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Published on: May 24, 2020
The role of hemostasis in infective endocarditis
Emanuele Durante-Mangoni1, Rosa Molaro, Domenico Iossa
1Internal Medicine, University of Naples S.U.N., Monaldi Hospital, Via L. Bianchi snc, 80131, Naples, Italy, emanuele.durante@unina2.it.
Insights
Infective endocarditis (IE) involves the heart
Area of Science:
- Cardiovascular Medicine
- Hematology
- Infectious Diseases
Background:
- Infective endocarditis (IE) is a complex thromboinflammatory condition affecting the heart's inner lining.
- Its pathophysiology is intricately linked to the interaction between pathogens and the hemostasis system.
Purpose of the Study:
- To systematically review and appraise existing experimental and clinical data on the role of hemostasis in IE.
- To explore the interplay between microorganisms, hemostasis modifiers, and IE development.
- To propose a hypothesis regarding thrombophilia as a potential trigger for IE.
Main Methods:
- Comprehensive review of experimental and clinical studies.
- Analysis of the dual role of platelets in IE pathogenesis.
- Examination of microbial interactions with the hemostasis system and nonspecific changes during sepsis.
Main Results:
- Hemostasis plays a critical, multifaceted role in IE susceptibility, progression, and treatment.
- Platelets exhibit a dual function in the context of IE.
- Microbial interactions significantly influence the hemostasis system.
Conclusions:
- The hemostasis system is a crucial factor in infective endocarditis.
- Thrombophilia is hypothesized as a potential trigger for IE.
- Pharmacological modulation of hemostasis presents a promising, yet largely unexplored, therapeutic avenue for IE.
Abstract:
Infective endocarditis (IE) is a thromboinflammatory disease of the endocardium, with pathophysiology mostly the result of the interplay between microorganisms and modifiers of the hemostasis system. In this setting, the evidence gathered so far warrants a more systematic appraisal. In this review article, experimental and clinical data on the role of hemostasis in IE are summarized. Starting from the current pathogenetic model of IE, we discuss the dual role of platelets in this condition, the microbial interaction with the hemostasis system, also describing nonspecific hemostasis changes during sepsis. We finally propose our hypothesis of thrombophilia as a possible trigger of IE, highlighting the challenges that the study of hemostasis in IE presents. The role of hemostasis in IE appears to be an exciting field of research. The activity of the hemostasis system is highly relevant in terms of susceptibility, progression, and treatment of IE. Pharmacologic modulation of hemostasis before and after IE onset is possible and represents still a largely unexplored area of study.
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Endocarditis I: Introduction
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