Use of RAS inhibitors in patients with COVID-19

Some concerns about the prescription of drugs acting on the renin-angiotensin system (RAS) have emerged due to SARS COV2 and COVID-19 pandemic and the revelation of the fundamental role of ACE2 (angiotensin-converting enzyme 2) in COVID-19 infection. Indeed, SARS COV2 utilizes ACE2 as a membrane receptor to enter target cells. Consequently, the question arises whether RAS modulating drugs impact the risk of developing severe or fatal severe acute respiratory syndrome in case of COVID-19 infection.  Here we discuss the evidence avilable on the impact of angiotensin-converting enzyme 1 inhibitors (ACEi) versus angiotensin II type 1 receptor blockers (ARB). Based on the currently available evidences, and as recommended by several medical societies, ACEi or ARB should not be systematically discontinued because to date no safety signal was raised with the use of these drugs.

Alexandre J, Cracowski JL, Richard V, Bouhanick B; French Society of Pharmacology and Therapeutics (SFPT). Drugs acting on renin angiotensin system and use in ill patients with COVID-19. Therapie. 2020;75(4):319-325.

doi: 10.1016/j.therap.2020.05.009.. PMID: 32553503

Gene Expression of Protein Tyrosine Phosphatase 1B and Endoplasmic Reticulum Stress During Septic Shock

Protein Tyrosine Phosphatase 1B (PTP1B) and endoplasmic reticulum stress (ERS) are involved in the septic inflammatory response. Their inhibition is associated with improved survival in murine models of sepsis. In a recent publication in Frontiers in Medicine Dr Clavier et al showed in a study of 40 patients with septic shock that gene expression variation in blood samples of PTPN1 and ATF6  partly correlate with the evolution of septic organ failure and with markers of endothelial dysfunction. The recent identification of PTP1B as a novel negative regulator of host defense against sepsis may have potential therapeutic implications. However, further studies are needed to better understand PTP1B and ERS implication during sepsis in humans.


Mechanisms of Acute Decompensation of Heart Failure

In a recent study from our laboratory, Pr Paul Mulder and colleagues have developed a new animal model of acute cardiac decompensation induced by salt overload. Using this model, they investigated whether heart rate reduction (HRR) opposes the acute decompensation‐related aggravation of cardiovascular dysfunction. Briefly, they found that acute HRR, induced by the If current inhibitor S38844, opposes cardiac decompensation by preventing aggravation of cardiovascular dysfunction, including reduced myocardial tissue perfusion and coronary relaxation. Importantly, the protective effects of HRR persist beyond the transient treatment, and led to partial prevention of the development of pulmonary congestion. Whether early transient HRR induced by If current inhibitors or other bradycardic agents, i.e. beta‐blockers, exerts beneficial effects in human ADHF warrants further investigation.

ESC Heart Failure

Thesis defense 2019

logo presThis autumn four PhD students have defended their thesis in our laboratory:

- Mouad Hamzaoui
- Bérénice Colleville
- Frédéric Roca
- Matthieu Leuillier



20191126 Mouad

Dr Mouad Hamzaoui (Dir. Dominique Guerrot)

"Rôle de la dysfonction endothéliale dans les complications cardiovasculaires et rénales de la polykystose rénale autosomique dominante: intérêt d’une modulation pharmacologique par agonistes dopaminergiques"

20191209 Berenice

Dr Bérénice Colleville (Dir. Eric Durand)

"Identification de nouvelles cibles thérapeutiques dans le rétrécissement aortique"

 20191212 Fred Roca

Dr Frédéric Roca (Dir Robinson Joannides)

"Évaluation in vivo de la viscosité pariétale des artères de conductance : impact du vieillissement, de la dysfonction endothéliale et de la réduction pharmacologique de la fréquence cardiaque"

20191216 Matthieu

Dr Matthieu Leuillier (Dir. Jeremy Bellien)

"Rôle de l'activité phosphatase de l'époxyde hydrolase soluble dans la régulation de l'homéostasie métabolique et cardiovasculaire"


Endothelium, Valvulopathy
& Heart Failure

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