E108 Bridging the gap in cardiovascular risk management in idiopathic inflammatory myopathies: insights from a single-centre cohort

Background/Aims Evidence suggests that patients with idiopathic inflammatory myopathies (IIM) are at an increased risk of atherosclerotic cardiovascular mortality. Cholesterol management is an important component of optimising cardiovascular health; however, IIM patients may be reluctant to take statins due to concerns about muscle-related side effects and misconceptions about statin-induced IIM. Although limited, the available literature suggests that statins are well tolerated in non-anti-HMGCR-IIM, and that alternative lipid-lowering agents (LLA) may be safely employed in patients with anti-HMGCR-IIM. This study aimed to assess statin use and cardiovascular risk, as estimated by QRISK3, in a cohort of IIM patients, and to compare findings between anti-HMGCR and non-anti-HMGCR subtypes. Methods A retrospective analysis was performed on patients attending the Myositis Clinic at Royal United Hospital, Bath. Data on demographics, cardiovascular risk factors, LLA use, and QRISK3 scores were collected. Results A total of 74 patients were included. Ten were anti-HMCGR positive, 16 seronegative, and 48 positive for other myositis-specific antibodies. Among the 10 anti-HMGCR-IIM patients (median age 70.5 years, 40% females), 9/10 (90%) had been on atorvastatin, 3 of whom had also taken an alternative statin. All presented with muscle symptoms and elevated CK, ranging from 5000-19,393 IU/L. Following diagnosis, statins were discontinued in all cases, with 6/9 (67%) switched to an alternative LLA and 3/9 (33%) ceasing lipid therapy entirely. In the non-anti-HMGCR cohort (n = 64; median age 63.5 years; 73% female), 7(11%) had previously been on statins, which were ceased with no alternative LLA prescribed. Seventeen(27%) remained on LLA, including 4 who were switched from statins to alternative LLA (10 atorvastatin, 1 colsevelam hydrocholoride, 3 ezetimibe, 1 ezetmibe/perbromic acid, 1 rosuvastatin, and 1 rosuvastatin and ezetimibe. Forty(63%) were not on and had never been on LLA. QRISK3 scores were available for 51/74 patients (4 excluded due to age cut-off and 19 due to missing data). There was anticipated variability in results, ranging from 17-36% in the HMGCR cohort and 0.6-65.3% in the non-HMGCR group. Median QRISK3 scores were similar between HMGCR and non-HMGCR groups (17.1% [IQR 15.9] vs 15.3% [IQR 17.4]). Concerningly, despite having at least a moderate cardiovascular risk score (QRISK3>10%), 14% of anti-HMGCR patients and 50% of non-anti-HMGCR patients were not on LLA. Traditional cardiovascular risk factors were more frequent in the anti-HMGCR-IIM group: previous cardiac events (30% vs 7.8%), hyperlipidaemia (70% vs 23%), diabetes (50% vs 11%), hypertension (50% vs 41%), and a higher median BMI (30.9 vs 26.0). Conclusion In our cohort, anti-HMGCR-IIM patients demonstrated a higher burden of traditional cardiovascular risk factors compared with non-anti-HMGCR IIM. Despite elevated QRISK3 scores, lipid-lowering therapy was often underutilised across both groups. These findings highlight a need for improved cardiovascular risk assessment and tailored lipid management strategies in patients with IIM. Disclosure K. Loh: Grants/research support; KL has received funding from the Australian Rheumatology Association (ARA) WA Research Fellowship grant.