Nicola Riccardo Pugliese1, Alessandro Mengozzi2, Stefano Masi2, Claudio Borghi3, Agostino Virdis2, Edoardo Casiglia4, Valerie Tikhonoff5, Arrigo F G Cicero3, Andrea Ungar6, Giulia Rivasi6, Massimo Salvetti7, Carlo M Barbagallo8, Michele Bombelli9, Raffaella Dell'Oro9, Berardino Bruno10, Luciano Lippa11, Lanfranco D'Elia12, Paolo Verdecchia13, Francesca Mallamaci14, Massimo Cirillo15, Marcello Rattazzi16, Pietro Cirillo17, Loreto Gesualdo17, Alberto Mazza18, Cristina Giannattasio19, Alessandro Maloberti19, Massimo Volpe20,21, Giuliano Tocci20,21, Georgios Georgiopoulos22, Guido Iaccarino23, Pietro Nazzaro24, Gianfranco Parati25,26, Paolo Palatini4, Ferruccio Galletti12, Claudio Ferri10, Giovambattista Desideri10, Francesca Viazzi27, Roberto Pontremoli27, Maria Lorenza Muiesan7, Guido Grassi9. 1. Department of Clinical and Experimental Medicine, University of Pisa, Via Roma, 67, 56126, Pisa, Italy. n.r.pugliese88@gmail.com. 2. Department of Clinical and Experimental Medicine, University of Pisa, Via Roma, 67, 56126, Pisa, Italy. 3. Department of Medical and Surgical Science, Hypertension and Cardiovascular Risk Factors Research Center, Alma Mater Studiorum University of Bologna, Bologna, Italy. 4. Department of Medicine, University of Padua, Padua, Italy. 5. Department of Medicine and Studium Patavinum, University of Padua, Padua, Italy. 6. Department of Geriatric and Intensive Care Medicine, Careggi Hospital and University of Florence, Florence, Italy. 7. Department of Clinical and Experimental Sciences, University of Brescia, Brescia, Italy. 8. Biomedical Department of Internal Medicine and Specialistics, University of Palermo, Palermo, Italy. 9. Clinica Medica, Department of Medicine and Surgery, University of Milano-Bicocca, Monza, Italy. 10. Department of Life, Health and Environmental Sciences, University of L'Aquila, L'Aquila, Italy. 11. Italian Society of General Medicine, Avezzano, L'Aquila, Italy. 12. Department of Clinical Medicine and Surgery, University of Naples 'Federico II', Naples, Italy. 13. Hospital S. Maria Della Misericordia, Perugia, Italy. 14. Clinical Epidemiology of Renal Diseases and Hypertension, Reggio Cal Unit, CNR-IFC, Reggio Calabria, Italy. 15. Department of Public Health, University of Naples 'Federico II', Naples, Italy. 16. Department of Medicine, Medicina Interna 1°, Ca' Foncello University Hospital, University of Padova, Treviso, Italy. 17. Department of Emergency and Organ Transplantation-Nephrology, Dialysis and Transplantation Unit, Aldo Moro University of Bari, Bari, Italy. 18. Department of Internal Medicine, Hypertension Unit, General Hospital, Rovigo, Italy. 19. Cardiology IV, A. De Gasperis Department, Health Science Department, Niguarda Ca' Granda Hospital, Milano-Bicocca University, Milan, Italy. 20. Hypertension Unit, Division of Cardiology, Department of Clinical and Molecular Medicine, Faculty of Medicine and Psychology, Sant'Andrea Hospital, University of Rome Sapienza, Rome, Italy. 21. IRCCS Neuromed, Pozzilli, IS, Italy. 22. First Department of Cardiology, Medical School, Hippokration Hospital, University of Athens, Athens, Greece. 23. Department of Advanced Biomedical Sciences, University of Naples 'Federico II', Naples, Italy. 24. Department of Medical Basic Sciences, Neurosciences and Sense Organs, University of Bari Medical School, Bari, Italy. 25. Department of Cardiovascular, Neural and Metabolic Sciences, Istituto Auxologico Italiano, IRCCS S. Luca Hospital, Lucca, Italy. 26. Department of Medicine and Surgery, University of Milan-Bicocca, Milan, Italy. 27. Department of Internal Medicine, University of Genoa and Policlinico San Martino, Genoa, Italy.
Abstract
INTRODUCTION: Serum uric acid (SUA) has been depicted as a contributory causal factor in metabolic syndrome (MS), which in turn, portends unfavourable prognosis. AIM: We assessed the prognostic role of SUA in patients with and without MS. METHODS: We used data from the multicentre Uric Acid Right for Heart Health study and considered cardiovascular mortality (CVM) as death due to fatal myocardial infarction, stroke, sudden cardiac death, or heart failure. RESULTS: A total of 9589 subjects (median age 58.5 years, 45% males) were included in the analysis, and 5100 (53%) patients had a final diagnosis of MS. After a median follow-up of 142 months, we observed 558 events. Using a previously validated cardiovascular SUA cut-off to predict CVM (> 5.1 mg/dL in women and 5.6 mg/dL in men), elevated SUA levels were significantly associated to a worse outcome in patients with and without MS (all p < 0.0001) and provided a significant net reclassification improvement of 7.1% over the diagnosis of MS for CVM (p = 0.004). Cox regression analyses identified an independent association between SUA and CVM (Hazard Ratio: 1.79 [95% CI, 1.15-2.79]; p < 0.0001) after the adjustment for MS, its single components and renal function. Three specific combinations of the MS components were associated with higher CVM when increasing SUA levels were reported, and systemic hypertension was the only individual component ever-present (all p < 0.0001). CONCLUSION: Increasing SUA levels are associated with a higher CVM risk irrespective of the presence of MS: a cardiovascular SUA threshold may improve risk stratification.
INTRODUCTION: Serum uric acid (SUA) has been depicted as a contributory causal factor in metabolic syndrome (MS), which in turn, portends unfavourable prognosis. AIM: We assessed the prognostic role of SUA in patients with and without MS. METHODS: We used data from the multicentre Uric Acid Right for Heart Health study and considered cardiovascular mortality (CVM) as death due to fatal myocardial infarction, stroke, sudden cardiac death, or heart failure. RESULTS: A total of 9589 subjects (median age 58.5 years, 45% males) were included in the analysis, and 5100 (53%) patients had a final diagnosis of MS. After a median follow-up of 142 months, we observed 558 events. Using a previously validated cardiovascular SUA cut-off to predict CVM (> 5.1 mg/dL in women and 5.6 mg/dL in men), elevated SUA levels were significantly associated to a worse outcome in patients with and without MS (all p < 0.0001) and provided a significant net reclassification improvement of 7.1% over the diagnosis of MS for CVM (p = 0.004). Cox regression analyses identified an independent association between SUA and CVM (Hazard Ratio: 1.79 [95% CI, 1.15-2.79]; p < 0.0001) after the adjustment for MS, its single components and renal function. Three specific combinations of the MS components were associated with higher CVM when increasing SUA levels were reported, and systemic hypertension was the only individual component ever-present (all p < 0.0001). CONCLUSION: Increasing SUA levels are associated with a higher CVM risk irrespective of the presence of MS: a cardiovascular SUA threshold may improve risk stratification.
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