Myocardial Perfusion in Rheumatoid Arthritis Patients: Associations with Traditional Risk Factors and Novel Biomarkers

Abstract

Introduction. Cardiovascular (CV) diseases are a major cause of death in rheumatoid arthritis (RA) patients. Novel biomarkers [B-type natriuretic peptide (BNP); osteoprotegerin (OPG)/receptor activator of nuclear factor-kappa B ligand (RANKL) ratio; and dickkopf-1 (DKK-1)] have been used in CV risk assessment. We analysed, in established RA patients, the presence of silent myocardial ischemia and its association with clinical variables, BNP, and bone and atheroma biomarkers. Methods. From a single-center tertiary referral hospital, RA patients asymptomatic for CV disease were submitted to myocardial perfusion scintigraphy (MPS) under adenosine stress and biomarkers measurements. Logistic regression was used to estimate crude odds ratios (OR) and 95% confidence intervals (CI). Results. In 189 patients, perfusion defects were frequent (25%) and associated with BNP ≥ 100 pg/mL (OR = 5.68; 95% CI: 2.038–15.830), fourth log OPG/RANKL ratio quartile (OR = 2.88; 95% CI: 1.091–7.622), and DKK-1 ≥ 133 pmol/L (OR = 2.69; 95% CI: 1.058–6.840). Similar associations were confirmed in those with C-reactive protein > or ≤ 3 mg/L. No relationship was found with the majority of traditional CV factors nor with disease variables. Conclusions. Our results corroborated the hypothesis that MPS could reveal subclinical CV dysfunction, supported the utility of BNP measurements as a screening tool, and put in perspective the potential usefulness of complementary approaches in CV risk assessment in RA patients.

Serum serotonin levels and bone in rheumatoid arthritis patients

“…All the specimens were measured in duplicate, according to the manufacturer's instructions and then averaged. OPG, DKK-1, RANKL, and sclerostin were determined as previously described [40]. Serotonin was measured using a kit from Labor Diagnostika Nord GmbH & Co, KG (Nordhorn, Germany); the intra-and inter-assay coefficients of variation were 3.9-5.4 and 6.0%, respectively.…”

Coronary artery calcium score in female rheumatoid arthritis patients: Associations with apolipoproteins and disease biomarkers

“…Lipid profile, glucose, insulin, CRP, ESR, rheumatoid factor (RF) and anticyclic citrullinated peptide antibodies (ACPA), homocysteine, uric acid, creatinine, 25(OH) vitamin D 3 , folic acid, intact parathyroid hormone, osteocalcin, beta‐carboxy‐terminal cross‐linking telopeptide of type I collagen (beta‐CTX), B‐type natriuretic peptide (BNP), OPG, receptor activator of nuclear factor–kappa B ligand (RANKL), dickkopf‐1 (Dkk‐1) and sclerostin levels were analyzed in a fasting blood sample. OPG, RANKL, Dkk‐1 and sclerostin were measured as previously described . Homeostasis model assessment for insulin resistance (HOMA‐IR) was calculated, using the formula: HOMA‐IR = (fasting insulin [mUI/L] × fasting glucose [mg/dL]/405) …”

“…CV comorbidities are indeed a major cause of mortality in RA patients and the relative risk of myocardial infarction is 1.5, against the general population . However, prediction of CV events in RA is far from being ideal, as has been shown in different studies . A deeper understanding of the mechanisms involved in vascular remodeling, including coronary calcification, is fundamental for the development of efficacious prevention strategies of CV disease in RA.…”

“…biological markers, bone mineral density, cardiovascular diseases, heart diseases, rheumatoid arthritis telopeptide of type I collagen (beta-CTX), B-type natriuretic peptide (BNP), OPG, receptor activator of nuclear factor-kappa B ligand (RANKL), dickkopf-1 (Dkk-1) and sclerostin levels were analyzed in a fasting blood sample. OPG, RANKL, Dkk-1 and sclerostin were measured as previously described 4. Homeostasis model assessment for insulin resistance (HOMA-IR) was calculated, using the formula: HOMA-IR = (fasting insulin [mUI/L] × fasting glucose [mg/dL]/405) 30.…”

Serum Osteoprotegrin, Total Srankl and Their Determinants in Adolescents with Type 1 Diabetes

“…OPG is a "fake" competitive receptor, binding to RANKL, preventing it from binding to RANK and signaling, causing the opposite effect -preventing bone loss [10]. The disorders of OPG / RANKL system not only affect bone metabolism but also play an important role in cardiovascular, inflammatory, cancer and autoimmune diseases [13][14][15]. Most available data on that issue come from the research in adults.…”