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Development of a systemic lupus erythematosus cardiovascular risk equation
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Objective
Accelerated atherosclerosis remains the major cause of late death (after 5 years) in SLE. Yet, the ‘traditional’ cardiovascular risk equations (such as Framingham) consistently underestimate the risk. We sought to construct a data-driven formula for cardiovascular risk in SLE, based on data collected during the first year in a longitudinal cohort, for research purposes.
Methods
Two risk formulas were derived: one was for a broad set of cardiovascular outcomes (myocardial infarction, stroke, onset of angina, coronary procedures such as bypass or stent, claudication, peripheral artery disease or congestive heart failure); and the other for hard outcomes (myocardial infarction or stroke). Traditional and SLE-specific risk factors for cardiovascular disease were measured during the first year of cohort participation. Using Cox proportional hazards modelling, SLE formulas to calculate the 10-year risk of a subsequent cardiovascular event were derived and compared with the Framingham (for the broader outcome) and American College of Cardiology formulas (for the hard outcomes).
Results
SLE-related risk factors for each model included mean disease activity score (as measured by the SELENA revision of the SLE Disease Activity Index), low C3 and history of lupus anticoagulant. In those with SLE-related risk factors, the estimated 10-year risk based on our formula was substantially higher than the risk estimated based on the formulas for the general population.
Conclusions
The excess cardiovascular risk among patients with SLE varies substantially depending on the SLE-related risk factors, age and traditional risk factors. Cardiovascular risk formulas based on individual data from patients with SLE may better estimate 10-year cardiovascular risk among patients with SLE than the Framingham or American College of Cardiology equations.
Title: Development of a systemic lupus erythematosus cardiovascular risk equation
Description:
Objective
Accelerated atherosclerosis remains the major cause of late death (after 5 years) in SLE.
Yet, the ‘traditional’ cardiovascular risk equations (such as Framingham) consistently underestimate the risk.
We sought to construct a data-driven formula for cardiovascular risk in SLE, based on data collected during the first year in a longitudinal cohort, for research purposes.
Methods
Two risk formulas were derived: one was for a broad set of cardiovascular outcomes (myocardial infarction, stroke, onset of angina, coronary procedures such as bypass or stent, claudication, peripheral artery disease or congestive heart failure); and the other for hard outcomes (myocardial infarction or stroke).
Traditional and SLE-specific risk factors for cardiovascular disease were measured during the first year of cohort participation.
Using Cox proportional hazards modelling, SLE formulas to calculate the 10-year risk of a subsequent cardiovascular event were derived and compared with the Framingham (for the broader outcome) and American College of Cardiology formulas (for the hard outcomes).
Results
SLE-related risk factors for each model included mean disease activity score (as measured by the SELENA revision of the SLE Disease Activity Index), low C3 and history of lupus anticoagulant.
In those with SLE-related risk factors, the estimated 10-year risk based on our formula was substantially higher than the risk estimated based on the formulas for the general population.
Conclusions
The excess cardiovascular risk among patients with SLE varies substantially depending on the SLE-related risk factors, age and traditional risk factors.
Cardiovascular risk formulas based on individual data from patients with SLE may better estimate 10-year cardiovascular risk among patients with SLE than the Framingham or American College of Cardiology equations.
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