![Sample our Medicine, Dentistry, Nursing & Allied Health journals, sign in here to start your FREE access for 14 days]({"type":"image" , "src" : "/sda/5944/TOC-Subject-Sample-2021-Medicine-Dentistry-Nursing-Allied-Health.jpg"})
Abstract
Introduction. Arterial calcification is a risk factor for atherosclerosis. Calumenin (CALU), a protein regulating proteins involved in coagulation and arterial calcification also has extracellular functions related to atherosclerosis. We recently described that CALU polymorphism A29809G was related to acenocoumarol requirements, and we wanted to evaluate its role in arterial calcification and prognosis.
Patients and methods. A total of 374 consecutive patients with non-ST-elevation acute coronary syndrome (nSTACS). In 175 of them, who underwent percutaneous coronary intervention, we assessed calcification in each main coronary artery. Follow-up at 1 and 6 months was performed for adverse end-points.
Results. CALU 29809G carriers were more frequent in the low calcium group (P = 0.037). The presence of ≥3 cardiovascular risk factors and CALU polymorphism were associated with arterial calcification (OR 2.34, P = 0.049; and OR 0.34, P = 0.019, respectively). CALU 29809G allele was the only variable associated with events at 1 month (HR 0.42; P = 0.042). Multivariate analysis showed that, at 6 months, age and severe anginal symptoms were associated with worse prognosis (HR 2.13, P = 0.023; and HR 2.01, P = 0.011, respectively), whereas CALU 29809G allele associated with good prognosis (HR 0.59, P = 0.044). Our results suggest that CALU A29809G is associated with arterial calcification and short-term prognosis of the outcome of patients with nSTACS.
Acknowledgements
This work was partially supported by 04515/GERM/06 from Fundación Séneca, SAF2009-08993 (MCYT & FEDER), RD06/0014/039 (RECAVA) from ISCIII, and PI081531 from ISCIII. Dr Hernández-Romero holds a post-doctoral position funded by Instituto de Salud Carlos III.
Declaration of interest: The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.