The Impact of Sclerostin Levels on Long-Term Prognosis in Patients Undergoing Coronary Angiography: A Personalized Approach with 9-Year Follow-Up.

Adam Kern,Jolanta Kiewisz,Dariusz Onichimowski,Marta Kiezun,Tomasz Stompór,Jerzy Górny,Jacek Bil,Ewa Sienkiewicz,Bartłomiej E Kraziński,Leszek Gromadziński,Jacek Kiezun

doi:10.3390/jpm11030186

Abstract

Sclerostin might play a role in atherosclerosis development. This study aimed to analyze the impact of baseline sclerostin levels on 9-year outcomes in patients without significant renal function impairment and undergoing coronary angiography. The primary study endpoint was the rate of major cardiovascular events (MACE), defined as a combined rate of myocardial infarction (MI), stroke, or death at 9 years. We included 205 patients with a mean age of 62.9 ± 0.6 years and 70.2% male. Median serum sclerostin concentration was 133.22 pg/mL (IQR 64.0–276.17). At 9 years, in the whole population, the rate of MACE was 34.1% (n = 70), MI: 11.2% (n = 23), stroke: 2.4% (n = 5), and death: 20.5% (n = 42). In the high sclerostin (>median) group, we observed statistically significant higher rates of MACE and death: 25.2% vs. 43.1% (HR 1.75, 95% CI 1.1–2.10, p = 0.02) and 14.6% vs. 26.5% (HR 1.86, 95% CI 1.02–3.41, p = 0.049), respectively. Similar relationships were observed in patients with chronic coronary syndrome and SYNTAX 0–22 subgroups. Our results suggest that sclerostin assessment might be useful in risk stratification, and subjects with higher sclerostin levels might have a worse prognosis.

Highlights

The osteocyte is considered the master cell that governs bone turnover and interactions between bone, the parathyroid gland, the kidneys, and possibly the cardiovascular system [1]
We revealed no evident association between sclerostin levels and coronary artery disease severity
The primary study endpoint was the rate of major cardiovascular events (MACE), defined as a combined rate of myocardial infarction (MI), stroke, or death at 9 years

Summary

Introduction

The osteocyte is considered the master cell that governs bone turnover and interactions between bone, the parathyroid gland, the kidneys, and possibly the cardiovascular system [1]. Osteocytes linked together in a lacunar–canalicular system are considered to be an active endocrine organ that releases sclerostin, fibroblast growth factor 23 (FGF23), Dickkopf (DKK-1), phosphate-regulating neutral endopeptidase, osteoprotegerin, matrix extracellular phosphoglycoprotein, and osteocalcin [2]. These proteins do not operate only locally but may influence remote organs [3]. The crosstalk between bone and the cardiovascular system via mentioned hormones and regulatory proteins is called the bone–kidney–heart axis [4,5]

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