J Wei1, M J Wood2, M Dubreuil3, G Tomasson4, M R LaRochelle5, C Zeng6, N Lu7, J Lin8, H K Choi9, G Lei10, Y Zhang11. 1. Health Management Center, Xiangya Hospital, Central South University, Changsha, Hunan, China; Division of Rheumatology, Allergy, and Immunology, Department of Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA; The Mongan Institute, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA. Electronic address: weij1988@csu.edu.cn. 2. Division of Cardiology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA. Electronic address: MJWOOD@mgh.harvard.edu. 3. Boston University School of Medicine, Boston, MA, USA; VA Boston Healthcare System, Boston, MA, USA. Electronic address: mdubreui@bu.edu. 4. Department of Public Health Sciences, University of Iceland, Stapi Hringbraut, 101 Reykjavik, Iceland. Electronic address: gunnar.tomasson@gmail.com. 5. Clinical Addiction Research and Education Unit at Boston University School of Medicine and Boston Medical Center, Boston, MA, USA. Electronic address: Marc.LaRochelle@bmc.org. 6. Division of Rheumatology, Allergy, and Immunology, Department of Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA; The Mongan Institute, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA; Department of Orthopaedics, Xiangya Hospital, Central South University, Changsha, Hunan, China. Electronic address: CZENG6@mgh.harvard.edu. 7. Division of Rheumatology, Allergy, and Immunology, Department of Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA; Arthritis Research Canada, Richmond, British Columbia, Canada. Electronic address: nhleo@channing.harvard.edu. 8. Department of Orthopaedic Surgery, Peking University People's Hospital, Beijing, China. Electronic address: linjianhao@pkuph.edu.cn. 9. Division of Rheumatology, Allergy, and Immunology, Department of Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA; The Mongan Institute, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA. Electronic address: hchoi@partners.org. 10. Department of Orthopaedic Surgery, Peking University People's Hospital, Beijing, China; National Clinical Research Center of Geriatric Disorders, Xiangya Hospital, Central South University, Changsha, Hunan, China. Electronic address: lei_guanghua@csu.edu.cn. 11. Division of Rheumatology, Allergy, and Immunology, Department of Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA; The Mongan Institute, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA. Electronic address: yzhang108@mgh.harvard.edu.
Abstract
OBJECTIVE: Tramadol has been widely used among patients with osteoarthritis (OA); however, there is paucity of information on its cardiovascular risk. We aimed to examine the association of tramadol with risk of myocardial infarction (MI) among patients with OA. DESIGN: Among OA patients aged 50-90 years without history of MI, cancer, or opioid use disorder in The Health Improvement Network database in the United Kingdom (2000-2016), three sequential propensity-score matched cohort studies were assembled, i.e., (1) patients who initiated tramadol or naproxen (negative comparator); (2) patients who initiated tramadol or diclofenac (positive comparator); and (3) patients who initiated tramadol or codeine (a commonly used weak opioid). The outcome was incident MI over six-months. RESULTS: Among tramadol and naproxen initiators (n = 33,024 in each cohort), 77 (4.8/1000 person-years) and 46 (2.8/1000 person-years) incident MI occurred, respectively. The rate difference (RD) and hazard ratios (HR) for incident MI with tramadol initiation were 1.9 (95% confidence interval [CI] 0.6 to 2.3)/1000 person-years and 1.68 (95% CI 1.16 to 2.41) relative to naproxen initiation, respectively. Among tramadol and diclofenac initiators (n = 18,662 in each cohort), 58 (6.4/1000 person-years) and 47 (5.1/1000 person-years) incident MIs occurred, respectively. The corresponding RD and HR for incident MI were 1.2 (95%CI -2.1 to 14.1)/1000 person-years and 1.24 (95%CI 0.84 to 1.82), respectively. Among tramadol and codeine initiators (n = 42,722 in each cohort), 127 (6.1/1000 person-years) and 103 (5.0/1000 person-years) incident MI occurred, respectively, and the corresponding RD and HR were 1.1 (95%CI:-0.3 to 2.5)/1000 person-years and 1.23 (95%CI:0.95 to 1.60), respectively. CONCLUSIONS: In this population-based cohort of patients with OA, the six-month risk of MI among initiators of tramadol was higher than that of naproxen, but comparable to, if not lower than, those of diclofenac or codeine.
OBJECTIVE:Tramadol has been widely used among patients with osteoarthritis (OA); however, there is paucity of information on its cardiovascular risk. We aimed to examine the association of tramadol with risk of myocardial infarction (MI) among patients with OA. DESIGN: Among OApatients aged 50-90 years without history of MI, cancer, or opioid use disorder in The Health Improvement Network database in the United Kingdom (2000-2016), three sequential propensity-score matched cohort studies were assembled, i.e., (1) patients who initiated tramadol or naproxen (negative comparator); (2) patients who initiated tramadol or diclofenac (positive comparator); and (3) patients who initiated tramadol or codeine (a commonly used weak opioid). The outcome was incident MI over six-months. RESULTS: Among tramadol and naproxen initiators (n = 33,024 in each cohort), 77 (4.8/1000 person-years) and 46 (2.8/1000 person-years) incident MI occurred, respectively. The rate difference (RD) and hazard ratios (HR) for incident MI with tramadol initiation were 1.9 (95% confidence interval [CI] 0.6 to 2.3)/1000 person-years and 1.68 (95% CI 1.16 to 2.41) relative to naproxen initiation, respectively. Among tramadol and diclofenac initiators (n = 18,662 in each cohort), 58 (6.4/1000 person-years) and 47 (5.1/1000 person-years) incident MIs occurred, respectively. The corresponding RD and HR for incident MI were 1.2 (95%CI -2.1 to 14.1)/1000 person-years and 1.24 (95%CI 0.84 to 1.82), respectively. Among tramadol and codeine initiators (n = 42,722 in each cohort), 127 (6.1/1000 person-years) and 103 (5.0/1000 person-years) incident MI occurred, respectively, and the corresponding RD and HR were 1.1 (95%CI:-0.3 to 2.5)/1000 person-years and 1.23 (95%CI:0.95 to 1.60), respectively. CONCLUSIONS: In this population-based cohort of patients with OA, the six-month risk of MI among initiators of tramadol was higher than that of naproxen, but comparable to, if not lower than, those of diclofenac or codeine.
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