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. 2021 Mar 6;11(3):186.
doi: 10.3390/jpm11030186.

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

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

Adam Kern et al. J Pers Med. .

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.

Keywords: Klotho; bone metabolism; cardiovascular events; coronary angiography; coronary artery disease; death; multivessel disease; myocardial infarction; osteocyte; sclerostin; stroke.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Study flow chart.
Figure 2
Figure 2
Whole population—Kaplan–Meier curves for MACE, myocardial infarction, and all-cause death, respectively.
Figure 3
Figure 3
Chronic coronary syndrome population—Kaplan–Meier curves for MACE, myocardial infarction, and all-cause death, respectively.
Figure 4
Figure 4
Acute coronary syndrome population—Kaplan–Meier curves for MACE, myocardial infarction, and all-cause death, respectively.
Figure 5
Figure 5
SYNTAX 0–22 population—Kaplan–Meier curves for MACE, myocardial infarction, and all-cause death, respectively.

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