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Hypercoagulation detected by routine and global laboratory hemostasis assays in patients with infective endocarditis
Ekaterina M Koltsova1,2, Maria A Sorokina1, Alexandra S Pisaryuk3,4
1Dmitry Rogachev National Medical Research Center of Pediatric Hematology, Oncology and Immunology, Moscow, Russian Federation.
Insights
Infective endocarditis (IE) involves hypercoagulability and platelet activation. Some patients show hypocoagulation, possibly indicating consumption coagulopathy, but genetic factors did not link to embolism or mortality in this IE study.
Area of Science:
- Cardiovascular Medicine
- Hematology
- Infectious Diseases
Background:
- The coagulation system plays a critical role in infective endocarditis (IE) vegetation development and embolization.
- Understanding coagulation and platelet status in IE is crucial for managing complications.
Purpose of the Study:
- To assess coagulation and platelet status in IE patients using diverse laboratory assays.
- To investigate the role of prothrombotic genetic polymorphisms in IE-related embolization and mortality.
Main Methods:
- 37 IE patients were studied, assessing coagulation via standard assays (APTT, prothrombin, fibrinogen, D-dimer) and integral assays (TEG, TD).
- Platelet functional activity was evaluated using flow cytometry.
- Genetic polymorphisms in coagulation system genes were analyzed.
Main Results:
- Elevated fibrinogen and fibrinogen-dependent TEG/TD parameters indicated systemic inflammation in IE patients.
- Most patients exhibited hypercoagulation, evidenced by clot growth rate and D-dimer levels.
- Some patients presented with hypocoagulation (prothrombin, TEG, TD), and resting platelets showed activation; decreased fibrinogen/TD correlated with fatal outcomes, while decreased TEG R parameter indicated embolism. No genetic associations were found.
Conclusions:
- IE is generally characterized by hypercoagulability and platelet pre-activation.
- A subset of IE patients may develop a hypocoagulant profile, potentially signifying consumption coagulopathy.
- Genetic polymorphisms were not associated with embolism or mortality in this IE cohort.
Background:
Coagulation system is heavily involved into the process of infective endocarditis (IE) vegetation formation and can facilitate further embolization. In this study we aimed to assess the coagulation and platelet state in IE implementing a wide range of standard and global laboratory assays. We also aim to determine whether prothrombotic genetic polymorphisms play any role in embolization and mortality in IE patients.
Methods:
37 patients with IE were enrolled into the study. Coagulation was assessed using standard coagulation assays (activated partial thromboplastin time (APTT), prothrombin, fibrinogen, D-dimer concentrations) and integral assays (thromboelastography (TEG) and thrombodynamics (TD)). Platelet functional activity was estimated by flow cytometry. Single nuclear polymorphisms of coagulation system genes were studied.
Results:
Fibrinogen concentration and fibrinogen-dependent parameters of TEG and TD were increased in patients indicating systemic inflammation. In majority of patients clot growth rate in thrombodynamics was significantly shifted towards hypercoagulation in consistency with D-dimers elevation. However, in some patients prothrombin, thromboelastography and thrombodynamics were shifted towards hypocoagulation. Resting platelets were characterized by glycoprotein IIb-IIIa activation and degranulation. In patients with fatal IE, we observed a significant decrease in fibrinogen and thrombodynamics. In patients with embolism, we observed a significant decrease in the TEG R parameter. No association of embolism or mortality with genetic polymorphisms was found in our cohort.
Conclusions:
Our findings suggest that coagulation in patients with infective endocarditis is characterized by general hypercoagulability and platelet pre-activation. Some patients, however, have hypocoagulant coagulation profile, which presumably can indicate progressing of hypercoagulation into consumption coagulopathy.
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