It has been suggested that manual removal of the placenta carries increased risk of endocarditis in cardiac patients.1 A small VSD may be a further risk factor. We feel there is a need for the two working parties to reach consensus, based on further objective assessment, on the indications for antibiotic prophylaxis against the risks of endocarditis during labour. an
R. M. EGDELL S. REID J. J. BENDING R. P. D. COOKE
Departments of Medicine and Microbiology, Eastbourne District General Hospital, East Sussex BN21 2UD, UK
Sugrue D, Blake S, Troy P, Macdonald D. Antibiotic prophylaxis against infective endocarditis after normal delivery-is it necessary? Br Heart J 1980; 44: 499-502. 2. McFaul PB, Dornan JC, Lank H, Bayle D. Pregnancy complicated by maternal heart disease: a review of 519 women. Br J Obstet Gynaecol 1988; 95: 861-67. 3. Working Party of the British Society for Antimicrobial Chemotherapy. Antibiotic prophylaxis of infective endocarditis. Lancet 1990; 335: 88-89. 4. Prevention of Bacterial Endocarditis. Recommendations by the American Heart Association. JAMA 1990; 264: 2919-22.
artery and vein samples are taken, it is impossible to confirm that a result comes from the artery and that sensible readings have been obtained. Perinatal Research Group, Department of Obstetrics, Plymouth General Hospital, Plymouth PL47JJ, UK
K. R. GREENE J. WESTGATE
1. STAN: an introduction. Molndal: Cinventa AB, 1992. 2. Westgate J, Keith RDF, Curnow JSH, Ifeachor EC, Greene KR. Suitability of fetal scalp electrodes for monitoring the fetal electrocardiogram during labour. Clin Phys Physiol Meas 1990; 11: 297-306. 3. Rosén KG, Murphy KW. How to assess fetal metabolic acidosis form cord samples.
J Perinat Med 1991;
Fetal ECG waveform for intrapartum
monitoring SIR,-We would like to reply to Dr Cockbum and colleagues’ (Sept 5, p 610) comments about the results of our randomised study (July 25, p 194) with respect to their experience with fetal
intrapartum ST waveform analysis. They do not provide details of their study design or of the numbers involved. However, they say that they record no reduction in operative intervention but a ten-fold reduction in fetal blood samples. There is the obvious possibility that they have substituted one intervention for another. As they point out, their method of monitoring is different from ours and we are concerned that in the fetal electrocardiogram (ECG) group they base this "wholly on the ST waveform". The interpretation model for clinical use of ST waveform has been carefully elucidated from clinical observational studies after laboratory animal studies and, as they know, depends on the use of both the CTG and the ST waveform. For example a raised ST waveform in the presence of a normal CTG needs no action, whereas a raised ST waveform plus an abnormal CTG does require action. How do they distinguish between the two? They therefore cannot comment on the use of fetal ECG monitoring with the ST waveform as proposed by ourselves and the manufacturers of the CTG/ST waveform recorder.1 The fetal physiological and pathophysiological events arising during labour are very complex (as shown by the enormous range of heart-rate patterns) and it would be remarkable if a single variable could convey fetal condition to the clinician. We have shown a highly significant difference in intervention rates for 1200 cases and this has continued to completion of the trial at 2400 cases (unpublished results). Subsequent analysis has revealed that results were significant at 600 cases. At 2400 cases we have also noted a significant reduction in total number of fetal blood samples which was not evident at 1200. The onus is now on others to repeat this trial to confirm or refute these data. We emphasise that the trial was done in a busy district general hospital and that all monitoring and clinical decision-making was done by the clinical staff on duty, on the basis of in-service training by research staff. Signal quality is important for ECG analysis and there is no substitute for correct application of a single spiral electrode.2 It is true that during the introduction of the ST analyser we provided technical trouble-shooting assistance to clinical staff, as should be done with the introduction of any new technology. This equipment is now used routinely without any special technical
Aortic distensibility and
hypercholesterolaemia SIR,—Dart et all reported that symptom-free adult patients with isolated hypercholesterolaemia have more distensible aortas than normocholesterolaemic controls. Using an echocardiographic technique of debatable accuracy, they found a positive correlation between low-density-lipoprotein (LDL) cholesterol and aortic distensibility in pooled data from hypercholesterolaemic and normocholesterolaemic subjects, such that an increase in LDLcholesterol was associated with an increase in aortic distensibility. We have measured blood-pressure-corrected aortic distensibility3 in 15 adult patients with heterozygous familial hypercholesterolaemia (FH) and 15 age and sex matched normocholesterolaemic controls with a computerised non-invasive pulse-wave-velocity doppler ultrasound technique.’ Symptom-free adults with FH had significantly less distensible aortas than normocholesterolaemic controls (unpaired t test p