Heparin Administration, but Not Myocardial Ischemia or Necrosis, Leads to Midkine Elevation

Autor: N. Collins, Andrew J. Boyle, Graham Robertson, M. Al-Omary, S. Sugito, Theo de Malmanche, Sharron T. Hall
Rok vydání: 2020
Předmět:
0301 basic medicine
medicine.medical_specialty
Time Factors
medicine.medical_treatment
Pharmaceutical Science
Renal function
Coronary Artery Disease
030204 cardiovascular system & hematology
Coronary artery disease
03 medical and health sciences
Percutaneous Coronary Intervention
0302 clinical medicine
Internal medicine
Genetics
medicine
Humans
Prospective Studies
cardiovascular diseases
Myocardial infarction
Non-ST Elevated Myocardial Infarction
Genetics (clinical)
Midkine
Dose-Response Relationship
Drug
biology
Heparin
business.industry
Anticoagulants
Percutaneous coronary intervention
medicine.disease
Troponin
Up-Regulation
Treatment Outcome
030104 developmental biology
Conventional PCI
Cardiology
biology.protein
ST Elevation Myocardial Infarction
Molecular Medicine
Cardiology and Cardiovascular Medicine
business
Biomarkers
medicine.drug
Zdroj: Journal of Cardiovascular Translational Research. 13:741-743
ISSN: 1937-5395
1937-5387
Popis: 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 naive, 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.
Databáze: OpenAIRE
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