Closed needle aspiration/biopsy was performed in 19 patients with suspected spinal disc space infection. A precise diagnosis was made, from the material obtained in 13 (68%); the infecting organism was isolated in 11 and malignant tumour diagnosed histologically in two. There were no important complications. The procedure which is described in detail is simple to perform and can be carried out early in the course of a patient's stay in hospital, thereby enabling prompt treatment.
Because it has been suggested that patients with obstructive sleep apnea have a narrower pharyngeal airway than normal persons, we performed lateral fluoroscopy and computed tomographic (CT) scans of the pharynx in patients with this syndrome. Fluoroscopy in 6 sleeping patients showed that the obstruction always began during inspiration when the soft palate touched the tongue and posterior pharyngeal wall. The CT scans in 9 awake subjects demonstrated that the narrowest section of the airway in patients and in control subjects was the region posterior to the soft palate. The cross-sectional area of this region was significantly narrower in patients than it was in control subjects (p less than 0.001). Because a narrow airway would be more likely to collapse during inspiration than a normal one would (Bernoulli's Principle), we conclude that the narrow airways we observed in awake patients may be an important contributing factor in the pathogenesis of obstructive sleep apnea.
SUMMARY In an attempt to assess the value of coronary sinus lactate estimation before and during atrial pacing for the diagnosis of obstructive coronary artery disease, 70 patients with angina were investigated in this way and by selective coronary arteriography. Thirty-five had radiologically normal coronary arteries and 35 had coronary artery disease. When the change in coronary arteriovenous lactate difference was less than 0-09 mmol/l (0.8 mg/100 ml) between the control and the peak atrial pacing sample, the coronary arteries were normal except in one patient who had distal disease of a single vessel. When the change was greater than 0-22 mmol/l (2.0 mg/100 ml) coronary artery disease was always found, and when the change was greater than 0 39 mmol/l (3.5 mg/100 ml) there was always disease of two or three vessels. Unfortunately, the presence or absence of coronary artery disease could not be predicted when the change fell between 0 09 and 0-22 mmol/l (0.8 and 2-0 mg/100 ml). Estimation of coronary sinus lactate before and during atrial pacing can thus frequently distinguish patients with normal coronary arteries from those with coronary artery disease.
SUMMARY Thirty-five patients with chest pain of sufficient severity to warrant coronary arteriography had normal coronary arteriograms. In each of them coronary sinus lactate was measured before and during atrial pacing. In 16 the lactate metabolism was normal as shown by a change between resting and peak pacing arteriovenous lactate difference of less than 0-09 mmol/l (0.8 mg/100 ml). Nineteen patients had abnormal lactate metabolism, the change being greater than 0-09 mmol/l (0.8 mg/100 ml). Sixteen (84%) of the group with abnormal lactate metabolism responded symptomatically to oral beta-blockade in contrast to only one patient in the normal group (P < 0.001). After 1 year all 16 patients with abnormal lactate metabolism who had responded to beta-blockade worsened when placebo was substituted. Fifteen of the 16 patients with normal lactate metabolism had become free of symptoms on no specific drug therapy; it is thus unlikely that their original pain was of cardiac origin.By estimating the coronary sinus lactate, it is, therefore, possible to divide patients with chest pain and normal coronary arteriograms into two groups. Those with pain ofnon-cardiac origin have normal lactate metabolism, are unlikely to respond to beta-blockade, and improve spontaneously. The group with abnormal lactate metabolism have genuine angina, usually respond to beta-blockade, and deteriorate when treatment is discontinued. Further observation is required to determine the prognosis of the two groups and to estimate the frequency of development of coronary artery disease.Up to 10 per cent of patients with suspected angina pectoris have normal coronary arteriograms (Kemp et al., 1973). Even when coronary arteries are normal, abnormal electrocardiograms at rest or on exercise and abnormal myocardial lactate metabolism after atrial pacing suggest myocardial ischaemia (Boudoulas et al., 1974;Richardson et al., 1974).We report here a series of 35 patients with chest pain who had normal coronary arteriograms. All had coronary sinus lactate estimations after atrial pacing to identify the development of anaerobic myocardial metabolism. Their response to treatment was also assessed. Patients and methods PATIENTSThirty-five patients, 16 men aged 26 to 58 years
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