Relation of plasma neuropeptide-Y with myocardial function and infarct severity in acute ST-elevation myocardial infarction

Christina Tiller; Martin Reindl; Magdalena Holzknecht; Ivan Lechner; Felix Troger; Fritz Oberhollenzer; Sebastian von der Emde; Thomas Kremser; Agnes Mayr; Axel Bauer; Bernhard Metzler; Sebastian J Reinstadler

doi:10.1016/j.ejim.2024.03.027

Relation of plasma neuropeptide-Y with myocardial function and infarct severity in acute ST-elevation myocardial infarction

Eur J Intern Med. 2024 Mar 29:S0953-6205(24)00137-7. doi: 10.1016/j.ejim.2024.03.027. Online ahead of print.

Affiliations

¹ University Clinic of Internal Medicine III, Cardiology and Angiology, Medical University of Innsbruck, Anichstrasse 35, A-6020 Innsbruck, Austria.
² University Clinic of Radiology, Medical University of Innsbruck, Anichstrasse 35, A-6020 Innsbruck, Austria.
³ University Clinic of Internal Medicine III, Cardiology and Angiology, Medical University of Innsbruck, Anichstrasse 35, A-6020 Innsbruck, Austria. Electronic address: Sebastian.Reinstadler@gmail.com.

PMID: 38555253
DOI: 10.1016/j.ejim.2024.03.027

Abstract

Background: Acute myocardial infarction is associated with the release of the co-transmitter neuropeptide-Y (NPY). NPY acts as a potent vasoconstrictor and is associated with microvascular dysfunction after ST-elevation myocardial infarction (STEMI). This study comprehensively evaluated the association of plasma NPY with myocardial function and infarct severity, visualized by cardiac magnetic resonance (CMR) imaging, in STEMI patients revascularized by primary percutaneous coronary intervention (PCI).

Methods: In this observational study, we included 260 STEMI patients enrolled in the prospective MARINA-STEMI (NCT04113356) study. Plasma NPY concentrations were measured by an immunoassay 24h after PCI from peripheral venous blood samples. Left ventricular ejection fraction (LVEF), global longitudinal strain (GLS), infarct size (IS) and microvascular obstruction (MVO) were determined using CMR imaging.

Results: Median plasma concentrations of NPY were 70 [interquartile range (IQR):35-115] pg/ml. NPY levels above median were significantly associated with lower LVEF (48%vs.52%, p=0.004), decreased GLS (-8.8%vs.-12.6%, p<0.001) and larger IS (17%vs.13%, p=0.041) in the acute phase after infarction as well as after 4 months (LVEF:50%vs.52%, p=0.030, GLS:-10.5vs.-12.9,p<0.001,IS:13%vs.10%,p=0.011). In addition, NPY levels were significantly related to presence of MVO (58%vs.52%, p=0.041). Moreover, in multivariable linear regression analysis, NPY remained significantly associated with all investigated CMR parameters (LVEF:p<0.001,GLS:p<0.001,IS:p=0.003,MVO:p=0.042) independent of other established clinical variables including high-sensitivity cardiac troponin T, pre-interventional TIMI flow 0 and left anterior descending artery as culprit lesion location.

Conclusion: High plasma levels of NPY, measured 24h after STEMI, were independently associated with lower LVEF, decreased GLS, larger IS as well as presence of MVO, indicating plasma NPY as a novel clinical risk marker post STEMI.

Keywords: Cardiac magnetic resonance imaging; Myocardial injury; Plasma neuropeptide-Y; Risk stratification; ST-segment elevation myocardial infarction.