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Chronic Thromboembolic Pulmonary Hypertension and Assessment of Right Ventricular Function in the Piglet
Published on: November 4, 2015
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From Acute to Chronic Thromboembolic Disease
Timothy Fernandes1, Benjamin Planquette2, Olivier Sanchez2
11 Division of Pulmonary and Critical Care Medicine, University of California San Diego, La Jolla, California; and.
Annals of the American Thoracic Society
|August 30, 2016
Summary
Pulmonary emboli can lead to chronic thromboembolic pulmonary hypertension (CTEPH). Persistent perfusion defects after anticoagulation increase CTEPH risk, influenced by clinical factors and cellular pathways.
Area of Science:
- Pulmonary vascular disease
- Thromboembolic disorders
Background:
- Acute pulmonary embolism (PE) has variable outcomes, ranging from complete resolution to persistent perfusion defects.
- Persistent perfusion defects are necessary but not sufficient for developing chronic thromboembolic pulmonary hypertension (CTEPH).
- Approximately 30% of PE patients have persistent defects after 6 months of anticoagulation; 10% of these develop CTEPH.
Purpose of the Study:
- To review the natural history of acute pulmonary emboli.
- To identify risk factors and pathogenic mechanisms associated with persistent perfusion defects and CTEPH development.
- To inform future prevention and treatment strategies for CTEPH.
Main Methods:
- Review of literature on the natural history of acute pulmonary emboli.
- Analysis of clinical risk factors associated with persistent perfusion defects.
- Examination of cellular and molecular pathways involved in thrombus resolution failure.
Main Results:
- Clinical risk factors for persistent defects include older age, delayed anticoagulation, and larger initial thrombus size.
- Pathogenic mechanisms include impaired fibrinolysis, altered fibrinogen, inflammation, and embolic remodeling.
- Current fibrinolytic therapy at presentation has not consistently improved perfusion recovery.
Conclusions:
- Understanding the interplay between clinical factors and pathogenic mechanisms is crucial for preventing and treating CTEPH.
- Further research into thrombus resolution pathways may lead to improved therapeutic targets.
- Identifying patients at high risk for persistent defects and CTEPH is essential.
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