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Biomedical subjects

C M Travill

Publications and source records attributed to C M Travill.

10 recordsLinked to original sources
PubMed1993

Coarctation of the aorta life and health 20-44 years after surgical repair.

OBJECTIVE: To examine the health and lifestyle of a group of patients who had repair of coarctation of the aorta 20-44 years ago (these were the first such operations in the United Kingdom) and to see how the results would influence current management strategies. DESIGN: Attempts were made to contact all patients by questionnaire. They were then requested to attend for a clinical examination. SETTING: Patients had their initial surgery at the Westminster Hospital (by Charles Drew) and the follow up examination at the same hospital. PATIENTS: 149 operations were performed. 70 of the 106 patients presumed to be alive were traced and 62 replied. 42 attended for examination. Only patients with the diagnosis of simple coarctation were included. Some patients had had coincidental ligation of a patent ductus arteriosus but none had any other cardiac abnormality requiring surgical or medical treatment. Those who died during the follow up period were described in paper by Bobby et al (Br Heart J 1991;65:271-6). MAIN OUTCOME MEASURES: Current symptoms and life situations, evidence of cardiac disease, further cardiac surgery, current and retrospective blood pressures, and Doppler echocardiographic examination. RESULTS: 29 (69%) had cardiovascular disorder. Doppler echocardiography did not show previously unrecognised major recoarctation. 19 (46%) had hypertension at follow up and there was evidence of enlargement of the aortic root or arch in seven (16%) patients, who tended to have had surgery at a later age. No evidence of cerebrovascular accident was found. CONCLUSIONS: In this group of patients with surgically repaired simple coarctation, late morbidity (particularly aortic aneurysm, aortic valve disease, and ischaemic heart disease) was common. The incidence of intracranial haemorrhage seemed to have been reduced by surgical repair. The integrity of the surgery remained good. Many patients did not have any regular cardiovascular review. Long-term anxiety related to early surgical experiences was evident. Even after apparently successful surgical repair of aortic coarctation. It would be prudent for all patients to have long-term review.

Adult↗
PubMed1992

Haemodynamic and neurohumoral response in heart failure produced by rapid ventricular pacing.

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.

Animals↗
PubMed1991

The incidence of malignant vasovagal syndrome in patients with recurrent syncope.

We reviewed 322 patients with recurrent syncope between 1984 and 1988. Investigation included limited intracardiac electrophysiological study in all cases with programmed extra-stimulus studies in 48 cases. In 93 patients (29%), all investigations were normal, (including negative extrastimulus in 30). In the other 229 cases syncope was explained by AV-block (n = 111, 34%), sinus node disease (n = 68, 21%), carotid sinus syndrome (n = 32, 10%) and inducible sustained tachyarrhythmia (n = 18, 6%). Prolonged 60 degrees head-up tilt was performed in 71 out of 93 patients with unexplained syncope, and reproduced vasovagal syncope and presenting symptoms in 53 (75%), or 16% of the whole population reported. These patients were diagnosed as having malignant vasovagal syndrome. Positive tilts were significantly less common in a group of 27 subjects of similar age without a history of syncope (7%), and a random sample of 37 patients with atrioventricular block (n = 16), sick sinus syndrome (n = 18) and inducible tachyarrhythmia (n = 3), (19%, 11% and 0% respectively, P less than 0.01). From this retrospective review it appears, therefore, that tilt testing is a valuable provocative tool for vasovagal syncope and may reduce the number of syncopal patients that remain undiagnosed, although these early observations do not allow an exact appraisal of the sensitivity and specificity of the tilt test.

Arrhythmias, Cardiac↗
PubMed1991

Natural history of sinus node chronotropy in paced patients.

The natural history of chronotropic incompetence is not clear. To assess this, we evaluated corrected sinus node recovery time (cSNRT) and sinus node chronotropy at rest and during exercise in two groups of syncopal patients with sinus node disease. Group A comprised patients with resting bradycardia but normal cSNRT and group B had resting bradycardia and prolonged cSNRT (greater than 1000 ms). An additional two groups (C and D) were studied. Group C comprised patients with complete AV (CAVB) and no evidence of sinus node disease and group D were asymptomatic controls of similar age. At diagnosis, patients with symptomatic bradycardia but normal cSNRT and no evidence of carotid sinus syndrome (group A) had resting bradycardia and impaired peak heart rate (PHR-I) on exercise compared to controls (P less than 0.001 and P less than 0.05, respectively), but no reduction in exercise duration. At follow-up group A patients demonstrated an increase in resting rate that was significantly slower than the controls (P less than 0.01). Peak heart rate (PHR-II) also remained significantly slower (P less than 0.05). There was no difference in exercise duration between groups A and D at follow-up. Group B was further subdivided according to follow-up findings of preservation of atrial activity in seven patients (group B-1) and junctional rhythm without any atrial activity in four patients (group B-2). Retrospective analysis showed no significant difference in resting heart rate at initial examination but group B-2 showed a significantly lower peak heart rate on exercise compared with B-1 (P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1990

Recurrent symptoms after ventricular pacing in unexplained syncope.

We report clinical and hemodynamic data in two cases of recurrent syncope. Both patients received permanent demand ventricular pacing (VVI) for unexplained syncope. Both patients experienced recurrent syncope after pacemaker implantation. They later underwent 60 degrees head-up tilt testing, initially noninvasively and then with hemodynamic profile. A vasovagal response to tilt occurred with bradycardia and was complicated by the onset of ventricular pacing and retrograde atrioventricular conduction (RAVC) with hemodynamic deterioration and rapid reproduction of syncope. Limited intracardiac electrophysiological study (EPS) excluded atrioventricular (AV) conduction disease, sinus node disease, and carotid sinus syndrome, and confirmed RAVC. Both patients were upgraded to dual chamber pacing, DDI mode, with 50/80 rate hysteresis. One patient was asymptomatic at repeat tilt testing; the other experienced continued symptoms due to the vasodepressor component of vasovagal syncope. Cardiac pacing alone is ineffective treatment for this phenomenon, and no proven therapy is presently available. Ventricular pacing applied to patients with unexplained syncope may lead to an increase in or continuation of symptoms rather than an amelioration. There is a need for full investigation of such patients, which must include tilt testing, to allow for the most accurate diagnosis possible and guide the most appropriate therapy.

Aged↗
PubMed1990

Mechanisms of impaired excretion of a fluid load after cardiac denervation in dogs.

The influence of cardiac innervation on the renal response to volume expansion was investigated. Systemic hemodynamic, plasma hormone, and renal clearance measurements were made before, during, and after intravenous administration of 1,000 ml 0.9% saline over 10 min to six control and six cardiac-denervated, chloralose-anesthetized mongrel dogs. Volume expansion resulted in a two- to threefold rise in plasma atrial natriuretic peptide (ANP) concentrations and a 50% rise in glomerular filtration rate (GFR) in both groups. Plasma renin activity (PRA) and plasma arginine vasopressin remained higher throughout in cardiac-denervated compared with control dogs. The marked increases in urine flow rate and sodium and free water clearances seen in the controls were attenuated or abolished after cardiac denervation. These differences were due to the influence of higher PRA and vasopressin in these animals compared with the controls, rather than differences in hemodynamic responses operating via GFR or in direct humoral responses via ANP secretion.

Animals↗
PubMedDate not supplied

The inotropic and hemodynamic effects of intravenous milrinone when reflex adrenergic stimulation is suppressed by beta-adrenergic blockade.

Milrinone is an inotropic and vasodilator agent proven to be effective in the treatment of heart failure. This study evaluated whether milrinone produces inotropic and hemodynamic effects independent of reflex adrenergic stimulation. Eleven stable heart failure patients (New York Heart Association class II to III) undergoing cardiac catheterization received intravenous (i.v.) milrinone (50 micrograms/kg for 10 minutes followed by 0.5 micrograms/kg/min for 50 minutes) during beta-adrenergic blockade. After beta-blockade with a 50-mg oral dose of metoprolol, heart rate decreased by a mean of 16.6%. The peak inotropic response to i.v. milrinone measured using the maximum rate of rise of left ventricular pressure (LV dP/dt) was fully developed at 20 minutes. Mean absolute inotropic response of LV dP/dt from baseline was statistically significant at 10, 20, 30, and 40 minutes (P < 0.05). Mean percentage increase in cardiac index from baseline was statistically significant at 20 and 30 minutes, and mean absolute decline from baseline for pulmonary capillary wedge pressure was statistically significant at 20 and 40 minutes (P < 0.05). The inotropic and hemodynamic effects of i.v. milrinone were thus preserved during beta-adrenergic blockade. This finding is consistent with a mechanism of action of i.v. milrinone--myocardial phosphodiesterase inhibition--that is independent of reflex adrenergic stimulation.

Adrenergic beta-Antagonists↗