Autor: |
Judith Kniffin, Marcia S. Foldes, William H. Baker, Harry L. Messmore, Jawed Fareed, Grace Squillaci |
Rok vydání: |
1981 |
Předmět: |
|
Zdroj: |
Oral Presentations. |
ISSN: |
2567-689X |
DOI: |
10.1055/s-0038-1653357 |
Popis: |
Activation of platelets as measured by monitoring thromboxane B2 levels, release specific proteins and quantitation of endogenous platelet aggregates has been reported in patients with angina pectoris. To study the relationship between the platelet-activation and intermittent claudication, 14 patients with demonstrated peripheral atherosclerosis were exercised to tolerance. Segmental limb pressures and platelet function studies were performed both pre and post exercise. A continuous EKG was recorded. All patients exhibited a drop in segmental limb pressures coinciding with complaints of claudication which was consistant with peripheral atherosclerosis. No significant alteration in the platelet release and aggregation pattern was noted in samples obtained prior to and immediately after exercise. Autoaggregation as measured by luminescence (luciferase-coupled) aggregometry to measure spontaneous ADP release and release specific proteins such as 3 thromboglobulin and platelet factor 4 also remained unchanged. Interestingly although 6 of 14 patients showed an abnormal exercise EKG, no angina pectoris was experienced. Although endogenous activation of platelets has been linked with anginal pain, the present study shows that platelet activation as studied by aggregation, release proteins and thromboxane measurement is not associated with intermittant claudication. The reduction in limb blood flow as evidenced by the drop in segmental pressures is most likely due to anatomic pathology rather than platelet mediated rheologic or vasospastic mechanisms. |
Databáze: |
OpenAIRE |
Externí odkaz: |
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