Julie Chezel1, Nathalie Costedoat-Chalumeau2, Cedric Laouénan3, Diane Rouzaud1, Camille Chenevier-Gobeaux4, Véronique Le Guern2, Alexis Mathian5, Drifa Belhadi3, Sébastien de Almeida Chaves6, Pierre Duhaut7, Olivier Fain8, Lionel Galicier9, Pascale Ghillani-Dalbin10, Jean Emmanuel Kahn11, Nathalie Morel2, Laurent Perard12, Micheline Pha5, Fanny Saidoune1, Francoise Sarrot-Reynauld13, Olivier Aumaitre14, François Chasset15, Nicolas Limal16, Helene Desmurs-Clavel17, Felix Ackermann18, Zahir Amoura5, Thomas Papo1, Karim Sacre1. 1. Département de Médecine Interne, Hôpital Bichat, Assistance Publique Hôpitaux de Paris (APHP), Institut national de la santé et de la recherche médicale (INSERM) U1149, Université de Paris, France. 2. Département de Médecine Interne, Hôpital Cochin, Centre de Reference Maladies Auto-immunes et Systémiques Rares, APHP, Université de Paris, CRESS, INSERM, INRA, France. 3. Departement d'Epidémiologie et de Recherche Clinique, Hôpital Bichat, France. 4. Service de Diagnostic Biologique Automatisé, Département médico-universitaire BioPhyGen, Hôpital Cochin, APHP, Université de Paris, Paris, France. 5. Département de Médecine Interne 2, French National Referral Center for Systemic Lupus Erythematosus, Antiphospholipid Antibody Syndrome and Other Autoimmune Disorders, Groupement Hospitalier Pitié-Salpêtrière, APHP, Sorbonne Université, Paris, France. 6. Département de Médecine Interne, Hôpital Purpan, Centre Hospitalo-Universitaire (CHU) de Toulouse, Toulouse, France. 7. Département de Médecine Interne, Hôpital Amiens Nord, CHU d'Amiens, Amiens, France. 8. Département de Médecine Interne, Hôpital Saint Antoine, APHP, Université Pierre et Marie Curie, Paris, France. 9. Département d'Immunologie Clinique, Hôpital Saint Louis, APHP, Université de Paris, Paris, France. 10. Département de Immunologie, Hôpital Pitié-Salpétrière, APHP, Université Pierre et Marie Curie, Paris, France. 11. Département de Médecine Interne, Hôpital Ambroise Paré, APHP, Université de Versailles-Saint-Quentin en Yvelines, Versailles, France. 12. Département de Médecine Interne, Hôpital St Joseph St Luc, Lyon, France. 13. Département de médecine interne, Hôpital Michallon, CHU de Grenoble Alpes, Grenoble, France. 14. Département de médecine interne, Hôpital Gabriel-Montpied, CHU de Clermont-Ferrand, Clermont-Ferrand, France. 15. Département de médecine interne, Hôpital Tenon, APHP Université Pierre et Marie Curie, Paris, France. 16. Département de médecine interne, Hôpital Henri Mondor, APHP Université Paris-Est Créteil, Paris, France. 17. Département de médecine interne, Hôpital Edouard Herriot, Hospices Civils de Lyon, Lyon, France. 18. Département de médecine interne, Hôpital Foch, Suresnes, France.
Abstract
OBJECTIVE: Identification of biological markers able to better stratify cardiovascular risks in SLE patients is needed. We aimed to determine whether serum cardiac troponin T (cTnT) levels measured with a highly sensitive assay [high sensitivity cTnT (HS-cTnT)] may predict cardiovascular events (CVEs) in SLE. METHOD: All SLE patients included between 2007 and 2010 in the randomized, double-blind, placebo-controlled, multicentre PLUS trial were screened. Patients with no past history of CVE at inclusion and a follow-up period of >20 months were analysed. HS-cTnT concentration was measured using the electrochemiluminescence method on serum collected at PLUS inclusion. The primary outcome was the incident CVE. Factors associated with the primary outcome were identified and multivariate analysis was performed. RESULTS: Overall, 442 SLE patients (of the 573 included in the PLUS study) were analysed for the primary outcome with a median follow up of 110 (interquartile range: 99-120) months. Among them, 29 (6.6%) experienced at least one CVE that occurred at a median of 67 (interquartile range: 31-91) months after inclusion. Six out of 29 patients had more than one CVE. In the multivariate analysis, dyslipidaemia, age and HS-cTnT were associated with the occurrence of CVE. Kaplan-Meier analysis showed that a concentration of HS-cTnT > 4.27 ng/l at inclusion increased by 2.7 [hazard ratio 2.7 (95% CI: 1.3, 5.6), P =0.0083] the risk of CVE in SLE. CONCLUSION: HS-cTnT measured in serum is the first identified biomarker independently associated with incident CVE in SLE patients.
OBJECTIVE: Identification of biological markers able to better stratify cardiovascular risks in SLEpatients is needed. We aimed to determine whether serum cardiac troponin T (cTnT) levels measured with a highly sensitive assay [high sensitivity cTnT (HS-cTnT)] may predict cardiovascular events (CVEs) in SLE. METHOD: All SLEpatients included between 2007 and 2010 in the randomized, double-blind, placebo-controlled, multicentre PLUS trial were screened. Patients with no past history of CVE at inclusion and a follow-up period of >20 months were analysed. HS-cTnT concentration was measured using the electrochemiluminescence method on serum collected at PLUS inclusion. The primary outcome was the incident CVE. Factors associated with the primary outcome were identified and multivariate analysis was performed. RESULTS: Overall, 442 SLEpatients (of the 573 included in the PLUS study) were analysed for the primary outcome with a median follow up of 110 (interquartile range: 99-120) months. Among them, 29 (6.6%) experienced at least one CVE that occurred at a median of 67 (interquartile range: 31-91) months after inclusion. Six out of 29 patients had more than one CVE. In the multivariate analysis, dyslipidaemia, age and HS-cTnT were associated with the occurrence of CVE. Kaplan-Meier analysis showed that a concentration of HS-cTnT > 4.27 ng/l at inclusion increased by 2.7 [hazard ratio 2.7 (95% CI: 1.3, 5.6), P =0.0083] the risk of CVE in SLE. CONCLUSION: HS-cTnT measured in serum is the first identified biomarker independently associated with incident CVE in SLEpatients.