IRD was associated with higher levels of both 25(OH)D and 1,25(OH)D. These findings argue against the hypothesis that patients with high systemic inflammatory burden (CAD+IRD) should have lower vitamin D levels than those with less inflammation (CAD only). Of note, when controlled for potential confounders, low 1,25(OH)D levels were associated with adventitial aortic inflammation.
Background Vitamin D is involved in immune reactions, and vitamin D deficiency is associated with autoimmune diseases and with cardiovascular diseases (CVDs). In Feiring Heart Biopsy Study (FHBS), we previously demonstrated a high occurrence of mononuclear cell infiltrates (MCIs) in subintimal layers of the aorta, related to inflammatory rheumatic disease (IRD). In theory, vitamin D deficiency might contribute to vascular inflammation involved in the pathogenesis of CVD along with the accelerated CVD in IRD. Objectives To look for differences in plasma levels of 25(OH)D3 and 1,25(OH)2D3 in patients with coronary artery disease (CAD) with and without IRD. To search for relationships between inflammation in subintimal aortic layers (in terms of MCIs) and plasma levels of 25(OH)D3 and 1,25(OH)2D3. Methods Plasma levels of 25(OH)D3 were examined by radioimmunoassay and 1,25(OH)2D3 by immunoassay in 53 patients with CAD and 68 patients with CAD and IRD from FHBS. The D vitamin levels were then related to the number of MCI previously identified in the subintimal aortic layers of these patients1. Results In crude analysis, we observed no significant differences in 25(OH)D3 and 1,25(OH)2D3 levels between patients with CAD and IRD and patients with CAD only (see Table). Nor did we observe any significant crude associations between vitamin D levels and occurrence of MCIs in the subintimal aortic layers. However, after adjustment for age, sex, CRP, glucocorticosteroids, daily vitamin and mineral supplementation, and IRD status, patients with MCIs in the subintimal aortic layers had lower levels of 1,25(OH)2D3 than patients without (inter-group difference = 17.0 pmol/l (95%CI: 2.8 to 31.3), p=0.019). Conclusions Our study does not support the hypothesis that patients with CVD and IRD have lower levels of vitamin D than patients with CVD only. Interestingly, based on multivariate analyses, low 1,25(OH)2D3 levels were associated with subintimal aortic inflammation. This finding should be explored in future studies. If a causal relationship exists, vitamin D supplementation could reduce vascular inflammation and thereby have potential therapeutic effect in CVD. References I. Hollan et al., Arthritis Rheum, 56 (2007), 2072-9. Disclosure of Interest None Declared
Background Systemic rheumatic diseases (SRDs) are associated with increased cardiovascular (CV) morbidity due to accelerated atherosclerosis. However, SRDs are also associated with cardiac vasculitis that may contribute to the increased CV risk. In the Feiring Heart Biopsy Study (FHBS) a high occurrence of inflammatory cell infiltrates (ICI) in the aorta of patients with coronary artery disease (CAD) and SRD were found and therefore we wanted to examine if this patient group also had a high occurrence of inflammation in the heart. Objectives To examine the occurrence and extent of ICI and small vessel vasculitis in all layers of the right atrium (epicardium, myocardium and endocardium) in patients with CAD with and without SRDs. Methods We examined biopsies from the right atrium taken in a standardized way during coronary artery bypass grafting from the edge of the openings for cannulation due to extracorporeal circulation from patients with and without SRD (matched for age, sex and acute coronary syndrome) included in FHBS (Hollan I, 2007). A 3-µm thick section from each paraffin fixed specimen was stained by hematoxylin and eosin and examined by light microscopy in a blinded manner. The number and extent of ICIs in the three layers of the heart wall were semi-quantified. Results Conclusions In patients with CAD, vasculitis was not observed, but the occurrence of ICIs in the right atrium was high, mostly localized around small vessels. The ICIs occured in the epicardium, and the occurrence and extent of epicardial ICIs was similar in SRD and non-SRD patients. In the myocardium and endocardium, the ICIs occurred in a low frequency, and in the non-SRD group only (but the difference was not statistically significant). In theory, the observed ICIs might be secondary to or independent of cardiovascular disease (CVD), but the inflammation might also contribute to CAD by compromising of the function of epicardial coronary arteries. Interestingly, abnormalities in epicardium (increased mass of epicardial adipose tissue) are related to CV prognosis, and we propose that inflammation in the epicardium might be of particular importance. Our findings do not support the hypothesis that inflammation in the heart including small vessel cardiac vasculitis is more common in SRD than non-SRD patients. However, this possibility cannot be completely ruled out as the number of examined specimens were small, taken from apparently healthy tissue, and the right atrium was the only site sampled. Disclosure of Interest None Declared
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