Session Type: ACR Poster Session B
Session Time: 9:00AM-11:00AM
Background/Purpose: Patients with various inflammatory rheumatic diseases (IRD) have increased cardiovascular morbidity caused by atherosclerosis. The aetiology of the accelerated atherosclerosis in IRD is still unclear, but both traditional cardiovascular risk factors and inflammation seem to play a role. There has been increasing attention to Lipoprotein (a) (LP(a)) as a risk factor for atherosclerotic cardiovascular disease (CVD). LP(a) exhibits homology to plasminogen, and thereby interfere with fibrinolysis. Moreover, through binding to macrophages it may promote foam cell formation and cholesterol deposition in atherosclerotic plaques. The aim of this study was to compare levels of Lp(a) in patients with CVD with and without IRD, and in healthy controls (HC).
Methods: We examined the plasma level of LP(a) and other plasma lipids in patients included in the Feiring Heart Biopsy Study, comprising patients referred to coronary artery bypass grafting (CABG): 69 patients with IRDs and 53 sex and age matched patients without IRDs called CVD. We also examined blood samples from a group of 30 HC, matched for sex and with the same age range as the CVD-IRD group. All measurements were done by standard laboratory methods.
Results: Patients with CVD and IRD had increased plasma levels of LP(a) compared to HC (631.4 vs 335.7 mg/l, p=0.0018), while they had reduced levels of the classical atherogenic lipids, i.e. total cholesterol (TC) (4.9 vs 6.1 mmol/l, p<0.0005) and Low Density Lipoprotein cholesterol (LDL) (3.1 vs 3.9 mmol/l, p=0.002) compared to HC potentially reflecting the use of statins as most CVD patients (78 %) are on statins at the time of CABG. The levels of Lp(a) were not significantly different between IRD and non-IRD CVD patients (631.4 vs 592.5 mg/l).
Conclusion: Despite reduced levels of TC and LDL, patients with CVD regardless of IRD have higher levels of LP(a) than HC. It is likely that the reduced levels of TC and LDL are result of statin treatment which seems to not normalize Lp(a) levels. This unmask a plausible role of Lp(a) in CVD and evokes a hypothesis that there might be a need for a better control of Lp(a), e.g. by TNF inhibition, to protect from CVD at least in the IRD population.1
1.Hjeltnes G, et al, ClinExp Rheumatol. 2013.
To cite this abstract in AMA style:Holm S, Oma I, Hagve TA, Saatvedt K, Mikkelsen K, Rydningen H, Almdahl SM, Aukrust P, Halvorsen B, Hollan I. Increased Levels of Lipoprotein(a) in RA Patients with Cardiovascular Disease [abstract]. Arthritis Rheumatol. 2016; 68 (suppl 10). https://acrabstracts.org/abstract/increased-levels-of-lipoproteina-in-ra-patients-with-cardiovascular-disease/. Accessed October 24, 2021.
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