Related Experiment Videos
Inflammatory joint diseases and atherosclerosis: time to look beyond the 'lipid paradox'
Rachel H Mackey1, Lewis H Kuller1, Larry W Moreland2
1Department of Epidemiology, University of Pittsburgh Graduate School of Public Health, University of Pittsburgh.
Insights
Lipids contribute to cardiovascular disease (CVD) risk in inflammatory joint disease (IJD). Quantifying lipoprotein particles, not just lipid content, offers better insights into managing CVD risk in IJD patients.
Area of Science:
- Rheumatology
- Cardiology
- Lipidology
Background:
- Rheumatoid arthritis and inflammatory joint diseases (IJD) are linked to increased cardiovascular disease (CVD) risk.
- Traditional lipid profiles may not fully capture CVD risk in IJD patients due to inflammation's complex effects.
Purpose of the Study:
- To review recent research on the contribution of lipids to CVD risk in IJD patients.
- To explore the utility of quantifying lipoprotein particles directly for assessing CVD risk.
Main Methods:
- Review of current scientific literature on IJD, CVD, and lipid metabolism.
- Analysis of studies comparing lipid content versus lipoprotein particle quantification for CVD risk assessment.
Main Results:
- Inflammation and anti-inflammatory treatments can increase atherogenic Apolipoprotein B (ApoB) particles, even if LDL cholesterol decreases.
- Cardiovascular risk factors like ApoB may precede IJD diagnosis, and cumulative exposure accelerates atherosclerosis.
- Non-atherosclerotic heart and lung diseases, heart failure, and mortality may relate to disease activity and HDL function.
Conclusions:
- Assessing CVD risk in IJD requires focusing on lipoprotein particles (especially ApoB) and cumulative risk factor exposure.
- Aggressive management of traditional CVD risk factors (smoking, obesity, hypertension, diabetes, inactivity) alongside disease control is crucial.
- Lipid-lowering therapies can mitigate increases in ApoB and LDL-C induced by anti-inflammatory drugs and reduce overall CVD risk.
Purpose Of Review:
Uncertainty persists about the contribution of lipids to the increased risk of cardiovascular disease (CVD) among rheumatoid arthritis and other inflammatory joint disease (IJD) patients. In reviewing recent research, we consider potential insights gained by quantifying lipoprotein particles directly, rather than by their lipid content.
Recent Findings:
Although inflammation often decreases LDL cholesterol (LDL-C), and anti-inflammatory medications often increase LDL-C, both inflammation and anti-inflammatory medications can increase atherogenic Apolipoprotein B (ApoB)-containing lipoprotein particles, attenuated by statins. CVD risk factors, that is, smoking, obesity, ApoB, may increase years prior to IJD diagnosis. Increased risks of nonatherosclerotic myocardial and pulmonary disease, heart failure and mortality may be directly related to disease activity, inflammation, and possibly to HDL particles and function.
Summary:
For IJD patients, higher cumulative lifetime exposure to CVD risk factors accelerates atherosclerosis and subsequent CVD risk that is underestimated by current risk factor levels. CVD risk reduction in IJD requires aggressive and earlier reduction in CVD risk factors (ApoB lipoproteins, smoking, hypertension, diabetes, lack of physical activity), in addition to control of disease activity and inflammation. Lipid-lowering medications can attenuate anti-inflammatory medication-induced increases in ApoB and LDL-C, but can also reduce CVD risk due to cumulative lifetime exposure.