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Importance of cumulative exposure to elevated cholesterol and blood pressure in development of atherosclerotic coronary artery disease in systemic lupus erythematosus: a prospective proof-of-concept cohort study

DOI: 10.1186/ar3473

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Abstract:

Patients in the Toronto lupus cohort had TC and BP measured at each clinic visit and were followed up prospectively for the occurrence of CAD. For each patient, arithmetic mean, time-adjusted mean (AM) and area-under-the-curve (AUC) were calculated for serial TC, SBP, and DBP measurements. Proportional hazards regression models were used to compare these summary measures with recent and first-available ("remote") measurements in terms of ability to quantify risk of CAD events, defined as myocardial infarction, angina, or sudden cardiac death.The 991 patients had a mean ± SD of 19 ± 19 TC measurements per patient. Over a follow-up of 6.7 ± 6.4 years, 86 CAD events occurred; although remote TC was not significantly predictive of CAD, mean and AM TC were more strongly predictive (hazard ratio (HR) 2.07; P = 0.003) than recent TC (HR 1.86, P = 0.001). AUC TC was not predictive of CAD. A similar pattern was seen for DBP and SBP. Older age, male sex, higher baseline and recent disease activity score, and corticosteroid use also increased CAD risk, whereas antimalarials were protective.In contrast to the population-based Framingham model, first-available TC and BP are not predictive of CAD among patients with SLE, in whom measures reflecting cumulative exposure over time are better able to quantify CAD risk. This is an important consideration in future studies of dynamic risk factors for CAD in a chronic relapsing-remitting disease such as SLE. Our findings also underpin the importance of adequate control of SLE disease activity while minimizing corticosteroid use, and highlight the cardioprotective effect of antimalarials.Systemic lupus erythematosus (SLE) is associated with a dramatically increased risk of atherosclerotic coronary artery disease (CAD), such that women with SLE aged 34 to 44 years are more than 50 times more likely to develop myocardial infarction (MI) than are age-matched peers [1]. Traditional risk factors measured at baseline, as defined in the Framing

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