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A case of pulmonary embolism in which the diagnosis was aided by transthorasic echocardiography is described. Echocardiography may be helpful in emergency presentations, as ECG changes can be neither sensitive nor specific for the diagnosis of acute massive pulmonary embolism.

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OBJECTIVE: To evaluate the role of haemostatic and haemodynamic variables in left atrial thrombosis in non-rheumatic atrial fibrillation. DESIGN: Case-control study. SUBJECTS: One hundred and nine patients with non-rheumatic atrial fibrillation. INTERVENTIONS: Peak blood velocity measured at three sites in the left atrium. Venous blood sampled for coagulant proteins and markers of haemostatic activation. MAIN OUTCOME MEASURES: Presence of left atrial thrombus and spontaneous echo contrast at transoesophageal echocardiography. RESULTS: Left atrial thrombus was identified in 19 patients (18%), 16 of whom had spontaneous echo contrast. Patients with thrombus had reduced peak left atrial appendage velocity compared with those without (0.17 v 0.26 m/s; P < 0.001), but no significant reductions in peak mid-left atrial or mitral valve outflow velocity. Patients with thrombus had increased plasma markers of platelet activation-beta thromboglobulin (56.8 v 30.4 IU/ml; P < 0.001) and platelet factor 4 (6.1 v 3.5 IU/ml; P < 0.01)-and of thrombogenesis: thrombin-antithrombin complexes (5.59 v 3.06 micrograms/ml; P < 0.001) and D-dimers (479 v 298 ng/ml; P < 0.01). von Willebrand factor was also increased (1.81 v 1.52 IU/ml; P < 0.05). A multiple logistic regression model identified left atrial appendage velocity (P = 0.001), beta thromboglobulin (P = 0.002), and von Willebrand factor (P = 0.04) as the independent associates of left atrial thrombosis, ahead of the presence of spontaneous echo contrast. CONCLUSIONS: Haemostatic and haemodynamic abnormalities are associated with left atrial thrombus in non-rheumatic atrial fibrillation, and may help stratify thromboembolic risk.

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Diastolic dysfunction may be the earliest marker of a diabetes-induced heart muscle disease which leads to the progressive development of cardiac failure. Left ventricular diastolic function was indirectly assessed using pulsed wave Doppler ultrasound mitral-flow velocities in 20 normotensive patients with a new diagnosis of type 2 diabetes mellitus, normal cardiac function and no evidence of coronary artery disease and in 16 age-matched normal subjects. Peak velocities of early (E) and late (A) left ventricular filling were measured. The median (interquartile ranges) peak E/A ratio was significantly reduced in the diabetic group 0.96 (0.8-1.2) vs 1.2 (1.1-1.3), P < 0.01. Despite improvements in glycaemic control over 3 months, HbA1c 9.9% (7.6%-10.5%) to 7.4% (6.5%-7.9%), P < 0.001, maintained at 6 months, HbA1c 7.0% (6.4%-7.3%), there were no changes in the E/A ratio, 0.96 (0.83-1.15) and 0.95 (0.83-1.17), respectively. Furthermore, there was no correlation between percentage change in HbA1c and E/A ratio over 6 months. The results of this study suggest that in patients with type 2 diabetes mellitus and normal systolic function, diastolic function was impaired at diagnosis and was not affected by an improvement in the glycaemic control.

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PURPOSE: Short-term therapy with angiotensin converting enzyme (ACE) inhibitors for hypertension is effective and well tolerated, and compared with beta blockers, may cause fewer adverse reactions. Furthermore, enalapril has been observed to have a greater effect on systolic blood pressure than beta blockers. We therefore decided to compare the ACE inhibitor enalapril and the beta blocker atenolol as monotherapy in a double-blind study of patients with mild to moderate hypertension. PATIENTS AND METHODS: After a four-week placebo run-in period, 162 patients were allocated randomly to receive atenolol (50 to 100 mg daily) or enalapril (20 to 40 mg daily) for 12 weeks. To assess the influence of these drugs on quality of life, a series of psychologic tests was performed, and a subset of patients also underwent treadmill exercise and pulmonary function tests. RESULTS: In 147 patients who completed the study, enalapril reduced supine blood pressure by 19/12 mm Hg, compared with 9/7 mm Hg for atenolol (p less than 0.001/p less than 0.005). The modest blood pressure response to atenolol was not due to poor compliance. A target blood pressure of 140/90 mm Hg or less was achieved by 35 percent of enalapril-treated atenolol (p less than 0.01). The frequency and severity of adverse effects with the two drugs were similar, and few important differences emerged from the quality-of-life assessments. CONCLUSION: At the doses used, enalapril induced a greater short-term blood pressure response than atenolol; long-term studies of its safety and efficacy are required.

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A failure of the usual increase in plasma adrenaline and noradrenaline concentrations during submaximal exercise has been suggested as a contributory cause of exercise induced asthma. Six normal subjects and six asthmatic patients underwent a standard graded maximal exercise test. Measurements of oxygen consumption, minute ventilation, exercise time, blood lactate concentration, and heart rate indicated that the two groups achieved similarly high work loads during exercise. Mean FEV1 fell by 20% in asthmatic patients after exercise. Basal plasma adrenaline concentrations (nmol/l) increased in normal subjects from 0.05 to 2.7 and in asthmatic patients from 0.12 to 1.6 at peak exercise. Noradrenaline concentrations (nmol/l) increased in normal subjects from 2.0 to 14.3 and in asthmatic patients from 1.9 to 13.7 at peak exercise. The increases in adrenaline and noradrenaline in the asthmatic patients did not differ significantly from the increases in normal subjects. Thus a reduced sympathoadrenal response to exercise seems unlikely to be an important mechanism in the pathogenesis of exercise induced asthma.

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The effect of selectivity of beta-adrenoceptor antagonists on resting and post-exercise airway calibre in normal subjects was studied. Eight normal subjects were given atenolol 50 mg, propranolol 80 mg and placebo orally, in random order, double-blind. Specific airways conductance and flow-volume curves (partial and complete) were recorded before, 2 hours after drug administration and after exercise. Neither beta-adrenoceptor antagonist had a measurable effect on lung function tests at rest. The post-exercise increase in flow rates measured from partial flow volume curves was inhibited by propranolol but not by the beta-1-selective adrenoceptor antagonist atenolol, whereas both drugs caused a decrease in specific airways conductance after exercise. Beta-adrenoceptor antagonists may have a dual effect on airway calibre. Firstly, a direct effect on the beta-2 receptors in airway smooth muscle may occur. Secondly, beta-adrenoceptor blockade may, in the large airways, inhibit vagal pre-junctional beta-1 receptors which normally inhibit acetylcholine release at the nerve ending, thereby permitting vagally-induced airway narrowing.

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Airway, cardiovascular and metabolic responses were measured in six asthmatic patients with stable asthma during separate adrenaline, noradrenaline and control infusions. Four incremental infusion rates (4, 10, 25 and 62.5 ng min-1 kg-1) produced circulating catecholamine concentrations within the physiological range. Specific airways conductance and maximal expiratory flow rates measured from complete and partial flow-volume curves increased significantly (P less than 0.05) during adrenaline infusion, in a dose-response manner. No changes in specific airways conductance or maximal expiratory flow rates were seen during the noradrenaline or control infusion. The highest adrenaline infusion rate caused a rise in systolic blood pressure (P less than 0.05) and plasma glucose (P less than 0.05) and a fall in plasma potassium (P less than 0.05). Noradrenaline infusion caused a slight increase in diastolic blood pressure (P less than 0.05) but no metabolic changes. No cardiovascular or metabolic changes occurred during the control infusion. Infused adrenaline, producing circulating concentrations within the physiological range, caused dose-related bronchodilatation in asthmatic patients. Circulating noradrenaline does not appear to have a role in the control of basal airway tone in asthmatic patients.

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Twenty-six patients, mean age 20.5 years (range 11-33 years) at last assessment or death, attended an adult cystic fibrosis clinic between 1975 and 1983. Twenty-one presented in infancy, and 5 later (3-17 years). Most morbidity was due to recurrent respiratory infection and 5 of the 7 deaths were from respiratory failure. Cor pulmonale occurred in 4 patients, pneumothorax in 3 and severe haemoptysis necessitating lobectomy in 2. Declining spirometric values and persistent isolation of Pseudomonas aeruginosa from sputum samples were associated with a poor prognosis. Minor gastrointestinal symptoms were common (19 patients). Four patients developed intestinal obstruction. Six patients had abnormal liver function tests and one patient died from hepatic cirrhosis. Diabetes was diagnosed in 3 patients and 9 patients experienced joint pains. The prognosis and quality of life for patients with cystic fibrosis appear to be improving, and all but 2 of the patients attending the clinic are at school, university or are employed.

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Airway, cardiovascular and metabolic responses were measured in six normal subjects during separate infusions of adrenaline and noradrenaline. Four incremental infusion rates of the catecholamines (4, 10, 25 and 62.5 ng X kg-1 X min-1) produced circulating levels of adrenaline and noradrenaline within the physiological range. Maximal expiratory flow rates at 25% of vital capacity measured from partial flow-volume curves increased sequentially with increasing adrenaline concentration. Increases in maximal expiratory flow rates at 25% and 50% of vital capacity measured from complete flow-volume curves were not statistically significant, nor were the changes in specific conductance. Small but insignificant changes were observed in heart rate and blood pressure during adrenaline infusion. Plasma glucose increased and serum potassium fell during adrenaline infusion. No significant airway, cardiovascular or metabolic responses were seen during noradrenaline infusion. These results suggest that adrenaline, at concentrations found in physiological circumstances, influences flow rates in small airways. Circulating noradrenaline does not appear to be important in the control of airway calibre in normal subjects.

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One hundred patients undergoing routine fibreoptic bronchoscopy were randomly allocated to receive premedication with either intramuscular papaveretum or oral temazepam in a double-blind manner. They all received atropine before and oxygen during the procedure. Patients found the drugs equally acceptable in terms of discomfort, anxiety and the possibility of repeat bronchoscopy, but more had recall of the procedure with papaveretum. There was no difference in secretions, coughing, relaxation and consciousness, as assessed by the bronchoscopist, but patients who had received papaveretum were more cooperative. Arterial blood gases were performed before and 45 minutes after bronchoscopy. Those given papaveretum had a significant fall in mean arterial oxygen tension of 0.96 kPa, while there was no significant change in the temazepam group. There was also a small mean rise in arterial carbon dioxide tension in both groups, with the mean rise in the papaveretum group (0.625 kPa) being significantly higher than the temazepam group (0.2 kPa). Premedication with temazepam is a useful alternative to papaveretum and has the advantage of oral administration and causing less respiratory depression.

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1 TIaramide, an anti-inflammatory drug, inhibits the action of mediators released from mast cells and has direct smooth muscle relaxant properties. It may therefore have a beneficial effect in asthma. 2 A double-blind crossover trial comparing the bronchodilator activity of tiaramide and placebo over 16 days was undertaken in 13 patients with asthma. 3 Peak expiratory flow rate (PEFR) was recorded on three separate occasions every day and frequency of salbutamol aerosol usage was noted on a diary card. 4 During treatment with tiaramide the mean mid-morning PEFR (362 1/min) was higher than mean PEFR on placebo (328) (P less than 0.001) as was the evening PEFR (378) compared with placebo (388) (P less than 0.001). 5 There was a significant reduction in daily use of the salbutamol inhaler whilst on tiaramide (1.8) compared with placebo (2.3) (P less than 0.05). 6. Tiaramide may be a useful addition to existing prophylactic treatment for asthma.

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Ten patients with exercise-induced asthma participated in a single-blind dose-response study comparing the protective effect of inhaled sodium cromoglycate in increasing concentrations from 2 to 40 mg/ml. Saline was used as a control. Effects were assessed from the mean maximal percentage fall in forced expiratory volume in one second (FEV1) after the patients had run on a treadmill for eight minutes. There was slight bronchodilation evident from the increase in baseline FEV1 after inhalation of sodium cromoglycate, the difference reaching statistical significance with the highest concentration (5.7%, p less than 0.05). After exercise the maximal percentage falls in FEV1 (means and SEM) after saline and after sodium cromoglycate at 2, 10, 20, and 40 mg/ml were 37.3 +/- 4.7, 17.3 +/- 4.1, 10 +/- 3.3, 7.6 +/- 2.4, and 12 +/- 2.9. Sodium cromoglycate inhibited the exercise-induced fall in FEV1 at all the concentrations used in the study (p less than 0.001) and its inhibitory effect increased from 2 to 20 mg/ml. The mean FEV1 returned to baseline values within 15 minutes at higher concentrations of sodium cromoglycate (20 and 40 mg/ml) and a small bronchodilator effect was noted at 30 minutes. The findings suggest that the protective effect of sodium cromoglycate in exercise asthma is dose related. At higher concentration the drug suppresses chemical mediator release from the lung mast cells and may also modify the bronchial reactivity to release mediators.

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