[Peroral nitroglycerin preparations with long-term effect in angina pectoris].
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Biomedical subjects
Publications and source records attributed to E Kjøller.
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A group of 43 consecutive patients with AMI were randomized to treatment with a novel platelet inhibitor, ticlopidine, or placebo in a double blind study. Treatment was started within 12 hr after onset of precordial pain. Patients who had taken drugs with known platelet inhibitory effect prior to the onset of therapy were excluded. Platelet survival time (PS) was measured 24-36 hr after onset of precordial pain and after 3 months of treatment in both groups. In the early phase of AMI CK-MB and ASAT were taken twice daily for estimation of infarction size. Platelet function, coagulation factors and fibrinolysis parameters were followed sequentially for 21 days and repeated after 3 months. In the placebo group a significant reduction in PS (5.62 +/- 1.63 S. D. days) was measured in the acute phase of AMI compared to PS 3 months after infarction (8.03 +/- 1.20 S.D. days). In the ticlopidine group PS was normal during the acute phase (8.35 +/- 1.82 S.D. days). After 3 months of treatment PS was normal in both groups. During the first two weeks after AMI significant changes in coagulation parameters and fibrinolysis indicated an increased risk of thrombosis in both groups. These parameters were unaffected by the platelet inhibitory therapy. Estimated by peak CK-MB and ASAT, infarction size was significantly reduced in the ticlopidine group.
14 patients with effort induced angina pectoris were treated with a specific TxB2 inhibitor Dazoxiben or verapamil for two weeks with a wash-out period of 14 days between the two regimens. A sub-maximal bicycle test was performed before treatment and at the end of each treatment period. The bicycle test induced a significant increase in serum TxB2 in patients without treatment and during verapamil therapy. This increase was significantly inhibited by Dazoxiben treatment. No alterations in plasma TxB2 or 6-keto-PGF1 alpha were observed on either regimen. Dazoxiben had no clinical effect, while verapamil caused a highly significant prolongation of exercise time.
A case of non-nosocomial, spontaneously occurring endocarditis caused by growth of Stomatococcus mucilaginosus on a prolapsed mitral valve is reported. Despite the organism's high susceptibility in vitro the patient responded slowly to antibiotic treatment. Colony adherence to agar surface and absent or weak catalase reaction differentiated this gram-positive coccus from coagulase-negative staphylococci and micrococci.
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The influence of propranolol on blood flow in peripheral tissues was studied in 10 normotensive subjects. Adequacy of beta-blockade was ascertained by an ergometric test. Perfusion of the subcutaneous tissue and skeletal muscle was measured by the local 133Xe-washout technique. The arteriolar dilatation underlying the autoregulatory response to a decrease in arterial perfusion pressurehead was not affected by beta-blockade. Propranolol did not change the magnitude of arteriolar constriction elicited by the local sympathetic veno-arteriolar reflex. Thus, the locally induced increase in the discharge rate along the peripheral sympathetic adrenergic fibres did not lead to measurable change in beta-receptor activity. The present results indicate that local bloodflow regulatory mechanisms are not affected by propranolol. They also indicate that the direct peripheral effects of propranolol are of no clinical importance in normotensive subjects in the supine position, when the general activity in the sympathetic nervous system is low.
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In 14 patients with coronary heart disease the effect of long-term treatment (mean 16 months, range 12-33) with alprenolol on platelet function and fibrinolytic activity was studied. While on the beta-blocker and two weeks after gradual withdrawal of it, the patients performed a bicycle-ergometer test and blood samples were obtained before and following exercise. Pre-exercise fibrinolytic activity, assessed by the euglobulin clot lysis time, was 183 +/- 27 min (mean +/- SEM) while on alprenolol as compared to 111 +/- 18 min (p less than 0.01) after its withdrawal. Activation of fibrinolysis following exercise was not significantly influenced by alprenolol. In patients treated with alprenolol, the pre-exercise threshold level of ADP, producing platelet aggregation was 3.3 muM (geometric mean) and 5.1 muM after stopping treatment (p less than or equal to 0.05). In patients receiving the beta-blocker, the ADP- threshold value dropped from 3.3 muM before exercise to 2.3 muM immediately after exercise (not significant). The corresponding values after withdrawal of alprenolol were 5.1 muM and 2.7 muM (p less than or equal to 0.02). Adrenaline - stimulated aggregation was not significantly influenced by alprenolol. Serotonin release from platelets following maximal ADP- and adrenaline stimuli was not significantly changed by exercise in patients on beta-blockade. After stopping treatment, ADP-induced serotonin release was 22 +/- 4.1% before and 15 +/- 4.7% after exercise (p less than 0.02). the corresponding values using the adrenaline stimulus were 29 +/- 5.7% and 17 +/- 4.7% (p less than 0.05). It is suggested that during physical stress alprenolol may protect platelets against aggregatory stimuli.
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