Longitudinal evolution of risk of coronary heart disease in systemic lupus erythematosus.

Pubmed ID: 22467935

Journal: The Journal of rheumatology

Publication Date: May 1, 2012

MeSH Terms: Humans, Male, Adult, Female, Risk Factors, Cohort Studies, Middle Aged, Longitudinal Studies, Coronary Disease, Disease Progression, Lupus Erythematosus, Systemic

Grants: MOP-42512

Authors: Abrahamowicz M, Pilote L, Karp I, Fortin PR, Neville C, Pineau CA, Esdaile JM

Cite As: Karp I, Abrahamowicz M, Fortin PR, Pilote L, Neville C, Pineau CA, Esdaile JM. Longitudinal evolution of risk of coronary heart disease in systemic lupus erythematosus. J Rheumatol 2012 May;39(5):968-73. Epub 2012 Apr 1.

Studies:

Abstract

OBJECTIVE: To produce evidence on the longitudinal evolution of risk factors for coronary heart disease (CHD) in patients with systemic lupus erythematosus (SLE). METHODS: Based on data for 115 patients from the Montreal General Hospital Lupus Clinic (1971-2003) and for 4367 control subjects from the Framingham Offspring Study (1971-1994), we investigated the temporal evolution of total serum cholesterol, systolic blood pressure (SBP), body mass index (BMI), blood glucose, and estimated risk for CHD (reflecting the balance of changes in different risk factors). In analyses limited to patients with SLE, we assessed the effect of SLE duration on each risk factor, adjusting for age, calendar time, sex, baseline level of the risk factor, and medication use. Next, we assessed how the adjusted difference in the values of the risk factors between SLE and controls changes over time. RESULTS: Among patients with SLE, longer disease duration was independently associated with higher SBP and blood glucose levels. Compared with controls, these patients appeared to have accelerated rates of increase in total cholesterol, blood glucose, and overall estimated CHD risk. The rate of increase in BMI was lower in patients with SLE than in controls. CONCLUSION: Elevated CHD risk in patients with SLE appears to be at least partially mediated by accelerated increases in some CHD risk factors, longitudinal trajectories of which increasingly diverge over time from those of population controls.