HYPERCOAGULABILITY IN HEART FAILURE AND ITS ASSOCIATION WITH THROMBOTIC EVENTS: A SYSTEMATIC REVIEW
- 1Universidade de Fortaleza (UNIFOR), Fortaleza, CE, Brazil
Abstract
Introduction: Chronic heart failure promotes a hypercoagulable state through blood stasis, endothelial dysfunction, and inflammation, increasing thrombotic risk. This leads to elevated markers such as D-dimer and von Willebrand factor, which reflect cardiac stress. Additionally, platelet activation contributes to thrombogenesis, making these mechanisms essential for risk stratification and clinical management. Objectives: To evaluate the association between hypercoagulability in patients with heart failure and the occurrence of thrombotic events, as well as to investigate the role of coagulation abnormalities as potential underlying mechanisms. Methods: This systematic review followed PRISMA guidelines. It evaluated the relationship between heart failure-associated hypercoagulability and the occurrence of thrombotic events. Searches were conducted in PubMed, Cochrane, and Embase using MeSH and DeCS terms: “Heart Failure”, “Blood Coagulation Disorders”, “Thrombosis”, “Thromboembolism”, “Fibrinogen” and “D-Dimer”, combined with AND/OR, covering publications from 2016 to 2026. Results and Conclusion: A total of 755 studies were identified, of which 5 were included, comprising 6416 patients. Most studies were observational, including prospective cohorts and retrospective analyses. Coagulation biomarkers such as D-dimer and von Willebrand factor (vWF) were significantly associated with markers of cardiac stress, particularly NT-proBNP, but did not independently predict the development of heart failure (HF). In contrast, Platelet Distribution Width (PDW), a marker of platelet activation, emerged as an independent predictor of mortality and adverse outcomes, especially among patients with diabetes and anemia. In the setting of acute pulmonary embolism, HF with reduced ejection fraction was identified as an independent predictor of 7-day mortality. Additionally, among outpatients with continuous-flow left ventricular assist devices (CF-LVAD), anticoagulation control proved critical: INR values below 2.0 were associated with increased thrombotic risk, whereas an optimal INR around 2.6 provided a balance between thrombotic and bleeding events. Overall, systemic activation of coagulation appears to be a key downstream effect of neurohormonal activation in heart failure.
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BibTeX
@article{oliveira2026hypercoagulability,
title = {{HYPERCOAGULABILITY IN HEART FAILURE AND ITS ASSOCIATION WITH THROMBOTIC EVENTS: A SYSTEMATIC REVIEW}},
author = {Maria Eduarda SANTOS DE OLIVEIRA and Lara DAMASCENO DUARTE and Clarissa FREIRE COUTINHO and Arthur BARROS MIRANDA CILIÃO LUCENA and Thaís FACÓ DE CASTRO and Beatriz BARSI CUNHA and Letícia MATOS LEANDRO and Mariz Beatriz MAGALHÃES PINHO and Clara SIMÕES NOBRE and Lucas CARTAXO TAVARES},
journal = {Hematology, Transfusion and Cell Therapy},
year = {2026},
month = oct,
doi = {10.1016/j.htct.2026.108487},
url = {https://doi.org/10.1016/j.htct.2026.108487},
note = {CC BY},
}
RIS
TY - JOUR
TI - HYPERCOAGULABILITY IN HEART FAILURE AND ITS ASSOCIATION WITH THROMBOTIC EVENTS: A SYSTEMATIC REVIEW
AU - Maria Eduarda SANTOS DE OLIVEIRA
AU - Lara DAMASCENO DUARTE
AU - Clarissa FREIRE COUTINHO
AU - Arthur BARROS MIRANDA CILIÃO LUCENA
AU - Thaís FACÓ DE CASTRO
AU - Beatriz BARSI CUNHA
AU - Letícia MATOS LEANDRO
AU - Mariz Beatriz MAGALHÃES PINHO
AU - Clara SIMÕES NOBRE
AU - Lucas CARTAXO TAVARES
PY - 2026
DA - 2026/10/23
JO - Hematology, Transfusion and Cell Therapy
DO - 10.1016/j.htct.2026.108487
UR - https://doi.org/10.1016/j.htct.2026.108487
AB - Introduction: Chronic heart failure promotes a hypercoagulable state through blood stasis, endothelial dysfunction, and inflammation, increasing thrombotic risk. This leads to elevated markers such as D-dimer and von Willebrand factor, which reflect cardiac stress. Additionally, platelet activation contributes to thrombogenesis, making these mechanisms essential for risk stratification and clinical management. Objectives: To evaluate the association between hypercoagulability in patients with heart failure and the occurrence of thrombotic events, as well as to investigate the role of coagulation abnormalities as potential underlying mechanisms. Methods: This systematic review followed PRISMA guidelines. It evaluated the relationship between heart failure-associated hypercoagulability and the occurrence of thrombotic events. Searches were conducted in PubMed, Cochrane, and Embase using MeSH and DeCS terms: “Heart Failure”, “Blood Coagulation Disorders”, “Thrombosis”, “Thromboembolism”, “Fibrinogen” and “D-Dimer”, combined with AND/OR, covering publications from 2016 to 2026. Results and Conclusion: A total of 755 studies were identified, of which 5 were included, comprising 6416 patients. Most studies were observational, including prospective cohorts and retrospective analyses. Coagulation biomarkers such as D-dimer and von Willebrand factor (vWF) were significantly associated with markers of cardiac stress, particularly NT-proBNP, but did not independently predict the development of heart failure (HF). In contrast, Platelet Distribution Width (PDW), a marker of platelet activation, emerged as an independent predictor of mortality and adverse outcomes, especially among patients with diabetes and anemia. In the setting of acute pulmonary embolism, HF with reduced ejection fraction was identified as an independent predictor of 7-day mortality. Additionally, among outpatients with continuous-flow left ventricular assist devices (CF-LVAD), anticoagulation control proved critical: INR values below 2.0 were associated with increased thrombotic risk, whereas an optimal INR around 2.6 provided a balance between thrombotic and bleeding events. Overall, systemic activation of coagulation appears to be a key downstream effect of neurohormonal activation in heart failure.
SN - 2531-1379
SN - 2531-1387
ER -