[Atherosclerosis, an inflammatory disease]. / L'athérosclérose, une maladie inflammatoire.

Chronic inflammation is recognized as a contributing factor to the development, progression and complications of atherosclerosis. The inflammatory nature of atherosclerosis has been proven by the presence of inflammatory cells, cytokines and chemokines at all stages of the disease. There is a widely accepted association between cardiovascular events and serum inflammatory markers, such as CRP, IL-6 and IL-1? produced via the inflammasome pathway. The involvement of inflammatory processes in atherosclerosis and progress in the therapeutic strategy are detailed in the article.

: L'inflammation chronique est reconnue comme un facteur contribuant au développement, à la progression et aux complications de l'athérosclérose. La nature inflammatoire de l'athérosclérose a été prouvée par la présence de cellules inflammatoires, de cytokines et chimiokines à tous les stades de celle-ci. Il existe une association largement acceptée entre les événements cardiovasculaires et les marqueurs inflammatoires sériques tels que la CRP, l'IL-6 et l'IL-1? produite via la voie de l'inflammasome. L'implication des processus inflammatoires dans l'athérosclérose et les progrès dans la stratégie thérapeutique sont détaillés dans l'article.

[European guidelines for the diagnosis and management of acute pulmonary embolism]. / Recommandations européennes concernant le diagnostic de l'embolie pulmonaire.

Pulmonary embolism (PE) is the third cause of cardiovascular death in industrialized countries. The difficulty lies on the diagnosis and is linked to the clinical pre-sentation which is often non-specific. The use of diagnostic scores and paraclinical examinations help the clinician in the management and assessment of the risk of death. This article aims to optimize knowledge and management of pulmonary embolism by revising the latest recommendations from the European Society of Cardiology 2019.

L'embolie pulmonaire (EP) représente la troisième cause de décès cardiovasculaire dans les pays industrialisés. La difficulté réside dans le diagnostic et est liée à la présentation clinique qui est souvent aspécifique. L'utilisation de scores diagnostiques et d'examens paracliniques permet d'aider le clinicien dans la prise en charge et l'évaluation du risque de mortalité. Cet article a pour objectif d'optimaliser les connaissances et la prise en charge de l'embolie pulmonaire en parcourant les dernières recommandations de la Société Européenne de Cardiologie de 2019.

Veno-venous extracorporeal CO2 removal improves pulmonary hemodynamics in a porcine ARDS model.

BACKGROUND: Protective lung ventilation is recommended in patients with acute respiratory distress syndrome (ARDS) to minimize additional injuries to the lung. However, hypercapnic acidosis resulting from ventilation at lower tidal volume enhances pulmonary hypertension and might induce right ventricular (RV) failure. We investigated if extracorporeal veno-venous CO2 removal therapy could have beneficial effects on pulmonary circulation and RV function. METHODS: This study was performed on an experimental model of ARDS obtained in eight anaesthetized pigs connected to a volume-cycled ventilator. A micromanometer-tipped catheter was inserted into the main pulmonary artery and an admittance micromanometer-tipped catheter was inserted into the right ventricle. RV-arterial coupling was derived from RV pressure-volume loops. ARDS was obtained by repeated bronchoalveolar lavage. Protective ventilation was then achieved, and the pigs were connected to a pump-driven extracorporeal membrane oxygenator (PALP, Maquet, Germany) in order to achieve CO2 removal. RESULTS: ARDS induced severe hypercapnic acidosis. Systolic pulmonary artery pressure significantly increased from 29.6±1.8 to 43.9±2.0 mmHg (P<0.001). After the PALP was started, acidosis was corrected and normocarbia was maintained despite protective ventilation. Pulmonary artery pressure significantly decreased to 31.6±3.2 mmHg (P<0.001) and RV-arterial coupling significantly improved (RV-arterial coupling index=1.03±0.33 vs. 0.55±0.41, P<0.05). CONCLUSION: Veno-venous CO2 removal therapy enabled protective ventilation while maintaining normocarbia during ARDS. CO2 removal decreased pulmonary hypertension and improved RV function. This technique may be an effective lung- and RV-protective adjunct to mechanical ventilation.