with exercise is limited in syndrome X as in heart failure. Arterial carbon dioxide tension (PCO2) homoeostasis during exercise was normal but the ventilatory cost of carbon dioxide excretion was increased in syndrome X (as in heart failure). End tidal PCO2 measurements correlated only poorly with arterial PCO2 in individual patients with syndrome X, providing a possible explanation for previous reports, based on end tidal PCO2 of inappropriate hyperventilation. Patients with syndrome X did not show inappropriate hyperventilation but they did show hyperventilation that was appropriate to maintain normal arterial PCO2 in the face of reduced cardiac reserve.
OBJECTIVE: To determine how severe tricuspid regurgitation influences exercise capacity and functional state in patients who have undergone successful mitral valve replacement for rheumatic mitral valve disease. DESIGN: 9 patients in whom clinically significant tricuspid regurgitation developed late after mitral valve replacement were compared with 9 patients with no clinical evidence of tricuspid regurgitation. The two groups were matched for preoperative clinical and haemodynamic variables. Patients were assessed by conventional echocardiography, Doppler echocardiography, and a maximal treadmill exercise test in which expired gas was monitored by mass spectrometry. SETTING: University Hospital of Wales, Cardiff. SUBJECTS: 18 patients who had been reviewed regularly since mitral valve replacement. MAIN OUTCOME MEASURE: Objective indices of exercise performance including exercise duration, maximal oxygen consumption, anaerobic threshold, and ventilatory response to exercise. RESULTS: Mitral valve prosthetic function was normal in all patients and estimated pulmonary artery systolic pressure and left ventricular function were similar in the two groups. Right ventricular diameter (median (range) 5.0 (4.3-5.6) v 3.7 (3.0-5.4) cm, p less than 0.01) and the incidence of paradoxical septal motion (9/9 v 3/9, p less than 0.01) were greater in the group with severe tricuspid regurgitation. Exercise performance--assessed by exercise duration (6.3 (5.0-10.7) v 12.7 (7.2-16.0) min, p less than 0.01), maximum oxygen consumption (11.2 (7.3-17.8) v 17.7 (11.8-21.4) ml min-1 kg-1, p less than 0.01), and anaerobic threshold (8.3 (4.6-11.4) v 0.7 (7.3-15.5) ml min-1 kg-1, p less than 0.05)--was significantly reduced in the group with severe tricuspid regurgitation. The ventilatory response to exercise was greater in patients with tricuspid regurgitation (minute ventilation at the same minute carbon dioxide production (41.0 (29.9-59.5) v 33.6 (26.8-39.3) l/min, p less than 0.01). CONCLUSIONS: Clinically significant tricuspid regurgitation may develop late after successful mitral valve replacement and in the absence of residual pulmonary hypertension, prosthetic dysfunction, or significant left ventricular impairment. Patients in whom severe tricuspid regurgitation developed had a considerable reduction in exercise capacity caused by an impaired cardiac output response to exercise and therefore experienced a poor functional outcome. The extent to which this was attributable to the tricuspid regurgitation itself or alternatively to the consequences of right ventricular dysfunction was not clear and requires further investigation.
The long-term cardiorespiratory effects of recombinant human erythropoietin treatment were investigated in ten haemodialysis patients by means of maximum exercise testing, lung function tests, echocardiography, chest X-ray, and rheological assessment over 12 months. There were significant rises in exercise time (mean [SD] 13.2 [5.5] to 20.0 [6.2] min), maximum oxygen consumption (19.1 [7.0] to 25.0 [6.7] ml.min-1.kg-1), and anaerobic threshold (11.7 [3.6] to 15.4 [4.8] ml.min-1.kg-1) after 2 months of erythropoietin treatment. The improvements were maintained but not augmented on repeat testing after 4, 8, and 12 months of therapy. Carbon monoxide transfer [corrected] rose from 15.5 (2.9) to 18.6 (3.7) ml.min-1.mm Hg-1. There was a substantial reduction in exercise-induced cardiac ischaemia (eight patients had significant ST segment depression before erythropoietin, only one after 2 months' treatment, and none after 12 months' treatment), despite a significant rise in whole blood viscosity. Left ventricular mass, as estimated by echocardiography, progressively decreased from 354 (169) g to 251 (95) g after 12 months' treatment, and four patients showed a reduction in cardiothoracic ratio on chest X-ray.
Fifteen severely anaemic patients receiving CAPD were treated with subcutaneous recombinant human erythropoietin (Epo). Ten subjects had a good response with the haemoglobin concentration increasing from less than 8 g/dl to greater than 10 g/dl within 16 weeks. Four patients had a poor response, which was due to infection in two, myelofibrosis in one and unknown cause in another. Epo was ineffective in the remaining individual, probably due to the presence of occult metastatic carcinoma. Iron supplementation in the form of intravenous iron dextran was given to 12 patients when transferrin saturation decreased below 20%. There was a significant increase in red cell volume (P less than 0.005), with a decrease in plasma volume (P less than 0.005). Red cell iron turnover increased (P less than 0.05) but there was no change in red cell lifespan or deformability. Biochemical parameters remained unaltered, as did peritoneal function. Exercise duration improved (P less than 0.001), as did maximal oxygen consumption (P less than 0.01). Four patients required an increased dose of hypotensive drugs. Epo is a safe effective therapy for the anaemia of CAPD subjects.
A pair of identical twins presented almost simultaneously at age 62 years with calcific aortic stenosis requiring surgery, one with bicuspid and one with tricuspid aortic valve. This suggests that bicuspid morphology may perhaps not be the cause, but may be a genetically linked marker of an inherited predisposition to calcific stenosis.
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1. Seventeen normal subjects were tilted on a tilt table and changes in blood pressure, heart rate and renal function were monitored in the absence of drug treatment; the same measurements were repeated during treatment with enalapril in eight of these subjects. 2. In the absence of drug, tilting of the whole body to the 45 degree head up position caused an antidiuresis, antinatriuresis and antikaliuresis; the antinatriuresis resulted from a transient fall in glomerular filtration and from a sustained increase in the tubular reabsorption of sodium, as reflected by a prolonged fall in fractional sodium excretion. 3. Enalapril caused a reduction in blood pressure in the upright position; there was no effect on heart rate. The antinatriuresis of tilt was significantly blunted by enalapril. This resulted from blunting of the transient fall in creatinine clearance and of the increase in tubular sodium reabsorption. Urinary potassium excretion during tilting was not altered by enalapril. 4. These findings are consistent with a direct intrarenal action of angiotensin II, mediating some of the alterations in renal function apparent on assumption of the upright position.
A mass with a diameter of 0.8 cm was detected in the aortic root of a 53 year old woman during routine preoperative cross sectional echocardiographic assessment of a secundum atrial septal defect. Intraoperative epicardial echocardiography showed that the mass was attached by a slender stalk to the tip of the left coronary cusp of the aortic valve, and histological examination showed that it was a papillary tumour. Intraoperative epicardial echocardiography can help in planning the excision of papillary tumours, and excision is advised even when there are no symptoms.
3H-Angiotensin II binding was studied in rat renal proximal tubular basolateral membranes. The characteristics of binding were found to be consistent with a receptor for angiotensin II at this site. Effects of angiotensin II on cAMP production were studied in the basolateral membranes. Angiotensin II had no effect on the time course of basal or parathyroid hormone stimulated cAMP production in basolateral membranes. Angiotensin II did not exhibit a concentration-dependent effect on cAMP production in basolateral membranes, either alone or in the presence of parathyroid hormone. The concentration-response curves of cAMP production in response to parathyroid hormone in basolateral membranes were similar in the presence or in the absence of angiotensin II. We conclude that adenylate cyclase production is not linked to the receptor for angiotensin II in rat renal proximal tubular basolateral membranes.
Basolateral membranes were prepared from rat renal cortex by density gradient centrifugation. Their purity was confirmed by electron microscopy and by marker enzyme enrichment. The basolateral membrane preparation was shown to be derived predominantly from the proximal renal tubule by measurement of hormone-stimulated adenylate cyclase; marked stimulation of adenylate cyclase was found with parathyroid hormone, but not with isoprenaline, antidiuretic hormone or calcitonin. A single class of specific high-affinity [3H]angiotensin II-binding site was identified in the basolateral membrane preparation which, after correction of results for tracer degradation, showed equilibrium dissociation constant of 0.23 nmol/l and binding site concentration of 485.8 fmol/mg protein. Binding sites for [3H]angiotensin II were measured in basolateral membranes prepared from rats fed diets with a low, normal or high sodium content. A trend of increased binding site density with reduced sodium intake was found which did not reach statistical significance. No effect on affinity was demonstrated. Treatment of rats on a low-sodium diet with captopril (500 mg/l drinking water) caused a significant reduction in binding site density; no effect on affinity was demonstrated. These findings suggest that the density of angiotensin II receptors at this site is altered by the activity of the renin-angiotensin system.
A patient in whom recurrence of Graves' disease after treatment with carbimazole was diagnosed after a disease-free interval of 31 years.
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