13 Dec Bone Protein May Be Marker of Cardiac Dysfunction

MedicalResearch.com Interview with:
Mette Bjerre, Associate Professor, PhD
Medical Research Laboratory
Aarhus University Hospital & Aarhus University
Aarhus C Denmark

Medical Research: What is the background for this study? What are the main findings?

Dr.Bjerre: Recently, a connection between bone regulatory proteins and vascular biology has attracted attention, suggesting osteoprotegerin (OPG), a secreted glycoprotein that regulates bone resorption, as a possible mediator of vascular calcification. Indeed, we and others has shown that high levels of circulating OPG predicts long-term outcome in patients with cardiovascular disease (CVD). However, the mechanism remains poorly understood. In order to elucidate the role of OPG in patients with ST-elevation myocardial infarction (STEMI) treated with primary percutaneous coronary intervention (pPCI), our study aimed to evaluate the progression of OPG levels, in four consecutive blood-samples obtained pre-PCI, post-PCI, day 1 and day 2.

OPG levels did indeed change during treatment. OPG levels peaked post-PCI and then decreased; mean concentrations (95% confidence interval) pre-PCI 2650ng/L (2315-3036ng/L), post-PCI 2778ng/L (2442-3363ng/L), day 1 2024ng/L (1775-2306ng/L) and day 2 1808ng/L (1551-2106), (repeated measures ANOVA, F=33.192, p<0.001). Additional, high OPG level is independently associated with impaired LVEF (LVEF < 40%). Adjustment for BMI and traditional cardiovascular risk factors (hypertension, hypercholesterolemia, diabetes and current smoking) did not significantly impact the association between OPG response and reduced LVEF.

Medical Research: What should clinicians and patients take away from your report?

Dr.Bjerre: Importantly, in patients who developed low LVEF during the infarction, OPG was already elevated at admission, suggesting that OPG may be an early marker of impaired systolic function. Interestingly, the OPG response was observed prior to the response in Troponin I and C-reactive protein. The fact that OPG decreased significantly in the days after the infarction indicates increased OPG production or release during or possibly before the infarction, further supporting a role of OPG in AMI possibly related to vascular inflammation.

Medical Research: What recommendations do you have for future research as a result of this study?

Dr.Bjerre: Whether osteoprotegerin is directly involved in myocardial damage after STEMI, or simply reflects vascular inflammation and/or extensive cardiovascular disease remains to be elucidated. Our findings suggest OPG as a possible marker of cardiac dysfunction, which may be included in a panel of cardiovascular-risk-stratification, in the future.

Citation:

Osteoprotegerin Levels Change During STEMI and Reflect Cardiac Function.

Lindberg S, Jensen JS, Hoffmann S, Iversen AZ, Pedersen SH, Mogelvang R, Galatius S, Flyvbjerg A, Bjerre M.
Can J Cardiol. 2014 Dec;30(12):1523-8. doi: 10.1016/j.cjca.2014.08.015. Epub 2014 Aug 23.

Last Updated on December 13, 2014 by Marie Benz MD FAAD