Juan C Quevedo-Abeledo1,2, Íñigo Rúa-Figueroa1,2, Hiurma Sánchez-Pérez1,2, Beatriz Tejera-Segura1,2, Antonia de Vera-González1,2, Alejandra González-Delgado1,2, Javier Llorca1,2, Miguel Á González-Gay1,2, Iván Ferraz-Amaro3,4. 1. From the Division of Rheumatology, Hospital Doctor Negrín, Las Palmas de Gran Canaria; Division of Rheumatology, Hospital Universitario de Canarias, Tenerife; Division of Rheumatology, Hospital Insular, Las Palmas de Gran Canaria; Central Laboratory Division, Hospital Universitario de Canarias, Tenerife; Department of Epidemiology and Computational Biology, School of Medicine, University of Cantabria; CIBER Epidemiología y Salud Pública (CIBERESP), Instituto de Investigacíon Sanitaria (IDIVAL); Division of Rheumatology, Hospital Universitario Marqués de Valdecilla, IDIVAL; Epidemiology, Genetics and Atherosclerosis Research Group on Systemic Inflammatory Diseases, Hospital Universitario Marqués de Valdecilla, IDIVAL; School of Medicine, University of Cantabria, Santander, Spain; Cardiovascular Pathophysiology and Genomics Research Unit, School of Physiology, Faculty of Health Sciences, University of the Witwatersrand, Johannesburg, South Africa. 2. J.C. Quevedo-Abeledo, MD, Division of Rheumatology, Hospital Doctor Negrín; I. Rúa-Figueroa, MD, PhD, Division of Rheumatology, Hospital Doctor Negrín; H. Sánchez-Pérez, MD, Division of Rheumatology, Hospital Universitario de Canarias; B. Tejera-Segura, MD, Division of Rheumatology, Hospital Insular; A. de Vera-González, MD, Central Laboratory Division, Hospital Universitario de Canarias; A. González-Delgado, MD, Central Laboratory Division, Hospital Universitario de Canarias; J. Llorca, MD, PhD, Department of Epidemiology and Computational Biology, School of Medicine, University of Cantabria, and CIBERESP, IDIVAL; M.A. González-Gay, MD, PhD, Division of Rheumatology, Epidemiology, Genetics and Atherosclerosis Research Group on Systemic Inflammatory Diseases, Hospital Universitario Marqués de Valdecilla, IDIVAL, and School of Medicine, University of Cantabria, and Cardiovascular Pathophysiology and Genomics Research Unit, School of Physiology, Faculty of Health Sciences, University of the Witwatersrand; I. Ferraz-Amaro, MD, PhD, Division of Rheumatology, Hospital Universitario de Canarias. 3. From the Division of Rheumatology, Hospital Doctor Negrín, Las Palmas de Gran Canaria; Division of Rheumatology, Hospital Universitario de Canarias, Tenerife; Division of Rheumatology, Hospital Insular, Las Palmas de Gran Canaria; Central Laboratory Division, Hospital Universitario de Canarias, Tenerife; Department of Epidemiology and Computational Biology, School of Medicine, University of Cantabria; CIBER Epidemiología y Salud Pública (CIBERESP), Instituto de Investigacíon Sanitaria (IDIVAL); Division of Rheumatology, Hospital Universitario Marqués de Valdecilla, IDIVAL; Epidemiology, Genetics and Atherosclerosis Research Group on Systemic Inflammatory Diseases, Hospital Universitario Marqués de Valdecilla, IDIVAL; School of Medicine, University of Cantabria, Santander, Spain; Cardiovascular Pathophysiology and Genomics Research Unit, School of Physiology, Faculty of Health Sciences, University of the Witwatersrand, Johannesburg, South Africa. iferrazamaro@hotmail.com miguelaggay@hotmail.com. 4. J.C. Quevedo-Abeledo, MD, Division of Rheumatology, Hospital Doctor Negrín; I. Rúa-Figueroa, MD, PhD, Division of Rheumatology, Hospital Doctor Negrín; H. Sánchez-Pérez, MD, Division of Rheumatology, Hospital Universitario de Canarias; B. Tejera-Segura, MD, Division of Rheumatology, Hospital Insular; A. de Vera-González, MD, Central Laboratory Division, Hospital Universitario de Canarias; A. González-Delgado, MD, Central Laboratory Division, Hospital Universitario de Canarias; J. Llorca, MD, PhD, Department of Epidemiology and Computational Biology, School of Medicine, University of Cantabria, and CIBERESP, IDIVAL; M.A. González-Gay, MD, PhD, Division of Rheumatology, Epidemiology, Genetics and Atherosclerosis Research Group on Systemic Inflammatory Diseases, Hospital Universitario Marqués de Valdecilla, IDIVAL, and School of Medicine, University of Cantabria, and Cardiovascular Pathophysiology and Genomics Research Unit, School of Physiology, Faculty of Health Sciences, University of the Witwatersrand; I. Ferraz-Amaro, MD, PhD, Division of Rheumatology, Hospital Universitario de Canarias. iferrazamaro@hotmail.com miguelaggay@hotmail.com.
Abstract
OBJECTIVE: Composite scores of cardiovascular (CV) risk factors underestimate the CV risk in patients with systemic lupus erythematosus (SLE). Carotid artery ultrasound (US) was found useful in identifying high CV-risk patients with inflammatory arthritis. We assessed the effect of carotid US assessments on the CV risk stratification of patients with SLE. METHODS: This cross-sectional study included 276 patients with SLE. These indices were measured: lipid profile, Systematic COronary Risk Evaluation (SCORE) risk calculation, and disease activity (SLE Disease Activity Index), severity (Katz), and damage [Systemic Lupus International Collaborating Clinics (SLICC)/American College of Rheumatology Damage Index]. Carotid plaques were assessed by US. A multivariable regression analysis, adjusted for classic CV-related factors, was performed to evaluate how risk reclassification was influenced by disease characteristics in patients with SLE. RESULTS: Thirty-six percent of patients had carotid plaques. However, only 6% of them fulfilled the definitions for high or very high risk according to the SCORE risk charts. Following carotid US assessment, 32% of the patients were reclassified as very high risk. Disease duration (OR 1.04, 95% CI 1.00-1.07, p = 0.025) and a SLICC > 0 (OR 2.48 95% CI 1.15-5.34, p = 0.020) were independently associated with a higher risk of reclassification. A predictive model for reclassification included age (cutoff 52 yrs, sensitivity 60%, specificity 86%), disease duration (cutoff 24 yrs, sensitivity 40%, specificity 82%), presence of hypertension, SLICC > 0, waist circumference (cutoff 102 cm, sensitivity 48%, specificity 84%), and C3 (cutoff 127 mg/dl, sensitivity 52%, specificity 92%) and triglyceride (cutoff 140 mg/dl, sensitivity 68%, specificity 79%) serum levels. CONCLUSION: Reclassification into a very high-risk category is frequent after carotid US assessments in patients with SLE. This is independently influenced by disease damage.
OBJECTIVE: Composite scores of cardiovascular (CV) risk factors underestimate the CV risk in patients with systemic lupus erythematosus (SLE). Carotid artery ultrasound (US) was found useful in identifying high CV-risk patients with inflammatory arthritis. We assessed the effect of carotid US assessments on the CV risk stratification of patients with SLE. METHODS: This cross-sectional study included 276 patients with SLE. These indices were measured: lipid profile, Systematic COronary Risk Evaluation (SCORE) risk calculation, and disease activity (SLE Disease Activity Index), severity (Katz), and damage [Systemic Lupus International Collaborating Clinics (SLICC)/American College of Rheumatology Damage Index]. Carotid plaques were assessed by US. A multivariable regression analysis, adjusted for classic CV-related factors, was performed to evaluate how risk reclassification was influenced by disease characteristics in patients with SLE. RESULTS: Thirty-six percent of patients had carotid plaques. However, only 6% of them fulfilled the definitions for high or very high risk according to the SCORE risk charts. Following carotid US assessment, 32% of the patients were reclassified as very high risk. Disease duration (OR 1.04, 95% CI 1.00-1.07, p = 0.025) and a SLICC > 0 (OR 2.48 95% CI 1.15-5.34, p = 0.020) were independently associated with a higher risk of reclassification. A predictive model for reclassification included age (cutoff 52 yrs, sensitivity 60%, specificity 86%), disease duration (cutoff 24 yrs, sensitivity 40%, specificity 82%), presence of hypertension, SLICC > 0, waist circumference (cutoff 102 cm, sensitivity 48%, specificity 84%), and C3 (cutoff 127 mg/dl, sensitivity 52%, specificity 92%) and triglyceride (cutoff 140 mg/dl, sensitivity 68%, specificity 79%) serum levels. CONCLUSION: Reclassification into a very high-risk category is frequent after carotid US assessments in patients with SLE. This is independently influenced by disease damage.
Authors: Juan Carlos Quevedo-Abeledo; Miguel Á González-Gay; Iván Ferraz-Amaro Journal: Ther Adv Musculoskelet Dis Date: 2022-04-19 Impact factor: 3.625