BEURTON, Antoine; MICHOT, Maxime; HERION, Francois-Xavier; RIENZO, Mario; ODDOS, Claire; COUFFINHAL, Thierry; IMBAULT, Julien; OUATTARA, Alexandre

doi:10.1097/MAT.0000000000002139

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BEURTON, Antoine
Biologie des maladies cardiovasculaires = Biology of Cardiovascular Diseases

MICHOT, Maxime
Biologie des maladies cardiovasculaires = Biology of Cardiovascular Diseases

HERION, Francois-Xavier
Biologie des maladies cardiovasculaires = Biology of Cardiovascular Diseases

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Ce document a été publié dans

ASAIO Journal. 2024-03-01, vol. 70, n° 3, p. 177-184

Résumé en anglais

Peripheral venoarterial extracorporeal membrane oxygenation (VA-ECMO) is increasingly being used in patients suffering from refractory cardiogenic shock (CS). Although considered life-saving, peripheral VA-ECMO may also be responsible for intracardiac hemodynamic changes, including left ventricular overload and dysfunction. Venoarterial extracorporeal membrane oxygenation may also increase myocardial wall stress and stroke work, possibly affecting the cellular cardioprotective and apoptosis signaling pathways, and thus the infarct size. To test this hypothesis, we investigated the effects of increasing the peripheral VA-ECMO blood flow (25-100% of the baseline cardiac output) on systemic and cardiac hemodynamics in a closed-chest CS model. Upon completion of the experiment, the hearts were removed for assessment of infarct size, histology, apoptosis measurements, and phosphorylation statuses of p38 and protein Kinase B (Akt), and extracellular signal-regulated kinase mitogen-activated protein kinases (ERK-MAPK). Peripheral VA-ECMO restored systemic perfusion but induced a significant and blood flow-dependent increase in left ventricular preload and afterload. Venoarterial extracorporeal membrane oxygenation did not affect infarct size but significantly decreased p38-MAPK phosphorylation and cardiac myocyte apoptosis in the border zone.< Réduire

Mots clés

article clinique

Mots clés en anglais

Humans

Shock

Cardiogenic

Extracorporeal Membrane Oxygenation

Hemodynamics

Myocardium

Signal Transduction