Heparin Administration, but Not Myocardial Ischemia or Necrosis, Leads to Midkine Elevation
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CORRESPONDENCE
Heparin Administration, but Not Myocardial Ischemia or Necrosis, Leads to Midkine Elevation Stuart Sugito 1,2,3 & Sharron Hall 2,3,4 & Mohammed S. Al-Omary 1,2,3 & Theo De Malmanche 2,3,4 & Graham Robertson 5 & Nicholas Collins 1,2,3 & Andrew Boyle 1,2,3,6 Received: 10 October 2019 / Accepted: 3 January 2020 # Springer Science+Business Media, LLC, part of Springer Nature 2020
Abstract Midkine (MK) is a heparin-binding growth factor, whose role as a biomarker of coronary artery disease, myocardial ischaemia and necrosis has not been well measured. This study quantified serial MK levels in patients undergoing coronary angiography (CA) and identified factors associated with MK. In this single-centre, parallel cohort study, forty patients undergoing CA had arterial samples collected prior, 10 and 20 min after heparin administration. Four groups were examined: 1—stable coronary artery disease (CAD) without percutaneous coronary intervention (PCI); 2—stable CAD for elective PCI; 3—non-ST elevation myocardial infarction (NSTEMI) with or without PCI; 4—ST elevation myocardial infarction (STEMI) with primary PCI. Groups 1, 2 and 4 were heparin naïve, allowing assessment of the effects of myocardial necrosis between baseline levels; group 3 had received low-molecular-weight heparin. MK levels were analysed by ELISA. Median MK at baseline did not differ between groups, demonstrating that myocardial ischaemia or necrosis does not affect MK levels. Heparin administration had an immediate effect on median MK at 10 min, showing an average 500-fold increase that is dose-dependent (R2 = 0.35, p = 0.001). Median MK levels remained elevated at 20 min following heparin administration. Multivariate analysis showed that the estimated glomerular filtration rate (eGFR) was the only predictor of elevated baseline MK (p = 0.02). Baseline MK did not correlate with high-sensitivity troponin-I (HsTnI) taken just before CA (p = 0.97), or peak HsTnI during admission (p = 0.74). MK is not a reliable marker of myocardial ischaemia or necrosis. MK increased significantly in all patients following heparin administration in a dose-dependent manner. Keywords Midkine . Biomarkers . Myocardial ischaemia . Coronary artery disease
Introduction
Associate Editor Craig Stolen oversaw the review of this article * Andrew Boyle [email protected] 1
Cardiology Department, John Hunter Hospital, Newcastle, NSW, Australia
2
University of Newcastle, Newcastle, NSW, Australia
3
Hunter Medical Research Institute, Newcastle, NSW, Australia
4
NSW Health Pathology, Newcastle, NSW, Australia
5
Cellmid Ltd, Sydney, NSW, Australia
6
Cardiovascular Department, John Hunter Hospital, University of Newcastle, Lookout Road, New Lambton Heights, NSW 2305, Australia
Midkine (MK) is a heparin-binding growth factor that has important pathophysiological functions in cardiac disease [1]. Animal experiments have shown that MK has cardioprotective properties [2], protecting from ischemia/ reperfusion injury through its anti-apoptotic effect and
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