Ntobeko A B Ntusi1, Jane M Francis2, Emily Sever2, Alexander Liu2, Stefan K Piechnik2, Vanessa M Ferreira2, Paul M Matthews3, Matthew D Robson2, Paul B Wordsworth4, Stefan Neubauer2, Theodoros D Karamitsos5. 1. University of Oxford Centre for Clinical Magnetic Resonance Research (OCMR), Division of Cardiovascular Medicine, Radcliffe Department of Medicine, John Radcliffe Hospital, Oxford, UK; Division of Cardiology, Department of Medicine, Groote Schuur Hospital, Cape Town, South Africa. 2. University of Oxford Centre for Clinical Magnetic Resonance Research (OCMR), Division of Cardiovascular Medicine, Radcliffe Department of Medicine, John Radcliffe Hospital, Oxford, UK. 3. GlaxoSmithKline Clinical Imaging Centre, London, UK; Division of Brain Sciences, Department of Medicine, Imperial College, London, UK. 4. Bortnar Institute, Nuffield Department of Orthopaedics, Rheumatology and Musculoskeletal Sciences, University of Oxford, Nuffield Orthopaedic Centre, John Radcliffe Hospital, Oxford, UK. 5. University of Oxford Centre for Clinical Magnetic Resonance Research (OCMR), Division of Cardiovascular Medicine, Radcliffe Department of Medicine, John Radcliffe Hospital, Oxford, UK; First Department of Cardiology, Aristotle University of Thessaloniki, AHEPA Hospital, Thessaloniki, Greece. Electronic address: tkaramitsos@auth.gr.
Abstract
BACKGROUND: Rheumatoid arthritis (RA), ankylosing spondylitis (AS) and psoriatic arthritis (PsA) are common disorders associated with increased rates of cardiovascular disease (CVD), but the contribution of cytokine-induced inflammation to impaired cardiovascular function in these conditions remains poorly understood. OBJECTIVES: We assessed the effect of anti-TNF therapy on myocardial and vascular function, myocardial tissue characteristics and perfusion in inflammatory arthropathy and systemic rheumatic disease (IASRD) patients, using cardiovascular magnetic resonance (CMR). METHODS: 20 RA patients, 7 AS patients, 5 PsA patients without previously known CVD scheduled to commence anti-TNF therapy and 8 RA patients on standard disease modifying antirheumatic drugs underwent CMR at 1.5 T, including cine, tagging, pulse wave velocity (PWV), T2-weighted, native and postcontrast T1 mapping, ECV quantification, rest and stress perfusion and late gadolinium enhancement (LGE) imaging. RESULTS: Following anti-TNF therapy, there was significant reversal of baseline subclinical cardiovascular dysfunction, as evidenced by improvement in peak systolic circumferential strain (p < 0.001), peak diastolic circumferential strain rate (p < 0.001), and total aortic PWV, (p < 0.001). This was accompanied by a reduction in myocardial inflammation, as assessed by T2-weighted imaging (p = 0.005), native T1 mapping (p = 0.009) and ECV quantification (p = 0.001), as well as in serum inflammatory markers like CRP (p < 0.001) and ESR (p < 0.001), and clinical measures of disease activity (DAS28-CRP, p = 0.001; BASDAI, p < 0.001). A trend towards improvement in myocardial perfusion was observed (p = 0.07). Focal myocardial fibrosis, as detected by LGE CMR was not altered by anti-TNF therapy (p = 0.92). CONCLUSIONS: Anti-TNF therapy reduces subclinical myocardial inflammation and improves cardiovascular function in RA, AS and PsA. CMR may be used to track disease progression and response to therapy. Future CMR-based studies to demonstrate effect of anti-TNF therapy modulation of vascular structure and function on hard clinical events and outcomes would be useful.
BACKGROUND:Rheumatoid arthritis (RA), ankylosing spondylitis (AS) and psoriatic arthritis (PsA) are common disorders associated with increased rates of cardiovascular disease (CVD), but the contribution of cytokine-induced inflammation to impaired cardiovascular function in these conditions remains poorly understood. OBJECTIVES: We assessed the effect of anti-TNF therapy on myocardial and vascular function, myocardial tissue characteristics and perfusion in inflammatory arthropathy and systemic rheumatic disease (IASRD) patients, using cardiovascular magnetic resonance (CMR). METHODS: 20 RApatients, 7 AS patients, 5 PsA patients without previously known CVD scheduled to commence anti-TNF therapy and 8 RApatients on standard disease modifying antirheumatic drugs underwent CMR at 1.5 T, including cine, tagging, pulse wave velocity (PWV), T2-weighted, native and postcontrast T1 mapping, ECV quantification, rest and stress perfusion and late gadolinium enhancement (LGE) imaging. RESULTS: Following anti-TNF therapy, there was significant reversal of baseline subclinical cardiovascular dysfunction, as evidenced by improvement in peak systolic circumferential strain (p < 0.001), peak diastolic circumferential strain rate (p < 0.001), and total aortic PWV, (p < 0.001). This was accompanied by a reduction in myocardial inflammation, as assessed by T2-weighted imaging (p = 0.005), native T1 mapping (p = 0.009) and ECV quantification (p = 0.001), as well as in serum inflammatory markers like CRP (p < 0.001) and ESR (p < 0.001), and clinical measures of disease activity (DAS28-CRP, p = 0.001; BASDAI, p < 0.001). A trend towards improvement in myocardial perfusion was observed (p = 0.07). Focal myocardial fibrosis, as detected by LGE CMR was not altered by anti-TNF therapy (p = 0.92). CONCLUSIONS: Anti-TNF therapy reduces subclinical myocardial inflammation and improves cardiovascular function in RA, AS and PsA. CMR may be used to track disease progression and response to therapy. Future CMR-based studies to demonstrate effect of anti-TNF therapy modulation of vascular structure and function on hard clinical events and outcomes would be useful.
Authors: Paras Karmacharya; Ravi Shahukhal; Cynthia S Crowson; M Hassan Murad; John M Davis; Pragya Shrestha; Delamo Bekele; Kerry Wright; Rikesh Chakradhar; Maureen Dubreuil Journal: Rheumatol Ther Date: 2020-11-10
Authors: Sven Plein; Bara Erhayiem; Graham Fent; Sarah Horton; Raluca Bianca Dumitru; Jacqueline Andrews; John P Greenwood; Paul Emery; Elizabeth Ma Hensor; Paul Baxter; Sue Pavitt; Maya H Buch Journal: Ann Rheum Dis Date: 2020-08-28 Impact factor: 19.103
Authors: George Markousis-Mavrogenis; George Poulos; Theodoros Dimitroulas; Aikaterini Giannakopoulou; Clio Mavragani; Vasiliki Vartela; Dionysia Manolopoulou; Genovefa Kolovou; Paraskevi Voulgari; Petros P Sfikakis; George D Kitas; Sophie I Mavrogeni Journal: Diagnostics (Basel) Date: 2021-03-15