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SummaryThe mortality risk showed a positive correlation as the number of subsequent fractures increased. Hip fracture showed the greatest association with mortality risk, followed by vertebral fracture. For the combination of hip and vertebral fracture, a hip fracture after a vertebral fracture showed the highest mortality risk.IntroductionIt is unclear whether subsequent fractures or a certain location and sequence of subsequent fractures are associated with mortality risk in the elderly. We aimed to investigate the relationship between subsequent fractures and mortality risk.MethodsUsing the Korean National Health Insurance Research Database, we analyzed the cohort data of 24,756 patients aged > 60 years who sustained fractures between 2002 and 2013. Cox regression was used to assess the mortality risk associated with the number, locations, and sequences of subsequent fractures.ResultsMortality hazard ratios (HRs) for women and men were shown to be associated with the number of subsequent fractures (one, 1.63 (95% confidence interval [CI], 1.48–1.80) and 1.42 (95% CI, 1.28–1.58); two, 1.75 (95% CI, 1.47–2.08) and 2.03 (95% CI, 1.69–2.43); three or more, 2.46(95% CI, 1.92–3.15) and 1.92 (95% CI, 1.34–2.74), respectively). For women, the mortality risk was high when hip (HR, 2.49; 95% CI, 1.80–3.44) or vertebral (HR, 1.40; 95% CI, 1.03–1.90) fracture occurred as a second fracture. Compared with a single hip fracture, there was a high mortality risk in the group with hip fracture after the first vertebral fracture (HR, 2.90; 95% CI, 1.86–4.54), followed by vertebral fracture after the first hip fracture (HR, 1.90; 95% CI, 1.12–3.22).ConclusionThe mortality risk showed a positive correlation as the number of subsequent fractures increased. Hip fracture showed the greatest association with mortality risk, followed by vertebral fracture. For the combination of hip and vertebral fracture, a hip fracture after a vertebral fracture showed the highest mortality risk.

Background:Systemic vasculitis is one of the most frequent extra-glandular manifestations in patients with Primary Sjögren syndrome (pSS), and further, small vessel vasculitis, particularly cryoglobulinaemic vasculitis is known as the most common vasculitis in patients with pSSObjectives:This study applied the 2022 American College of Rheumatology/European Alliance of Association for Rheumatology (ACR/EULAR) criteria for antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) to patients with pSS accompanied by signs and symptoms suggestive of small- and medium-vessel vasculitis and investigated the overall frequency of and the major contributing factors to the reclassification of overlap syndrome of pSS with AAV (OS-pSS-AAV).Methods:This study included 116 patients with pSS according to the inclusion criteria, and defined signs and symptoms suggestive of small- or medium-vessel vasculitides as lung parenchymal lesions supporting AAV, peripheral neuropathy, and suspected renal vasculitis. The classification could be made when the total scores for microscopic polyangiitis (MPA) and granulomatosis with polyangiitis (GPA) are 5 points or more, and that for eosinophilic GPA (EGPA) is 6 points or more.Results:The median age of the patients was 56.0 years, and 87.1% were women. Ninety-five, 12, and 37 patients had lung parenchymal lesions supporting AAV, peripheral neuropathy, and suspected renal vasculitis. According to the 2022 ACR/EULAR criteria for AAV, 35 of 116 (30.2%) patients were reclassified as having OS-pSS-AAV. Among these 35 patients, four were reclassified as having both OS-pSS-MPA and OS-pSS- GPA, whereas, one as having both OS-pSS-MPA and OS-pSS-EGPA simultaneously. The major contributing factor to the reclassification of OS-pSS-AAV was ANCA positivity.Conclusion:The overall frequency of the reclassification of OS-pSS-AAV was 30.2% in pSS patients accompanied by signs and symptoms suggestive of small- and medium-vessel vasculitis. Its likelihood increased according to ANCA positivity.REFERENCES:[1] Argyropoulou OD, Tzioufas AG. Common and rare forms of vasculitis associated with Sjögren’s syndrome. Curr Opin Rheumatol 2020;32:21-8.[2] Scofield RH. Vasculitis in Sjögren’s Syndrome. Curr Rheumatol Rep 2011;13:482-8.Acknowledgements:NIL.Disclosure of Interests:None declared.

Background:The monocyte-to-high-density lipoprotein-cholesterol (HDL-cholesterol) ratio (MHR) was introduced, and MHR at diagnosis or study entry was reported to be associated with all-cause mortality, acute coronary syndrome (ACS), and atherosclerosis.Objectives:In this study, the association between the MHR at diagnosis and poor outcomes of atherosclerosis-related antineutrophil cytoplasmic antibody-associated vasculitis (AAV) during follow-up in patients with AAV was investigated.Methods:This retrospective study included 138 patients diagnosed with AAV. Their comprehensive medical records were meticulously reviewed. All-cause mortality, cerebrovascular accident (CVA), and ACS were evaluated as atherosclerosis-related poor outcomes of AAV. MHR was obtained by dividing monocyte counts (/mm3) by HDL-cholesterol (mg/dL) levels.Results:The median age of the 138 patients was 58.3 years with 44 being male (31.9%). Among the 138 patients, 11 (8.0%) died, and 11 (8.0%) and nine (6.5%) had CVA, and ACS, respectively. MHR at diagnosis was significantly correlated with the Birmingham Vasculitis Activity Score, erythrocyte sedimentation rate, and C-reactive protein at diagnosis. Among the three poor outcomes of AAV, only CVA during follow-up was significantly associated with MHR at diagnosis, and thus, only CVA was considered an atherosclerosis-related poor outcome of AAV. In the multivariable Cox hazards model analysis, MHR (hazard ratio [HR] 1.195) and serum albumin (HR 0.203) at diagnosis were independently associated with CVA during follow-up. Additionally, patients with MHR at diagnosis ≥3.0 exhibited a significantly higher risk for CVA and lower cumulative CVA-free survival rate than those with MHR at diagnosis <3.0.Conclusion:This study is the first to demonstrate clinical implications of MHR suggesting that MHR at diagnosis is significantly and independently associated with CVA during follow-up in patients with AAV.REFERENCES:[1] Jiang M, Yang J, Zou H, Li M, Sun W, Kong X (2022) Monocyte-to-high-density lipoprotein-cholesterol ratio (MHR) and the risk of all-cause and cardiovascular mortality: a nationwide cohort study in the United States. Lipids Health Dis 21(1):30. https://DOI:10.1186/s12944-022-01638-6.[2] Xi J, Men S, Nan J, Yang Q, Dong J (2022) The blood monocyte to high density lipoprotein cholesterol ratio (MHR) is a possible marker of carotid artery plaque. Lipids Health Dis 21(1):130. https://DOI:10.1186/s12944-022-01741-8.Figure 1.Relative risk.Patients with MHR at diagnosis ≥3.0 exhibits a significantly higher risk of CVA than those with MHR at diagnosis <3.0MHR: monocyte-to-high-density lipoprotein-cholesterol; CVA: cerebrovascular accident.Acknowledgements:NIL.Disclosure of Interests:None declared.

BackgroundDecreased muscle mass is frequently observed in patients with autoimmune rheumatic diseases; however, the relationship between muscle quality and patient outcomes has not been well understood.ObjectivesThis study evaluated the influence of muscle quality on the outcomes of antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV).MethodsRecords of patients with AAV (microscopic polyangiitis, granulomatosis with polyangiitis, and eosinophilic granulomatosis with polyangiitis) at the Severance Hospital having computed tomography (CT) images at disease diagnosis were retrospectively reviewed. For muscle quality measures, normal attenuation muscle area (NAMA), low attenuation muscle area (LAMA), total abdominal muscle area (TAMA), and intramuscular adipose tissue (IMAT) in the axial muscles of the middle third lumbar vertebra level was calculated. Correlations between NAMA, LAMA, and IMAT and patient characteristics and outcomes were assessed.ResultsA total of 136 patients with CT images at AAV diagnosis were identified. Correlation analyses revealed that age, female sex, total cholesterol, and alanine aminotransferase were significantly associated with NAMA. LAMA was associated with age, body mass index (BMI), five-factor score (FFS), and C-reactive protein, while a relationship between IMAT and age and BMI was observed. Cox-proportional hazard analysis demonstrated that NAMA/TAMA≤0.46 (odds ratio [OR] 5.612, 95% confidence interval [CI] 1.758-17.909, p=0.004), female sex (OR 0.228, 95% CI 0.075, 0.684, p=0.008), dyslipidemia (OR 3.819, 95% CI 1.380, 10.571, p=0.010), and FFS (OR 2.160, 1.298-3.595, p=0.003), were independent factors associated with mortality.ConclusionHigher mortality was observed in patients with AAV with NAMA/TAMA ≤ 0.46, indicating that cautious monitoring is required in these patients.References[1]An HJ, Tizaoui K, Terrazzino S et al (2020) Sarcopenia in Autoimmune and Rheumatic Diseases: A Comprehensive Review. Int J Mol Sci 2020;21. https://doi.org/10.3390/ijms21165678[2]Lee MJ, Kim HK, Kim EH, Bae SJ, Kim KW, Kim MJ, Choe J (2021) Association Between Muscle Quality Measured by Abdominal Computed Tomography and Subclinical Coronary Atherosclerosis. Arterioscler Thromb Vasc Biol 2021;41:e128-e140. https://doi.org/10.1161/atvbaha.120.315054Figure : Kaplan Meier-analysis with clinical outcomes according to NAMA/TAMA cut-off value of 0.46.Acknowledgements:NIL.Disclosure of InterestsNone Declared.

Background:RA-ILD (interstitial lung disease) is a heterogeneous disease with a chronic course and potential for flares. Serum biomarkers are needed to identify those at risk for RA-ILD progression.Objectives:To investigate the associations of baseline and change of pulmonary damage biomarkers (serum Kreb von den Lungen 6 [KL-6], human surfactant protein D [hSP-D], and matrix metalloprotein 7 [MMP7]) with ILD progression among patients with RA-ILD.Methods:We investigated RA-ILD progression in the Korean RA-ILD (KORAIL) cohort, a prospective, longitudinal observational study. We enrolled patients with RA based on either 1987 ACR or 2010 ACR/EULAR criteria and ILD based on chest computed tomography (CT) scans from January 2015 to July 2018 and followed for 3 years. Pulmonary function tests and chest CT scans were conducted annually, and ILD extent on chest CT was scored independently by two radiologists. ILD progression was defined as both physiological and radiological evidence of disease progression adapted from the 2023 ATS/ERS/JRS/ALAT definition of progressive pulmonary fibrosis.[1] Serum KL-6 level was measured using the latex-enhanced immunoturbidimetric assay method, and hSP-D and MMP7 levels using R-Plex assays. We performed multivariable Cox regression to investigate the associations of baseline biomarkers (baseline value and annual change) with RA-ILD progression, adjusted for age, sex, smoking status, and DAS28-ESR score at baseline, and baseline biomarker value (in models using annual change in biomarker value as a predictor).Results:We analyzed 136 RAILD patients who had biomarker measurement (mean age 66.5 [SD 8.3] years, 30% male, 60% definite/probable usual interstitial pneumonia pattern). During a median 2.5 [IQR 1.3, 3.2] years follow-up, 35% (n=47) of patients had progression. Higher baseline levels of KL-6 and hSP-D were associated with higher risk of ILD progression (HRs 1.36 per SD, 95%CI 1.02-1.81 and 1.50 per SD, 95%CI 1.09-2.07, respectively) (Table 1). Having high serum KL-6 was associated with the worst progression-free survival (HRs 2.86, 95%CI 1.21-6.74 compared to quartile 1) (Figure 1). Having increasing levels of serum KL-6 and serum MMP7 were significantly associated with progression in the multivariable model (ΔKL-6 level HR 1.84 per SD, 95%CI 1.20-2.81, and ΔMMP7 level HR 1.56 per SD, 95%CI 1.00-2.43, respectively) adjusting for potential confounders including baseline biomarker level, while change in hSP-D were not.Conclusion:Higher levels of serum KL-6 and hSP-D were each associated with increased risk of RA-ILD progression. Higher KL-6 levels were most consistently associated with progression. At follow-up, increasing serum KL-6 and MMP7 level was also associated with increased risk of progression. These data provide evidence that serial measurements of serum biomarkers of pulmonary damage, particularly KL-6, may predict RA-ILD progression and may be helpful in monitoring patients and treatment decisions.REFERENCES:[1] Raghu, G. et al. Idiopathic Pulmonary Fibrosis (an Update) and Progressive Pulmonary Fibrosis in Adults: An Official ATS/ERS/JRS/ALAT Clinical Practice Guideline. Am J Respir Crit Care Med 205, e18-e47 (2022).Table 1.Hazards ratios for RA-ILD progression by pulmonary damage biomarkers at baseline and 1-year change (n=136).Multivariable* HR (95%CI)Baseline measurementKL-6 level (per SD)1.36 (1.02 – 1.81)hSPD level (per SD)1.50 (1.09 – 2.07)MMP7 level (per SD)1.10 (0.77 – 1.56)1-year change of biomarker**ΔKL-6 level (per SD)1.84 (1.20 – 2.81)ΔhSPD level (per SD)1.23 (0.81 – 1.85)ΔMMP7 level (per SD)1.56 (1.00 – 2.43)*Adjusted for age, sex, smoking, and DAS28-ESR at baseline.**Additionally adjusted for baseline value of each biomarker.Figure 1.Kaplan-Meier curves for RA-ILD progression-free survival and hazard ratios for RA-ILD progression, stratified by quartiles of pulmonary damage biomarkers at baseline (n=136). Multivariable models were adjusted for age, sex, smoking, and DAS28-ESR at baseline.Acknowledgements:The KORAIL cohort investigators.Disclosure of Interests:None declared.

Background: Patients with similar grade diastolic dysfunction at rest may have a spectrum of alterations in diastolic function during exercise. Objective: To evaluate (a) whether exercise could unmask further diastolic abnormalities not evident during rest; (b) whether diastolic functional reserve during exercise is associated with exercise capacity. Methods: 141 subjects (77 male, mean (SD) age 62 (9)) with abnormal left ventricular (LV) relaxation (mitral E/A <0.75) and/or deceleration time >240 ms, underwent graded supine bicycle exercise with simultaneous respiratory gas analysis and two-dimensional and Doppler echocardiographic study. Mitral inflow and annular velocities were measured at rest and during exercise. The LV diastolic function reserve index (DFRI) was calculated. Results: Patients were classified into two groups: group 1 (n = 64), DFRI <13.5; group 2 (n = 77), DFRI ⩾13.5. The ratio of E/E′ to stroke volume was used as an index of ventricular elastance (Ed). No significant differences between the groups in mitral inflow and annular velocities at rest were found. Mean (SD) Ed was not significantly different at rest between the groups (0.19 (0.07) vs 0.18 (0.06), p = 0.29). Ed was significantly higher during exercise in group 1 than in group 2 (25 W, 0.21 (0.09) vs 0.14 (0.04), p<0.001; 50 W, 0.22 (0.10) vs 0.15 (0.04), p<0.001). Group 1 subjects had a shorter exercise duration (8.2 (2.7) vs 9.4 (3.7) min, p = 0.04) and lower peak oxygen consumption (17.5 (4.5) vs 20.2 (5.4) ml/kg/min, p = 0.005). Conclusions: Despite similar mitral flow and annular velocities at rest, different responses to exercise were seen in patients with abnormal LV relaxation at rest. Lower LV diastolic functional reserve was associated with higher ventricular elastance during exercise, and reduced exercise capacity.

Contrast enhanced image obtained by magnetic resonance imaging showed prominent delayed hyperenhancement localised at the visceral and parietal pericardium (left panel).

Coronary artery spasm has been proposed as a definite cause of vasospastic angina and as a contributor to other acute cardiac events, including unstable angina, acute myocardial infarction, and sudden cardiac death. It has also been demonstrated that silent ischaemia caused by coronary artery spasm could initiate potentially fatal arrhythmias in patients without flow limiting structural coronary artery lesions. We report a case of prolonged sinus arrest after an attack of coronary artery spasm.