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Biomedical subjects

S Sherry

Publications and source records attributed to S Sherry.

At least 37 records · Page 2Linked to original sources
PubMed1988

Unresolved clinical pharmacologic questions in thrombolytic therapy for acute myocardial infarction.

Thrombolytic therapy has now become established as a useful therapeutic measure for the immediate treatment of an acute evolving transmural infarction. Nevertheless, several important and fundamental aspects of a pharmacologic nature remain to be resolved. Prominent among these is whether or not fibrin specificity of a thrombolytic agent provides important benefits, and whether heparin therapy as commonly employed to prevent rethrombosis has been effective. Review of the available data raises serious questions as to the validity of current views and the appropriateness of prevailing trends.

Fibrin↗
PubMed1988

Anxiety, depression, and menstrual symptoms among freshman medical students.

Based on data from a larger longitudinal study of medical students and physicians, this study establishes the incidence of some menstrual symptoms in a nonclinical population of 82 healthy, female, first-year medical students and investigates the correlation of self-reported anxiety and depression scores with these symptoms. Findings show that nearly half reported the frequent occurrence of at least one menstrual symptom that appeared to cause discomfort but did not interfere with performance. The data suggest an association between anxiety and depression scores and certain self-reported menstrual symptoms in this population. The study suggests the need for further investigation of the nature of the relationship between dysphoric moods and menstrual symptoms in healthy women.

Adult↗
PubMed1987

Appraisal of various thrombolytic agents in the treatment of acute myocardial infarction.

The immediate therapeutic objective after the onset of symptoms of an evolving myocardial infarction is to stop the process from progressing. Evidence has accumulated that this can be accomplished by the early dissolution of the clot within an acutely thrombosed artery, resulting in reperfusion of the ischemic area. There are five clot-dissolving agents currently being evaluated by intravenous administration for their ability to dissolve coronary thrombi and to produce clinical benefit; all are plasminogen activators and each has distinctive properties. Streptokinase, because it has been the agent most extensively studied and its clinical benefits have been established, now serves as a standard for comparison with the others (anisoylated plasminogen-streptokinase activator complex, urokinase, recombinant tissue plasminogen activator, and recombinant pro-urokinase). It is apparent that each of the agents has advantages and disadvantages and that none has established its superiority over the others as of yet.

Anistreplase↗
PubMed1987

The FDA Advisory Panel's decision on rt-PA.

Considerable dissatisfaction has been expressed over the FDA's Cardio-renal Advisory Panel's recommendation on May 29, 1987 that approval of rt-PA as a thrombolytic agent for the treatment of acute myocardial infarction be delayed. Justification for the Advisory Panel's action appears to be based on a lack of adequate data supporting the clinical benefit and safety of a specific therapeutic regimen of rt-PA, i.e., its molecular form, dosage, and duration of therapy. Although not an issue in the Panel's decision, questions can be raised concerning claims that rt-PA, in comparison to streptokinase, is a safer agent as far as bleeding complications are concerned, and is twice as effective in dissolving coronary thrombi during a period of potential clinical benefit. Also to be considered is the association of its use with a higher incidence of rethrombosis and a much greater cost.

Myocardial Infarction↗
PubMed1987

Thrombolytic therapy in acute myocardial infarction. A perspective.

This paper deals with the history of thrombolytic therapy from its inception to its application in acute myocardial infarction. It describes the discovery of streptococcal fibrinolysin, followed by the elucidation of the plasma proteolytic enzyme system concerned with fibrinolysis. An outline is given of the therapeutic basis for the decision to concentrate on the development of activators of the enzyme, rather than the enzyme itself. Early attempts to demonstrate the value of streptokinase and urokinase in the treatment of myocardial infarction are examined. Finally, the more encouraging approaches in current use, especially the early application of thrombolytic therapy after the onset of the morbid event, are discussed.

Clinical Trials as Topic↗
PubMed1987

The fibrinolytic system and its pharmacologic activation for thrombolysis.

When in 1977 the Food and Drug Administration approved streptokinase for the treatment of deep vein thrombosis and pulmonary embolism, a new and exciting field of therapies was opened up for the clinician. In the period since the approval of streptokinase, the number of pharmacologic agents that activate the fibrinolytic system for thrombolysis has increased. Hence, this article reviews the history of this evolving field of therapies.

Fibrin↗
PubMed1987

Intra-arterial thrombolytic therapy in peripheral vascular disease.

This is a prospective analysis of patients undergoing 34 treatments for arterial thromboses and emboli with intra-arterial thrombolytic therapy. These included acute arterial thromboses, graft thromboses, arterial emboli and pulmonary emboli. Twenty-seven of 34 patients treated had evidence of lysis, 14 had complete lysis, 13 had partial lysis and seven had no lysis. Both patients with occlusions for longer than three weeks failed to respond to treatment. Thirty-two patients presented with ischemia of the extremity. Twenty-four of 32 patients had limb salvage with eight subsequently undergoing amputation. No patient who was treated for claudication or who had a patent popliteal artery distal to the acute thrombosis failed to respond. Extensive tibioperoneal occlusion generally responded poorly compared with femoropopliteal or more proximal thrombi. Complications are divided into direct (drug related) and indirect (technique related). Four of 34 patients had an extensive hemorrhagic event with two suffering intracranial bleeding who ultimately died. All of the patients with extensive hemorrhagic episodes had serum fibrinogen levels of less than 50 milligrams per cent. During infusion, extensive distal emboli occurred in three with two of these patients requiring thrombectomy; one instance resolved with infusion. Minor distal emboli occurred in three and all resolved with continued infusion. We believe that intra-arterial thrombolytic therapy is a valuable adjunct in the treatment of acute arterial occlusion. The local infusion of lytic agents appears to be more efficient than systemic therapy. The tip of the infusion catheter should be placed into the thrombus for optimal lysis, but not advanced too far. The fibrinogen level is a sensitive indicator of systemic lysis and should be maintained above 50 milligrams per cent. Systemic lysis is obtained even with low dose infusion when therapy exceeds six hours. Intra-arterial infusion of thrombolytic agents can be performed safely in the immediate postoperative period as well as intraoperatively if specific guidelines are followed. Patients with massive unilateral pulmonary embolism can be efficiently treated with intra-arterial lytic therapy.

Fibrinogen↗
PubMed1986

High-dose, brief-duration intravenous infusion of streptokinase in acute myocardial infarction: description of effects in the circulation.

The effects in the circulating blood of a 1-hour intravenous infusion of 1.5 X 10(6) units of streptokinase (SK) were measured during the subsequent 24-hour period in 7 patients with acute myocardial infarction. At the end of the infusion, the activator activity, expressed in SK units, averaged 65 U/ml, all of the plasminogen had disappeared, only a small amount of free plasmin was still present and functionally active alpha 2 antiplasmin had been reduced to 21% of the preinfusion level. All of the native fibrinogen had been degraded and the thrombin-coagulable protein was composed entirely of fragment X species, but the circulating plasma also contained significant amounts of the more extensively degraded fragments Y, D and E. The biologic half-life of the SK-induced activator activity was 23 minutes and that of the fibrinogen degradation products was 6.3 hours. The lytic effects persisted for 4 hours before any signs of recovery from the hemostatic defect were evident; considerable recovery was present at 25 hours.

Fibrin Fibrinogen Degradation Products↗