Post-infarction inflammation influences diastolic function after STEMI - 12/05/23
, Smaranda Filip 1, Hélène Thibault 1, Cyrille Bergerot 1, Alexandre Paccalet 2, Ahmad Hayek 3, Gilles Rioufol 4, Eric Bonnefoy-Cudraz 3, Cyril Prieur 3, Claire Crola Da Silva 2, Camille Brun 2, Léa Azar 3, Iyad Abou Saleh 3, Nathan Mewton 5, Laura Mechtouff 6, Thomas Bochaton 3Résumé |
Introduction |
Diastolic dysfunction after STEMI is under documented despite its impact on cardiovascular events. We focused on inflammatory biomarkers within hours after STEMI and their association with diastolic dysfunction at one month post-STEMI.
Objective |
Our aim was to identify an inflammatory profile promoting diastolic dysfunction in STEMI patients.
Method |
We prospectively included STEMI patients admitted in our hospital from 2016 to 2019. We collected sera at 5 time points [admission (H0), 4hours (H4), H24, H48 an 1 month]. Inflammatory biomarkers serum levels were assessed using ELISA assays (cytokines, chemokines and endothelial activation biomarkers). Transthoracic echocardiogram and cardiac MRI to assess diastolic function and infarct size were carried out at one month post-STEMI. We used last guidelines from the EACVI to grade diastolic function. Patients were followed for 12months.
Results |
Complete echocardiographic data were available for 236 patients. There were 163 patients with normal diastolic function and 73 patients with diastolic dysfunction. As expected, patients with diastolic dysfunction had higher BNP level (197.0ng/L versus 68ng/L, P<0.001) and were more likely to have a MACE during the first 12months after STEMI compared to patients normal diastolic function (HR=3.0, CI [1.1–7.9], P=0.01). Patients with diastolic dysfunction at one month had higher inflammatory biomarkers within the first 48h post-STEMI compared with patient with normal diastolic function (Fig. 1): CRP AUC (660.2mg.h.L−1 vs. 361.4mg.h.L−1 P=0.02), IL-6 AUC (206.0pg.h.mL−1 vs. 173.1pg.h.mL−1 P=0.03) sTNFR1 AUC (27.6ng.h.mL−1 versus 24.1ng.h.mL−1, P=0.03), sTNFR2 AUC (44.7ng.h.mL−1 vs. 43.5ng.h.mL−1, P=0.03) sST2 AUC (30.4pg.h.mL−1 vs. 27.3pg.h.mL−1, P=0.046), GDF15 AUC (10.8ng.h.mL−1 vs. 8.1ng.h.mL−1, P=0.050) and IL-10 AUC (174.6pg.h.mL−1 vs. 122.8pg.h.mL−1, P=0.02). There was no significant difference in infarct size (13 versus 17% of left ventricular mass, P=0.06) or LVEF (58 versus 54%, P=0.0523) between the two groups.
Conclusion |
Diastolic function seems influenced by the early post-STEMI inflammatory environment. These results should be considered in future mechanistical study and in patients’ care.
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Vol 15 - N° 2
P. 199-200 - mai 2023 Retour au numéro
Article précédent
- P2Y4 nucleotide receptor: A novel target for anti-inflammatory therapies to improve myocardial infarction outcome
- Michael Horckmans, Esteban Diaz Villamil, Mariaelvy Bianchini, Céline Verdier, Jean-Bernard Ruidavets, Laurent O. Martinez, Didier Communi
- RANTES (CCL5) as a biomarker of clinical outcomes in STEMI patients
- Camille Brun, Florentin Moulin, Simon Leboube, Ahmad Hayek, Abou Saleh Lyad, Alexandre Paccalet, Gilles Rioufol, Cyril Prieur, Eric Bonnefoy-Cudraz, Nathan Mewton, Gabriel Bidaux, Melanie Paillard, Claire Crola Da Silva, Sylvie Ducreux, Thomas Bochaton
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