کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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3003138 | 1180767 | 2009 | 7 صفحه PDF | دانلود رایگان |
Background and aimTo evaluate the prevalence of subclinical cardiovascular (CV) abnormalities in systemic lupus erythematosus (SLE) stratified according to SLE-related organ damage using the Systemic Lupus International Collaborating Clinics (SLICC) damage index.Methods and resultsWe selected SLE patients without clinically overt CV events (n = 45, 56% with SLICC = 0, 44% with SLICC = 1–4). CV evaluation was performed using cardiac and vascular echo-Doppler techniques. Post-ischemic flow-mediated dilation (FMD) over nitroglycerine-mediated dilation (NMD) of the brachial artery <0.70 defined endothelial dysfunction.The prevalence of preclinical CV abnormalities (CVAbn, including at least one of the following—carotid atherosclerosis, left ventricular (LV) hypertrophy, low arterial compliance, LV wall motion abnormalities, aortic regurgitation, FMD/NMD < 0.70)—was 64% (16/25) in patients with SLICC = 0 and 80% (16/20) in those with SLICC > 0 (p = not significant (NS)). In particular, the prevalence of carotid atherosclerosis (28% vs. 16%), of LV hypertrophy (12% vs. 6%) and of LV wall motion abnormalities (15% vs. 12%), of low global arterial compliance (18% vs. 10%), prevalence of aortic regurgitation (30% vs. 18%) and/or aortic valve fibrosclerosis (10% vs. 8%), FMD < 10% (14 ± 5% vs. 14% ± 6) and prevalence of FMD/NMD < 0.70 (53% vs. 52%) were comparable in SLE patients with SLICC > 0 and in those with SLICC = 0 (all p = NS). Of the SLE patients without carotid atherosclerosis, LV hypertrophy, low arterial compliance, LV wall motion abnormalities and aortic regurgitation (n = 17), endothelial dysfunction was detected in 50% of those with SLICC = 0 (6/12) and in 40% of those with SLICC > 0 (2/5, p = NS).ConclusionsSLE patients with SLICC = 0 often have an elevated CV risk profile due to subclinical manifestations of CV disease detectable by cardiac and vascular echo-Doppler evaluations.
Journal: Nutrition, Metabolism and Cardiovascular Diseases - Volume 19, Issue 4, May 2009, Pages 234–240