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Oliver Moore
Oliver Moore

Download Syndrome Cardio RГnal Pdf EXCLUSIVE


Inflammatory arthritides including rheumatoid arthritis (RA), psoriatic arthritis (PsA) and ankylosing spondylitis (AS) are associated with increased risk of cardiovascular disease. This process may be driven by systemic inflammation, and the use of tumour necrosis factor (TNF) inhibitors could therefore potentially reduce cardiovascular risk by reducing this inflammatory burden. The aims of this study were to evaluate whether the risk of cardiovascular events (CVEs) in patients with inflammatory arthritis is associated with treatment with anti-TNF therapy, compared with other biologics or non-biologic therapy, and to compare the CVE risk between participants with RA, PsA and AS.




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Data from consecutive participants in the Australian Rheumatology Association Database with RA, PsA and AS from September 2001 to January 2015 were included in the study. The Cox proportional hazards model using the counting process with time-varying covariates tested for risk of having CVEs, defined as angina, myocardial infarction, coronary artery bypass graft, percutaneous coronary intervention, other heart disease, stroke/transient ischaemic attack or death from cardiovascular causes. The model was adjusted for age, sex, diagnosis, methotrexate use, prednisone use, non-steroidal anti-inflammatory use, smoking, alcohol consumption, hypertension, hyperlipidaemia, diabetes and functional status (Health Assessment Questionnaire Disability Score).


Inflammatory arthritides such as rheumatoid arthritis (RA), ankylosing spondylitis (AS) and psoriatic arthritis (PsA) impose a heavy burden of morbidity and mortality on populations worldwide. A significant component of this is the two-fold increased risk of cardiovascular events (CVEs) [1], with some evidence for increasing risk with longer disease duration [2,3,4]. It has been proposed that this is due to inflammatory processes driven by cytokines such as tumour necrosis factor (TNF), with a high inflammatory burden driving autoantibody production and apoptosis of endothelial cells to cause vascular damage [5] and a pro-thrombotic state [6].


The use of TNF inhibitors could therefore potentially reduce cardiovascular risk by controlling systemic inflammation. A recent study demonstrated that an RA cohort with disease onset after the year 2000 did not have an increased mortality risk compared to the general population, whereas those with disease onset prior to 2000 were at increased risk [7]. Several studies have demonstrated that treatment of inflammatory arthritis with TNF inhibitors is associated with an improvement in surrogate markers of cardiovascular health such as endothelial stiffness, biochemical lipid profile and carotid intima-media thickness [8,9,10,11,12,13].


There is conflicting evidence regarding clinical cardiovascular endpoints such as rate of myocardial infarction, stroke and cardiovascular-related death after treatment with biologics in patients with RA. Some studies report a lower risk of CVEs [14, 15], while others report no significant difference [16, 17]. Studies assessing cardiovascular risk in RA have been performed in locations including North America [14, 18, 19], Britain [20] and Sweden [21], but as yet no studies have been undertaken in the Australian context where there are stringent criteria for accessing biologic therapy. Furthermore, little research has been done to establish the effect of biologics on the CVE rate for inflammatory arthritis apart from RA. Thus, wider research is warranted in a range of arthritic conditions to examine whether biologic therapy is helpful beyond direct arthritic control in these patients.


The study period comprised a total of 19,627 patient-years. Therapy was primarily anti-TNF (12,555 patient-years, 64.0%) or other biologics (1963 patient-years, 10.1%), while 10.0% (1955 patient-years) had ceased biologic therapy and 15.9% (3116 patient-years) were biologic-naïve. Only 29 patient-years (0.1%) included unknown DMARD therapy. Across the study period, 552 participants (13.3%) experienced a composite cardiac event and 10 died secondary to cardiovascular causes, with only one of these 10 participants reporting a CVE during the study period before dying of a cardiovascular cause.


This study has demonstrated a reduction in CVEs associated with biologic use for both anti-TNF and other biologic agents in ARAD participants with RA, PsA or AS, compared with ARAD participants who were biologic-naïve. However, this protective effect for the CVE rate was not observed in those who had ceased using biologic agents. Previous studies have shown that people with any inflammatory arthritis have increased rates of both cardiovascular morbidity and cardiovascular mortality compared to the general population [4, 34,35,36]. However, there are few primary studies directly comparing event rates between different forms of inflammatory arthritis.


Our study explored the relationship between anti-TNF use and CVEs in the Australian context and was also able to examine three different types of inflammatory arthritis in the same cohort. A reduced risk of myocardial infarction for RA patients treated with anti-TNF agents compared with conventional DMARDs was also reported in a recently updated analysis of the British Society for Rheumatology Biologic Register (BSRBR-RA) [37]. The baseline characteristics of patients entered in the ARAD are similar to the biologic-exposed population in the BSRBR-RA [20]. A similar reduction in acute coronary syndrome events for patients with RA using anti-TNF therapy was also found in a recent Swedish cohort study [38]. A recent systematic review reported a decreased risk of CVEs in patients with RA treated with TNF inhibitors or with methotrexate, and an increased risk in those using glucocorticoids or NSAIDs [39]. This review also reported that treatment with systemic therapy decreased the risk of CVEs in patients with PsA or psoriasis. However, there was insufficient data to compare the CVE risk between individual therapies.


Apart from cardiovascular death, in this study CVEs were identified through participant self-report and it is possible that there was under-reporting of events. It is not possible to directly compare the incidence of CVEs in our study with data for the general population in Australia due to differences in the definitions of CVEs used in the Australian Institute of Health and Welfare (AIHW) analysis of the AIHW National Hospital Morbidity Database and AIHW National Mortality Database [41].


Furthermore, we used a composite measure for biologic use due to the small numbers of patients treated with each individual agent. It was therefore not possible to ascertain whether there was any difference in the CVE risk between individual biologic therapies. Although the ARAD collects information on reasons for biologic cessation, it was difficult to isolate a single cause to explain the finding that the CVE risk in the group who had ceased using biologic agents was not significantly different from the biologic-naïve group. This could be because those who had ceased biologic therapy were generally resistant to biologic therapy and thus did not derive any improvement in either disease status or the CVE rate, or it could be because any protective effect from biologic use is not sustained after biologic cessation and participants returned to their previous level of cardiovascular risk. Medication use was self-reported and dosages of glucocorticoid and DMARDs were not collected. Furthermore, some participants reported they were unsure if they had certain medical conditions, or had taken some medications. However, this made up only a small proportion of data points, and is unlikely to have affected the overall results.


Current use of biologics, whether anti-TNF or another mechanism of action, is associated with a reduction in the CVE rate compared to the rate among people with inflammatory arthritis who are biologic-naïve. This event reduction was no longer observed in those who had ceased biologic use. There was no difference in the CVE risk between RA, PsA and AS. These findings support the hypothesis that control of systemic inflammation in these conditions may reduce the cardiovascular risk.


There are several ways to increase the specificity and the PPV of a diagnosis in the IPR. In a paper on sepsis in celiac disease by Ludvigsson et al [23] sensitivity analyses were performed among patients with (1) sepsis diagnosed in a department of infectious diseases (i.e. in a department where sepsis is likely to be correctly diagnosed), (2) sepsis listed as the primary diagnosis and (3) the risk of having at least two hospital admissions with sepsis. All these measures could increase the specificity of a diagnosis. For instance, there is a risk that individuals discharged from a dermatology department with a diagnosis of MI (ICD-10: I20.9) actually had an incorrectly recorded eczema (ICD-10: L20.9). When Parikh et al examined parity and risk of later cardiovascular disease, they restricted their discharges to patients with a primary diagnosis of cardiovascular disease (or death from cardiovascular disease)[24]. In their recent paper on schizophrenia, substance abuse and violent crime Fazel et al resolved to study patients with at least two hospital admissions with schizophrenia [25].


However, a positive calcium balance arises easily because the intestinal absorption of calcium is greater than the renal excretion capacity, therefore, the excretion of this mineral in the kidneys decreases and does not increase [52]. In addition, because hypocalcemia is common in ESRD, routine calcium supplementation exists. However, high levels are associated with undesirable and harmful effects, such as vascular calcification, cardiovascular disease and mortality [53]. As with our findings, Inaguma et al. (2017) [53] evidenced in their multivariate analysis that high serum calcium levels are an independent risk factor for a poor survival prognosis. 041b061a72


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