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1.
Thromb Res ; 184: 67-76, 2019 Dec.
Article in English | MEDLINE | ID: mdl-31710860

ABSTRACT

Surviving an embolism exposes patients to potential long-term complications, such as altered quality of life, persistent dyspnea, impaired exercise capacity or pulmonary hypertension. The common objective factor in most of these situations is the presence of residual pulmonary vascular obstruction (RPVO). Planar ventilation/perfusion scintigraphy (V/Q lung scan) is the gold standard for assessing RPVO, which occurs in 46 to 66% of patients at 3 months and persists in 25 to 29% of patients a year after acute PE. Assessed early (i.e. before discharge), RPVO could predict acute PE development with a high negative predictive value. Evaluated after anticoagulation therapy, RPVO could help to manage anticoagulation treatment and predict the risk of PE recurrence and patients identified at risk of developing chronic thromboembolic pulmonary hypertension. In this comprehensive review, we provide an overview of the current knowledge of RPVO after PE from imaging diagnosis to clinical consequences. In the first part, we mainly focus on the imaging modalities capable of detecting and quantifying RPVO. We then focus on the symptoms and syndromes linked with this residual obstruction after PE. Although the occurrence of RPVO and long-term complications varies greatly from one patient to another, we finally aim to identify the patients and diseases at risk of developing residual obstruction.


Subject(s)
Lung/blood supply , Pulmonary Embolism/complications , Pulmonary Embolism/diagnostic imaging , Thrombosis/diagnostic imaging , Thrombosis/etiology , Vascular Diseases/diagnostic imaging , Vascular Diseases/etiology , Female , Humans , Male , Pulmonary Embolism/pathology , Risk Factors
2.
Rev Pneumol Clin ; 72(1): 49-60, 2016 Feb.
Article in French | MEDLINE | ID: mdl-26657351

ABSTRACT

This general review deals with the mechanisms which underlie the genetic factors in COPD. Many cellular and biochemical mechanisms occur in bronchial inflammation. We present the experimental models of COPD, insisting on the importance of oxydative stress, and on recent knowledge about the lung microbiome. Starting from this pathophysiology basis, we show how various genetic targets are able to interfere with the disease model. Thanks to these genetic targets, new markers in exhaled breath condensates and new drug targets are rising.


Subject(s)
Pulmonary Disease, Chronic Obstructive/pathology , Disease Progression , Disease Susceptibility , Environment , Epithelial Cells/pathology , Humans , Lung/pathology , Lung/physiopathology , Oxidative Stress/genetics , Oxidative Stress/physiology , Pulmonary Disease, Chronic Obstructive/etiology
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