Background: The objective measurement of exercise tolerance is an important component of heart failure trials. The use of laboratory-based treadmill exercise testing has attracted criticism, however, as being unrepresentative of patients' true capabilities. Aim: To examine the relationships between tests of exercise capacity, quality of life and haemodynamics in patients with stable symptomatic heart failure. Methods: Thirty-six patients with mild-moderate chronic heart failure were studied. Exercise capacity was assessed in the laboratory by maximal treadmill tests and self-paced corridor walk tests, and in the patients' homes by hipborne pedometers. Quality of life was assessed by a disease-specific questionnaire. Cardiac output and limb blood flow were measured by non-invasive techniques. Results: Customary activity as assessed by pedometer scores correlated with quality of life questionnaire scores (r s0.47, Ps0.04), and both variables correlated with limb (calf) blood flow (pedometer scores: r s0.39, S SPs0.03; quality of life scores: r s0.50, Ps0.04). The laboratory-based maximal treadmill test correlated with the self-paced S corridor walk test, but neither of these tests correlated with pedometer scores, quality of life or haemodynamics. Conclusions: Different methods of assessing exercise capacity do not appear to give comparable results and bear different relationships to haemodynamic variables and quality of life. Pedometer scores of customary activity may better reflect patients' quality of life and appear to be more closely related to limb blood flow than the maximal treadmill exercise test or the corridor walk test. The sole use of laboratory-based exercise tests in therapeutic trials may give a misleading assessment of treatment efficacy in heart failure patients. ᮊ
To quantitate embolic risk we studied a retrospective series of 61 patients with strictly defined bacterial endocarditis. Eighteen patients had neurological complications attributable to cerebral embolism. Seventeen embolic episodes occurred prior to antibiotic treatment and 8 episodes after its commencement. The rate of embolism per patient-week during a 20-week observation period showed a highly significant almost 4-fold reduction to a low level soon after antibiotics were started. Patients already on anticoagulation for prosthetic valves had the same embolic risk as those not so treated. The evidence suggests that anticoagulation at the time of diagnosis of bacterial endocarditis is not warranted.
Transient neurological disturbances occurring in patients with disseminated sclerosis have recently been receiving increasing attention (Andermann, Cosgrove, Lloyd-Smith, and Walters, 1959;Espir, Watkins, and Smith, 1966). Espir et al. (1966) described six patients with frequent short-lived attacks of dysarthria with or without other symptoms of brain-stem dysfunction. The nature of the attacks was not clear, but by analogy with trigeminal neuralgia they were treated with phenytoin (Epanutin) and carbamazepine (Tegretol) (Espir et al., 1966;Kuroiwa and Shibasaki, 1967; Espir and Walker, 1967 There was bilateral optic atrophy and first degree nystagmus to right and left and on vertical gaze. Tone was slightly reduced in the arms and increased in the legs. Power was normal. There was cerebellar ataxia of all four limbs. The tendon reflexes were pathologically brisk, with bilateral extensor plantar responses. Sensory testing revealed subjective diminution of vibration sensibility in the legs. His gait was spastic and ataxic.Each attack lasted for 15 to 20 seconds and consisted of diplopia, a severe scanning and slurring dysarthria, and severe ataxia of Lhe right arm and leg. If he were talking when an attack started he became almost unintelligible; if walking, he was forced to stop and seek support to prevent a fall. The attacks were of sudden onset and cessation and were not accompanied by any clouding of consciousness. They were sometimes precipitated by emotional stress, but no other factors appeared to influence their timing, frequency, or content.As a test of co-ordination of the right hand the patient was requested to draw a regular sine curve on moving paper (Fig. 1), and to copy a paragraph from a journal (Fig. 2)
Background: The AT receptor antagonists differ from the angiotensin converting enzyme inhibitors by achieving a more 1 complete blockade of angiotensin II's actions and by not affecting bradykinin metabolism. There is little information on whether this causes clinically significant differences in haemodynamics, neurohormones and exercise tolerance in heart failure. Aims: To compare the effects of losartan and captopril upon central and regional haemodynamics, neurohormones and exercise capacity in heart failure. Methods: In a double-blind, randomised trial 18 patients aged G 65 years with symptomatic Ž . Ž . heart failure were allocated to treatment with losartan 10 patients or captopril eight patients . Patients underwent assessment at baseline, after the first dose, at 12 weeks and at 24 weeks. Results: Systolic blood pressure fell by y10.7% 1 h Ž . Ž . after captopril 6.25 mg Ps 0.007 and by y4.8% 3 h after losartan 12.5 mg Ps 0.02 . The blood pressure reduction was Ž . sustained with losartan at 12 and 24 weeks. Systemic vascular resistance fell acutely after captopril y16.4%, Ps 0.01 . Ž . Captopril caused an acute and sustained rise in superior mesenteric artery blood flow q22.9%, Ps 0.04 , and a slower rise in Ž . renal artery blood flow q31.7%, Ps 0.01 . Losartan had no acute effects on regional haemodynamics but had increased Ž . superior mesenteric artery blood flow by 38.1% at 12 weeks Ps 0.02 . There were no substantial differences between losartan and captopril, and no changes occurred in neurohormones or exercise capacity. Conclusion: No substantial differences were observed between losartan and captopril on central or regional haemodynamics, neurohormones or exercise capacity in elderly patients with stable symptomatic heart failure. ᮊ
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