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Primary Outcome Assessment in a Pig Model of Acute Myocardial Infarction
Published on: October 14, 2016
Alterations in prothrombin time and activated partial thromboplastin time in patients with acute myocardial
Haseeb A Khan1, Abdullah S Alhomida, Tamader Y Al Rammah
1Department of Biochemistry, College of Science,King Saud University Riyadh, Saudi Arabia.
Prothrombin time (PT) and activated partial thromboplastin time (aPTT) respectively measures the extrinsic and intrinsic pathways of coagulation and are used to determine the bleeding or clotting tendency of blood. We compared PT and aPTT levels in acute myocardial infarction (AMI) patients and normal subjects. There were significant increases in PT levels in patients with STEMI (15.98 ± 0.96 s), NSTEMI (16.03 ± 0.97 s) and chest pain (15.02 ± 0.54 s) as compared to control group (8.86 ± 0.08 s). The level of aPTT in control subjects was 31.35 ± 0.48 s. Patients with STEMI (40.79 ± 1.83 s), NSTEMI (41.33 ± 2.06) and chest pain (37.84 ± 1.66 s) showed significantly higher levels of aPTT. There was a significant correlation between PT and aPTT levels. Both PT and aPTT were significantly correlated with age however there was no correlation between these coagulation markers and gender or body mass index. In conclusion, both PT and aPTT are significantly increased in AMI patients on anticoagulation therapy. The elevations in PT values were more than 2.5-fold greater than aPTT suggesting a high potential of PT for predicting blood clotting tendency in patients receiving anticoagulation therapy.
Prothrombin time (PT) and activated partial thromboplastin time (aPTT) respectively measures the extrinsic and intrinsic pathways of coagulation and are used to determine the bleeding or clotting tendency of blood. We compared PT and aPTT levels in acute myocardial infarction (AMI) patients and normal subjects. There were significant increases in PT levels in patients with STEMI (15.98 ± 0.96 s), NSTEMI (16.03 ± 0.97 s) and chest pain (15.02 ± 0.54 s) as compared to control group (8.86 ± 0.08 s). The level of aPTT in control subjects was 31.35 ± 0.48 s. Patients with STEMI (40.79 ± 1.83 s), NSTEMI (41.33 ± 2.06) and chest pain (37.84 ± 1.66 s) showed significantly higher levels of aPTT. There was a significant correlation between PT and aPTT levels. Both PT and aPTT were significantly correlated with age however there was no correlation between these coagulation markers and gender or body mass index. In conclusion, both PT and aPTT are significantly increased in AMI patients on anticoagulation therapy. The elevations in PT values were more than 2.5-fold greater than aPTT suggesting a high potential of PT for predicting blood clotting tendency in patients receiving anticoagulation therapy.
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