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Fibrinolysis is the body's process that prevents blood clots. The investigators hypothesize that patients presenting with acute pulmonary embolism (PE) or blood clots in the lungs differ in their fibrinolytic deficit phenotype. The investigators aim to use biomarkers directly involved in endogenous fibrinolytic cascade including PAI-1, Alpha-2-Antiplasmin (A2A), TAFI, D-dimer, and Fibrinogen to phenotypically characterize patients presenting with acute PE and to correlate these biomarkers with clinical, echocardiographic, computed tomography (CT), and functional status outcomes.
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Patients (n=100) identified by the Pulmonary Embolism Response Team (PERT) suffering from a PE will be identified by the PI. Blood plasma samples from these patients which have been drawn for routine lab tests will be identified and the Sub-I who will pick the samples up from the clinical lab after the routine analysis has been completed. These samples will be de-identified by giving them a study number. These samples will be recentrifuged and aliquoted. Samples will be stored in a -80ᵒC freezer in the Hemostasis & Thrombosis Research Laboratory. When all 100 de-identified samples have been collected they will be analyzed blindly by the technical staff of the hemostasis laboratory for the fibrinolytic parameters PAI-1, Alpha-2-Antiplasmin, TAFI, tPA, D-dimer, Plasminogen, and Fibrinogen. PAI-1 and TAFI will be quantified with an Enzyme Linked-Immuno-Sorbent Assay (ELISA), while A2A is measured using functional assay. PAI-1 is measured as ug/ml, while TAFI and A2A are measured as % of normal controls. Normal controls are derived from pooled normal human plasma from volunteers purchased from outside vendor. Results will be compiled and sent to the PERT team for analysis and correlation withclinical, echocardiographic, computed tomography (CT), and functional status outcomes.
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Amir Darki, MD
Data sourced from clinicaltrials.gov
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