Thromboembolic and bleeding risk in cardiac amyloidosis
(2024) In Journal of Thrombosis and Haemostasis 22(9). p.2381-2392- Abstract
Cardiac amyloidosis represents a spectrum of conditions characterized by the accumulation of insoluble fibrils, resulting in progressive deposition and myocardial dysfunction. The exact mechanisms contributing to the heightened risk of thromboembolic events and bleeding tendencies in cardiac amyloidosis remain unclear. Proteins such as transthyretin in transthyretin amyloidosis and light chains in light-chain amyloidosis, along with acute phase proteins in amyloid A (AA) amyloidosis, play complex roles in the coagulation cascade, affecting both coagulation initiation and fibrinolysis regulation. The increased occurrence of atrial fibrillation, systolic and diastolic left ventricular dysfunction, and atrial myopathy in patients with... (More)
Cardiac amyloidosis represents a spectrum of conditions characterized by the accumulation of insoluble fibrils, resulting in progressive deposition and myocardial dysfunction. The exact mechanisms contributing to the heightened risk of thromboembolic events and bleeding tendencies in cardiac amyloidosis remain unclear. Proteins such as transthyretin in transthyretin amyloidosis and light chains in light-chain amyloidosis, along with acute phase proteins in amyloid A (AA) amyloidosis, play complex roles in the coagulation cascade, affecting both coagulation initiation and fibrinolysis regulation. The increased occurrence of atrial fibrillation, systolic and diastolic left ventricular dysfunction, and atrial myopathy in patients with cardiac amyloidosis may predispose them to thrombus formation. This predisposition can occur regardless of sinus rhythm status or even with proper anticoagulant management. Bleeding events are often linked to amyloid deposits around blood vessels, which may increase capillary fragility and cause coagulation disturbances, leading to unstable international normalized ratio levels during anticoagulant therapy. Thus, comprehensive risk assessment for both thrombotic and hemorrhagic complications, especially before commencing anticoagulant therapy, is imperative. This review will explore the essential pathophysiological, epidemiologic, and clinical aspects of thromboembolic and bleeding risk in cardiac amyloidosis, evaluating the existing evidence and uncertainties regarding thrombotic and bleeding risk assessment and antithrombotic treatment.
(Less)
- author
- Tana, Marco ; Tana, Claudio ; Rossi, Davide ; Mantini, Cesare ; Gallina, Sabina ; Ricci, Fabrizio LU and Porreca, Ettore
- organization
- publishing date
- 2024-09
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- anticoagulants, cardiac amyloidosis, hemostasis, pathophysiology, thrombosis
- in
- Journal of Thrombosis and Haemostasis
- volume
- 22
- issue
- 9
- pages
- 12 pages
- publisher
- Wiley-Blackwell
- external identifiers
-
- pmid:38810701
- scopus:85196497869
- ISSN
- 1538-7933
- DOI
- 10.1016/j.jtha.2024.05.018
- language
- English
- LU publication?
- yes
- id
- 69fd7403-e7fb-4043-add2-45847e2aa895
- date added to LUP
- 2024-09-09 11:23:00
- date last changed
- 2024-09-09 11:24:20
@article{69fd7403-e7fb-4043-add2-45847e2aa895,
abstract = {{<p>Cardiac amyloidosis represents a spectrum of conditions characterized by the accumulation of insoluble fibrils, resulting in progressive deposition and myocardial dysfunction. The exact mechanisms contributing to the heightened risk of thromboembolic events and bleeding tendencies in cardiac amyloidosis remain unclear. Proteins such as transthyretin in transthyretin amyloidosis and light chains in light-chain amyloidosis, along with acute phase proteins in amyloid A (AA) amyloidosis, play complex roles in the coagulation cascade, affecting both coagulation initiation and fibrinolysis regulation. The increased occurrence of atrial fibrillation, systolic and diastolic left ventricular dysfunction, and atrial myopathy in patients with cardiac amyloidosis may predispose them to thrombus formation. This predisposition can occur regardless of sinus rhythm status or even with proper anticoagulant management. Bleeding events are often linked to amyloid deposits around blood vessels, which may increase capillary fragility and cause coagulation disturbances, leading to unstable international normalized ratio levels during anticoagulant therapy. Thus, comprehensive risk assessment for both thrombotic and hemorrhagic complications, especially before commencing anticoagulant therapy, is imperative. This review will explore the essential pathophysiological, epidemiologic, and clinical aspects of thromboembolic and bleeding risk in cardiac amyloidosis, evaluating the existing evidence and uncertainties regarding thrombotic and bleeding risk assessment and antithrombotic treatment.</p>}},
author = {{Tana, Marco and Tana, Claudio and Rossi, Davide and Mantini, Cesare and Gallina, Sabina and Ricci, Fabrizio and Porreca, Ettore}},
issn = {{1538-7933}},
keywords = {{anticoagulants; cardiac amyloidosis; hemostasis; pathophysiology; thrombosis}},
language = {{eng}},
number = {{9}},
pages = {{2381--2392}},
publisher = {{Wiley-Blackwell}},
series = {{Journal of Thrombosis and Haemostasis}},
title = {{Thromboembolic and bleeding risk in cardiac amyloidosis}},
url = {{http://dx.doi.org/10.1016/j.jtha.2024.05.018}},
doi = {{10.1016/j.jtha.2024.05.018}},
volume = {{22}},
year = {{2024}},
}