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A letter to the editor is presented in response to the article on the increased prevalence of antithyroid antibodies in rheumatoid arthritis (RA) patients by Dr. F. Atzeni and colleagues.

Introduction: The first step-down defibrillation studies in the subcutaneous implantable cardioverter-defibrillator (S-ICD) described a defibrillation threshold (DFT) of 32.5 ± 17.0 J and 36.6 ± 19.8 J. Therefore, the default shock output of the S-ICD was set at 80 J. In de novo implants, the DFT is lower in optimally positioned S-ICDs. However, a retrospective analysis raised concerns about a high DFT in S-ICD replacements, possibly related to fibrosis., Objective: We aimed to find the DFT in patients undergoing S-ICD generator replacement., Methods: This prospective study enrolled patients who underwent S-ICD generator replacement with subsequent defibrillation testing. A pre-specified defibrillation testing protocol was used to determine the DFT, defined as the lowest shock output that effectively terminated the induced ventricular arrhythmia., Results: A total of 45 patients were enrolled, 6.0 ± 2.1 years after initial implant. Mean DFT during replacement in the total cohort was 27.4 ± 14.3 J. In patients with a body mass index (BMI) 18.5-25 kg/m 2 (N = 22, BMI 22.5 ± 1.6), median DFT was 20 J (IQR 17.5-30). In 18/22 patients, the DFT was ≤30 J and 5/22 patients were successfully defibrillated at 10 J. One patient with hypertrophic cardiomyopathy had a DFT of 65 J. In patients with a BMI >25 kg/m 2 (N = 23, BMI 29.5 ± 4.2), median DFT was 30 J (IQR 20-40). In 15/23 patients, the DFT was ≤30 J and 4/23 patients had a successful defibrillation test at 10 J., Conclusions: This study eases concerns about a high DFT after S-ICD generator replacement. The majority of patients had a DFT ≤30 J, regardless of BMI, suggesting that the shock output of the S-ICD could be safely reduced., Competing Interests: Declaration of Competing Interest Van Halm reports consultancy or speaker fees and research grants from Abbott, Biotronik, Medtronic and Microport. Wilde is consultant for ARMGO and Thryv Therapeutics. Knops reports consultancy fees and research grants from Abbott, Boston Scientific, Cairdac, and Medtronic and has stock options from AtaCor Medical Inc. The other authors report no conflicts of interest., (Copyright © 2023 The Author(s). Published by Elsevier B.V. All rights reserved.)

Objectives: To extend our investigation of cardiovascular diseases (CVD) in rheumatoid arthritis (RA) patients to a follow up of more than 20 years, with a special focus on patients without prevalent CVD., Methods: The CARRÉ study is an ongoing prospective cohort study on CV endpoints in RA patients. Results were compared to those of a reference cohort (n = 2484) enriched for type 2 diabetes mellitus (DM). Hazard ratios (HR) for RA and DM patients compared to non-RA/-DM controls were calculated with cox proportional hazard models, and adjusted for baseline SCORE1 (estimated 10-year CVD mortality risk based on CV risk factors)., Results: 238 RA patients, 117 DM patients and 1282 controls, without prevalent CVD at baseline were included. Analysis of events in these patients shows that after adjustment, no relevant 'RA-specific' risk remains (HR 1.16; 95%CI 0.88 - 1.53), whereas a 'DM-specific' risk is retained (1.73; 1.24 - 2.42). In contrast, adjusted analyses of all cases confirm the presence of an 'RA-specific' risk (1.50; 1.19 - 1.89)., Conclusions: In RA patients without prevalent CVD the increased CVD risk is mainly attributable to increased presence of traditional risk factors. After adjustment for these factors, an increased risk attributable to RA only was thus preferentially seen in the patients with prevalent CVD at baseline. As RA treatment has improved, this data suggests that the 'RA-specific' effect of inflammation is preferentially seen in patients with prevalent CVD. We suggest that with modern (early) treatment of RA, most of the current increased CVD risk is mediated through traditional risk factors., Competing Interests: Declaration of Competing Interests None., (Copyright © 2022. Published by Elsevier Inc.)

Objective: To develop recommendations for cardiovascular risk (CVR) management in gout, vasculitis, systemic sclerosis (SSc), myositis, mixed connective tissue disease (MCTD), Sjögren's syndrome (SS), systemic lupus erythematosus (SLE) and antiphospholipid syndrome (APS)., Methods: Following European League against Rheumatism (EULAR) standardised procedures, a multidisciplinary task force formulated recommendations for CVR prediction and management based on systematic literature reviews and expert opinion., Results: Four overarching principles emphasising the need of regular screening and management of modifiable CVR factors and patient education were endorsed. Nineteen recommendations (eleven for gout, vasculitis, SSc, MCTD, myositis, SS; eight for SLE, APS) were developed covering three topics: (1) CVR prediction tools; (2) interventions on traditional CVR factors and (3) interventions on disease-related CVR factors. Several statements relied on expert opinion because high-quality evidence was lacking. Use of generic CVR prediction tools is recommended due to lack of validated rheumatic diseases-specific tools. Diuretics should be avoided in gout and beta-blockers in SSc, and a blood pressure target <130/80 mm Hg should be considered in SLE. Lipid management should follow general population guidelines, and antiplatelet use in SLE, APS and large-vessel vasculitis should follow prior EULAR recommendations. A serum uric acid level <0.36 mmol/L (<6 mg/dL) in gout, and disease activity control and glucocorticoid dose minimisation in SLE and vasculitis, are recommended. Hydroxychloroquine is recommended in SLE because it may also reduce CVR, while no particular immunosuppressive treatment in SLE or urate-lowering therapy in gout has been associated with CVR lowering., Conclusion: These recommendations can guide clinical practice and future research for improving CVR management in rheumatic and musculoskeletal diseases., Competing Interests: Competing interests: GCD, DV, EH, LB, SB, DTB, NB, GK, FM, CM, MR-C, KS, SS, VPvH, GJM, MMW and MN have nothing to declare. FA: research grants from BMS, Celgene, Novartis and Sandoz and consulting fees from AbbVie, Biogen, BMS, Celgene, Janssen, Lilly, Novartis, Pfizer and Sanofi-Aventis, all unrelated to this manuscript; INB: grant from GSK paid to institution, consulting fees from Astra Zeneca, GSK, Eli lilly, UC, MSD paid to institution, support for attending meetings and/or travel from GSK, participation on a data safety monitoring board/or advisory board from Aurinia, Astra Zeneca and ILTOO paid to institution, all unrelated to this manuscript; MÁG-G: grants/research support from AbbVie, MSD, Jansen and Roche paid to institution and personal consulting fees/participation in company sponsored speakers bureau from AbbVie, Pfizer, Roche, Celgene, MSD, Novartis, SOBI and Sanofi, all unrelated to this manuscript; SJ: grants from BMS paid to institution, personal consulting fees from Astra Zeneca, and personal fees from Danish Medicolegal Council, all unrelated to this manuscript; NS: grants paid to institution from Astrazeneca, Boehringer Ingelheim and Roche Diagnostics, personal consulting fees from Afimmune, Amgen, Astrazeneca, Boehringer Ingelheim, Eli-Lilly, Hanmi Pharamceuticals, MSD, Novartis, Novo Nordisk, Pfizer and Sanofi, all unrelated to this manuscript; ES: grant from Merck and honoraria from Janssen, all unrelated to this manuscript; ZS: research grants from Pfizer paid to institution and personal consulting fees from Pfizer, MSD, Lilly, Novartis, Roche, Gedeon Richter, Boehringer Ingelheim, Abbvie, all unrelated to this manuscript; A-KT: speakers fee from Berlin Chemie Menarini, Novarti and personal fees and non-financial support from AstraZeneca and Grünenthal, all unrelated to this manuscript; AT: consulting fees from Magenta Therapeutics and personal fees from Novartis and Idorsia for participation on a Data Safety Monitoring Board or Advisory Board, all unrelated to this manuscript; AV: personal consulting fees from Astra Zeneca and GS, all unrelated to this manuscript; MGT: research grants from Genesis, GSK, MSD, Pfizer and UCB paid to institution, and personal consulting fees from Genesis, GSK and Novartis, all unrelated to this manuscript., (© Author(s) (or their employer(s)) 2022. No commercial re-use. See rights and permissions. Published by BMJ.)

An 81-year-old male with a history of systolic heart failure due to an underlying ischemic cardiomyopathy with a left ventricular ejection fraction of 13% and QRS duration of 130 ms had undergone an uncomplicated cardiac resynchronization therapy defibrillator implantation (Quadra Assura MP, St. Jude Medical, LV lead (SJM Quartet 1458Q-86), RA lead (Biotronik Safio S53) and RV shocklead (Biotronik Linox Smart S65 ProMRI) in 2015., (© 2020 The Authors. Journal of Cardiovascular Electrophysiology Published by Wiley Periodicals LLC.)

Background: Diastolic left ventricular (LV) dysfunction appears more prevalent in ankylosing spondylitis (AS). The effects of tumor necrosis factor alpha (TNF-α) blocking therapy, a strong and effective anti-inflammatory drug, on diastolic LV function in AS are unknown. The objective of the study was to find the effects of 1-year treatment with golimumab 50 mg subcutaneously once per month on systolic and diastolic LV dysfunction in AS patients., Methods: Forty consecutive AS patients were treated with TNF-α blocking therapy for 1 year. Transthoracic echocardiography was performed in all patients at baseline and after 1 year of treatment., Results: Diastolic LV function improved after treatment in four out of six (67%) AS patients who completed follow-up ( P =0.125), and did not develop or worsen in any of the other patients. Treatment with TNF-α blocking therapy had no effect on systolic LV function., Conclusion: These findings give support to the hypothesis that diastolic LV dysfunction improves during treatment with TNF-α blocking therapy., Competing Interests: Disclosure The authors report no conflicts of interest in this work.

Introduction: Tumour necrosis factor (TNF) blocking therapy is an effective treatment for chronic inflammatory arthritis. As circulating TNF might induce or exacerbate the development of congestive heart failure (CHF), several trials have investigated the effect of TNF blocking therapy on CHF. However, due to inefficacy and even a risk of exacerbation of CHF, TNF blocking therapy has since then been contraindicated in patients with advanced CHF, New York Heart Association class III and IV. We review current knowledge on the pathophysiological mechanisms and safety of TNF blocking therapy in chronic inflammatory arthritis patients with regard to CHF., Methods: A systematic search of the literature published up till December 2013 was conducted in MEDLINE, EMBASE and the Cochrane Library to identify all studies investigating the effect of TNF blocking therapy on the occurrence and risk of CHF in patients with rheumatoid arthritis (RA), ankylosing spondylitis (AS) and psoriatic arthritis (PsA). All articles reporting data on the prevalence or incidence of CHF during treatment with TNF blocking therapy in patients with in RA, AS or PsA were included. Also imaging studies and studies with biomarkers, investigating the effect of TNF blocking therapy on cardiac function were included., Results: In total, 54 studies were included. Results from large prospective registries suggest that first, a potentially harmful effect of TNF blocking therapy on the incidence of CHF in older RA patients cannot be excluded and that no harmful effect was observed of TNF blocking therapy in other patients. Second, we found that TNF blocking therapy potentially improves several echocardiographic parameters of cardiac function in RA, AS and PsA, but due to small sample sizes, these results require validation in larger studies. Third, we found improvement in NT-proBNP levels after use of TNF blocking therapy in both RA and AS., Conclusion: Based on current literature, in patients with chronic inflammatory arthritis and concomitant symptomatic mild-tomoderate CHF (NYHA class I or II), treatment with TNF blocking therapy is not contraindicated. In chronic inflammatory arthritis patients with concomitant symptomatic moderate-to-severe CHF, NYHA class III-IV, treatment with TNF blocking therapy should be avoided if possible. Whenever, treatment with TNF-blocking therapy is considered in these patients consultation with a cardiologist is recommended before treatment is initiated.