Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “SULFINPYRAZONE”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 793 records · Page 44Linked to original sources
PubMed1985

Clinical trials on the efficacy of pharmacologic intervention reducing mortality from cardiovascular diseases.

Results of recent clinical trials on secondary prevention of ischemic heart disease indicate that judicious, long-term administration of adrenergic beta blockers and platelet-active drugs such as aspirin and Persantine (dipyridamole) would seem to yield protection against mortality associated with acute myocardial infarction, including sudden death. These drugs are beneficial also in prevention of recurrent myocardial infarction, especially among patients with unstable angina. These drugs should be considered as soon as the diagnosis of myocardial infarction or unstable angina is confirmed clinically. In terms of primary prevention of ischemic heart disease and cerebrovascular disease (stroke), the results of the Hypertension Detection and Follow-Up Program provide an excellent set of data on the efficacy of rigorous treatment of hypertension, especially those with mild hypertension. To be effective, treatment must start before there is evidence of target end organ damage, such as left ventricular hypertrophy. Recent data from the Australian Therapeutic Trial in Mild Hypertension also confirms these findings.

Adrenergic beta-Antagonists↗
PubMed1987

Overview of completed sudden death trials: European experience.

Progress in understanding the epidemiology and mechanism of sudden cardiac death (SCD) has been rapid over the past two decades. This, together with the availability of drugs with actions that potentially may counter the pathophysiology of sudden death, has led to myriad trials aimed at prolonging life for high-risk individuals. European countries have contributed a major share both to the development of these drugs and to subsequent tests of their efficacy. Ventricular fibrillation (VF), either unheralded or secondary to fresh myocardial ischemia, is by far the most common cause of SCD. The classes of drugs with profiles that might be expected to influence the occurrence of VF directly are antiarrhythmics, calcium channel blockers, platelet-active agents, and beta-adrenoceptor antagonists. Twenty-four of the European trials that employed agents from these groups have special significance because of their design and size. Studies of two of the calcium channel blockers have not demonstrated any life-saving potential to date. One platelet-active agent - aspirin - has shown favorable trends. Results with the use of antiarrhythmic agents have been disappointing, probably because their adverse effects, including arrhythmogenesis in some patients, have countered the antiarrhythmic effects that other patients have achieved. Nevertheless, evidence suggests that lidocaine can reduce the incidence of VF; this can reasonably be equated with life-saving potential whenever defibrillation is not available. Trials with beta-blocking drugs have been the most encouraging; seven of the 11 trials that have been considered demonstrated a significant reduction in sudden death, which was variously defined, and a strong trend toward reduction was observed with another. None of the trials showed an unfavorable trend. The results of completed trials now offer practical guidance to physicians with responsibility for the care of patients with ischemic heart disease, especially those who have features that indicate high risk.

Adrenergic beta-Antagonists↗
PubMed1981

Haemostatic function changes in a trial on the secondary prevention of myocardial infarction with sulphinpyrazone.

The trend of some haemostatic parameters was investigated in a series of 186 myocardial infarction patients randomly allocated to sulphinpyrazone and placebo 15-25 days after the myocardial infarction episode in order to ascertain if one or more of these parameters may be considered as forecasting elements. The tests were performed a treatment allocation (basal values) and after 1, 6, and 12 months. In comparison with 44 healthy volunteers, the results have provided striking confirmation of 'hyperactive' platelets in the early phase of myocardial infarction expressed by the shorter bleeding time, increasing plasmatic beta-thromboglobulin, increased platelet factor 4 release and shorter heparin thrombin clotting time, and by the increased platelet sensitivity to threshold concentrations of adenosine diphosphate and collagen. Significant changes in bleeding time, platelet factor 4 release and heparin thrombin clotting time persist at successive testing times. Platelet aggregation by low collagen concentrations was inhibited in the sulphinpyrazone subsample patients.

Adult↗
PubMed1979

A study of the relationship between ex vivo and in vivo effects of sulphinpyrazone in the guinea pig.

In guinea pigs, sodium arachidonate-induced platelet aggregation ex vivo proved a more sensitive method for detecting drug-related effects after the administration of sulphinpyrazone than collagen-induced platelet aggregation. It was possible to detect inhibition of platelet aggregation after giving sulphinpyrazone orally in a single dose of 3 mg/kg. Excellent correlation was achieved between ex vivo and in vivo inhabition of platelet function with sulphinpyrozone using the Arthus reaction. The results are consistent with the formation, in the guinea pig of metabolites more potent than the parent molecule.

Administration, Oral↗
PubMed1981

The effects of two different dosage regimens of sulphinpyrazone on platelet function ex vivo and blood chemistry in man.

When sulphinpyrazone (either 200 mg q.d.s. for 7 days or 400 mg b.d.s. for 5 days) was administered to human volunteers, inhibition of platelet function was observed ex vivo. The inhibitory effect was measured by the increase in the concentration of sodium arachidonate required to cause platelet aggregation and a decrease in the biosynthesis by the platelets of malondialdehyde from added sodium arachidonate. ADP-induced primary platelet aggregation was statistically significantly inhibited only on 1 day of the two studies. The inhibitory effect did not correlate with the plasma concentrations of unchanged sulphinpyrazone nor with its sulphone metabolite but correlated with the plasma concentration of the thioether metabolite (r = 0.577, p less than 0.001). Platelet count, plasma fibrinogen, beta-thromboglobulin, urea and creatinine concentrations were not changed by the drug but there was a clinically insignificant increase in bleeding time in all but one subject.

Bleeding Time↗
PubMed1981

The effect of sulphinpyrazone and its metabolites on platelet function in vitro and ex vivo.

The thioether metabolite of sulphinpyrazone is between 8 and 13 times more potent than the parent compound as a competitive inhibitor of human, guinea pig and rabbit platelet aggregation induced by sodium arachidonate. Of the other known metabolites, the sulphone is approximately equipotent and the p-hydroxy compounds are much less potent that sulphinpyrazone itself. Malondialdehyde biosynthesis from sodium arachidonate by washed human platelets and collagen-induced aggregation of all three species is also inhibited by the thioether. It is 10 times more potent than sulphinpyrazone. ADP-induced aggregation is not affected by sulphinpyrazone, its thioether metabolite, nor the other metabolites. After intravenous administration of the thioether metabolite to groups of guinea pigs the inhibitory effect on sodium arachidonate-induced platelet aggregation ex vivo was long lasting (up to 24 h). In view of the recent information about the metabolism of sulphinpyrazone to its thioether in guinea pigs, we conclude that the thioether metabolite is the substance responsible for the prolonged effect of sulphinpyrazone on platelet fuction in this species and in man.

Animals↗
PubMed1975

Platelet survival time following aortic valve replacement.

Thromboembolism continues to complicate the course of patients following aortic valve replacement. In patients with prosthetic and homograft mitral valves, platelet survival time has been shown to correlate with occurrence of thromboembolism. This study extends these observations to patients with aortic valve disease. Platelet survival time was measured (by the chromium-51 method) in 73 patients with aortic valve disease. Eighteen patients were studied preoperatively and had platelet survival times of 3.4 plus or minus 0.14 days (mean plus or minus standard error of the mean), almost the same as normal (3.7 plus or minus 0.4 days). Platelet survival time was shortened (P less than 0.001) following aortic valve replacement with Starr-Edwards prosthesis - Model 1000: 2.5 plus or minus 0.13 days (N = 6); Model 1200-1260: 3.0 plus or minus 0.10 (n = 14); model 2300-2320: 3.0 plus or minus 0.15 days (N = 9) - and with stented aortic homografts: 3.0 plus or minus 0.10 days (N = 16). Platelet survival time was normal following aortic valve replacement in patients with directly sewn aortic homografts 3.7 dats plus or minus 0.24 days (N = 10). Eleven patients with Starr-Edwards prostheses had a history of thromboembolism and all also showed shortened platelet survival time (2.7 plus or minus 0.12 days, P less than 0.001), a measurement which was significantly different (P less than 0.01) from the 18 patients with Starr-Edwards prostheses and no thromboembolism (3.0 plus or minus 0.09 days). Platelet suppressant therapy prolonged platelet survival in eight patients with Starr-Edwards devices, thromboembolism, and shortened platelet survival time. These results suggest that insertion of Starr-Edwards valves and stented aortic homografts alter platelet survival time but that direct homografts do not. A correlation between occurrence of thromboembolism after aortic valve replacement and shortened platelet survival time has been shown.

Adult↗
PubMed1981

The randomized clinical trial: bias in analysis.

The realization that bias in patient selection may influence the results of clinical studies has helped to establish the randomized controlled clinical trial in medical research. However, bias can be equally important at other stages of a trial, especially at the time of analysis. Withdrawing patients from consideration in the analysis because of ineligibility on account of study entry criteria, lack of compliance to the protocol, or data of poor quality may be a source of systematic error. Examples to illustrate the possible consequences are taken from trials in the cardiovascular field. We recommended that reported study results should include outcome data from all subjects randomized in the group to which they were originally assigned.

Acute Disease↗