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Background: It is plausible that optimal cardiovascular disease (CVD) risk management differs in patients with rheumatoid arthritis (RA) from low or middle income compared to high income populations. This study aimed at producing evidence-based points to consider for CVD prevention in South African RA patients. Methods: Five rheumatologists, one cardiologist and one epidemiologist with experience in CVD risk management in RA patients, as well as two patient representatives, two health professionals and one radiologist, one rheumatology fellow and 11 rheumatologists that treat RA patients regularly contributed. Systematic literature searches were performed and the level of evidence was determined according to standard guidelines. Results: Eighteen points to consider were formulated. These were grouped into 6 categories that comprised overall CVD risk assessment and management (n = 4), and specific interventions aimed at reducing CVD risk including RA control with disease modifying anti-rheumatic drugs, glucocorticoids and non-steroidal anti-inflammatory drugs (n = 3), lipid lowering agents (n = 8), antihypertensive drugs (n = 1), low dose aspirin (n = 1) and lifestyle modification (n = 1). Each point to consider differs partially or completely from recommendations previously reported for CVD risk management in RA patients from high income populations. Currently recommended CVD risk calculators do not reliably identify South African black RA patients with very high-risk atherosclerosis as represented by carotid artery plaque presence on ultrasound. Conclusions: Our findings indicate that optimal cardiovascular risk management likely differs substantially in RA patients from low or middle income compared to high income populations. There is an urgent need for future multicentre longitudinal studies on CVD risk in black African patients with RA., The first meeting held amongst local Rheumatologists was funded by the South African Arthritis and Rheumatology Association. The studies by Professor González-Gay have been supported by grants from “Fondo de Investigaciones Sanitarias” PI06/0024, PS09/00748, PI12/00060, PI15/00525, PI18/00043, and RD12/0009/0013 and RD16/0012 (RIER) from “Instituto de Salud Carlos III” (ISCIII) (Spain), co-funded by FEDER funds

Objective.Arterial properties influence cardiovascular disease (CVD) risk. We identified potential determinants of arterial function in patients with rheumatoid arthritis (RA).Methods.Relationships of traditional cardiovascular risk factors and RA characteristics with arterial stiffness (pulse wave velocity), wave reflection (augmentation index, reflected wave pressure, and reflection magnitude), and pressure pulsatility (central systolic and pulse pressure, peripheral pulse pressure, pulse pressure amplification, and forward wave pressure) were identified in multivariable backward regression models among 177 patients without established CVD (118 white, 32 Asian, 22 black, 5 mixed ancestry).Results.Recorded characteristics explained 37% (pulse wave velocity) to 71% (reflected wave pressure) of the variability in arterial function. These factors were particularly associated with wave reflection and pressure pulsatility: RA duration (p = 0.04), rheumatoid factor status (p = 0.01 to 0.03), leukocyte counts (p = 0.02 to 0.05), and total cholesterol (p < 0.01 to 0.03). Body mass index (p < 0.01 to 0.02) and insulin resistance (p < 0.01 to 0.01) were related to reduced wave reflection and peripheral pulse pressure. Exercise (p = 0.02) and alcohol consumption (p < 0.01) were associated with increased pulse pressure amplification and decreased peripheral pulse pressure, respectively. Tumor necrosis factor-α inhibition (p < 0.01) was related to reduced pulse wave velocity, and tetracycline use (p = 0.02) to decreased peripheral pulse pressure.Conclusion.Traditional cardiovascular risk factors and disease characteristics are consistently associated with vascular hemodynamic alterations in RA. The relative effect of arterial stiffness, wave reflection, and pressure pulsatility on CVD risk in RA needs further study.

To the Editor: Leptin is an adipokine that regulates appetite and energy expenditure1. Both high and low leptin production can further increase cardiovascular (CV) risk1. Leptin is also produced in inflamed joints and implicated in the pathophysiology of rheumatoid arthritis (RA)2. Whether leptin increases CV risk in RA is currently uncertain. Two studies reported a lack of association between leptin concentrations and carotid artery intima-media thickness (cIMT) in RA3,4. Leptin concentrations were also found to be unrelated to coronary artery classification scores in RA5. However, we recently reported an independent relationship between leptin concentrations and surrogate markers of early atherogenesis in young patients with RA2. Importantly, in the present context, carotid artery plaque is a more reliable indicator of atherosclerosis than cIMT6. In our present study, we examined the independent relationships of leptin concentrations with cIMT and plaque in 217 (112 black and 105 white) patients with RA. Because the production and effects of adipokines on CV risk depend on pathophysiological context1,2,7, we also determined whether the presence of conventional and nonconventional CV risk factors modified leptin concentrations and their associations with atherosclerosis. … Address correspondence to Prof. P.H. Dessein, P.O. Box 1012, Melville 2109, Johannesburg, South Africa. E-mail: dessein{at}telkomsa.net

We examined the potential impact of demographic characteristics on the independent leptin-metabolic cardiovascular risk factor and leptin–endothelial activation relationships in black and white patients with RA. Leptin concentrations and those of endothelial activation molecules including soluble E-selectin, vascular cell adhesion molecule-1, intercellular adhesion molecule-1 and monocyte chemoattractant protein-1 were measured in 217 RA patients (51.6 % black). We determined associations in potential confounder and mediator-adjusted mixed regression models. No independent associations between leptin concentrations and cardiovascular risk were present in all patients and either women and men or black and white patients. However, age impacted on several leptin–cardiovascular risk relations (interaction P < 0.05). In patients aged

Vitamin D is a steroid hormone that is best known for its central role in calcium and phosphate homeostasis1,2,3. Vitamin D deficiency [serum 25 OH-hydroxyvitamin D (25(OH)D) < 20 ng/ml] is complicated by rickets in children and osteomalacia in adults. Further, vitamin D deficiency and insufficiency [serum 25(OH)D < 30 ng/ml] contribute to osteoporosis and osteoporotic fractures through reduced bone mineral density and muscle mass, strength, and function, thus increasing the risk of falls. In persons 65 years of age or older, adequate vitamin D supplementation reduces the risk of hip and any nonvertebral fracture by 30% and 14%, respectively2. Impaired vitamin D status is prevalent worldwide, and vitamin D concentrations may have fallen further by 20% over the past 10 years3. The past 10 years have also witnessed a dramatically increased interest in vitamin D metabolism. This is because impaired vitamin D status was found to have — aside from its classical role in bone disease — numerous additional nonclassical adverse effects1,3,4,5. Thus, the vitamin D receptor (VDR), which is a member of the nuclear receptor superfamily, and key activating enzyme 25-OH-1α hydroxylase (CYP27B1), which converts 25(OH)D to its active metabolite 1,25 (OH)2D3, were shown to be present in multiple cell types. By its local synthesis and regulation of the transcription of as much as ∼ 3% of the human genome4, vitamin D can mediate its nonclassical effects through autocrine and paracrine mechanisms. Congruently, impaired vitamin D status has now been linked to a wide range of chronic conditions that include cardiovascular disease (CVD), diabetes, and autoimmune disorders. How relevant could these findings be to patients with rheumatoid arthritis (RA)? RA results in enhanced … Address correspondence to Professor Patrick H. Dessein, P.O. Box 1012, Melville 2109, Johannesburg, South Africa. E-mail: Dessein{at}telkomsa.net

Objective.Black Africans currently experience a distinctly low frequency of atherosclerotic cardiovascular disease. Whether this protection persists in those with rheumatoid arthritis (RA) is unknown. We compared the carotid atherosclerosis burden and its relationships with cardiovascular (CV) risk factors between Africans with RA from a developing black and developed CV population.Methods.We performed high resolution B-mode ultrasonography and assessed CV risk factors in 243 patients with established RA, of whom 121 were black and 122 white. Data were analyzed in age, sex, and healthcare center-adjusted regression models.Results.The mean ± SD common carotid intima-media thickness (cIMT) was 0.694 ± 0.097 mm in black and 0.712 ± 0.136 mm in white patients (adjusted p = 0.8). Plaque prevalence was also similar in black compared to white cases (35.5% and 44.3%, respectively; adjusted OR 0.83, 95% CI 0.32–2.20, p = 0.7). Interactions between population grouping and several CV risk factors were independently associated with cIMT and plaque. In stratified analysis, that is, in each population group separately, risk factors associated with cIMT or/and plaque comprised the systolic blood pressure (p = 0.02), serum cholesterol/high-density lipoprotein cholesterol ratio (p = 0.004), C-reactive protein concentrations (p = 0.01), and the presence of extraarticular manifestations (p = 0.01) in whites but, contrastingly, the Arthritis Impact Measurement Scales tension score (p = 0.04) and use of nonsteroidal antiinflammatory agent (p = 0.03) in black patients. The Framingham score was significantly associated with atherosclerosis only in whites (p < 0.0001).Conclusion.The carotid atherosclerosis burden is similar in black compared to white Africans with RA, but relationships between modifiable CV risk factors and atherosclerosis vary substantially among Africans with RA.