Are Antiphospholipid Antibodies an Independent Risk Factor for Atherosclerosis?

Abstract

The purpose of this study was to check whether antiphospholipid antibodies (aPL) could be an independent risk factor for atherosclerosis. Eighty-five subjects were studied: 45 with primitive antiphospholipid antibody syndrome and 40 controls affected by deep vein thrombosis secondary to known causes. The two groups were homogeneous for age, sex, and risk factors for atherosclerosis. All the subjects submitted to echo-color doppler of the carotid arteries, femoral arteries, and abdominal aorta. The cases were then subdivided into three subgroups on the basis of the positivity to the three subpopulations of aPL. Results demonstrate that there is no correlation between aPL and atherosclerosis. The different positivity to aPL does not modify this conclusion.

Premature atherosclerosis in primary antiphospholipid syndrome: preliminary data

“…When compared with healthy controls, patients with PAPS differ for three variables: the presence and persistence of aPL, the occurrence of thrombosis, and continuing oral anticoagulation. Bilora et al correctly employed thrombotic controls, 5 but with thrombosis of unknown cause, and their duration of anticoagulation might have differed from that of the patients with PAPS. In addition, the authors focused on the relationship between plaque frequency and cumulative positivity in three subgroups of aPL, but not on their titre.…”

β3 integrin deficiency promotes atherosclerosis and pulmonary inflammation in high-fat-fed, hyperlipidemic mice

“…Mice with deficiency of von Willebrand factor, critical for platelet adhesion under high-flow conditions, have less atherosclerosis at discrete sites after eating a toxic diet (5). However, studies in von Willebrand-deficient pigs (6,7) and humans (8,9) provide conflicting data about the role of platelet adhesion in plaque formation. In humans, the antiplatelet and antiinflammatory drug aspirin is effective for the primary prevention of coronary disease in some groups but not others (10).…”

Atherosclerosis in Primary Antiphospholipid Syndrome: Summary of Clinical and Pathogenic Evidence

“…Two of these series did not find intima-media thickening in PAPS: in one study, IMT and plaque prevalence were similar in 45 PAPS patients with deep vein thrombosis and in non-APS thrombotic controls matched by age, sex and other vascular risk factors. Having examined the abdominal aorta, the carotid and femoral arteries the authors concluded that atherosclerosis was not a feature of their PAPS cohort [4]. Another survey of PAPS, SLE related APS and normal controls revealed similar IMT across groups though there was a higher plaque frequency in SLE related APS (37.5%) vs. PAPS (8%) [5].…”

“…Early observations suggesting that aPL contributed to atherosclerosis in Systemic Lupus Erythematosus (SLE) lead to testing the atherosclerosis hypothesis in primary APS (PAPS) through the measurement of Intima Media Thickness (IMT) in large enough PAPS series [2][3][4][5][6][7][8][9][10][11]. This review will survey the pathways associated with premature atherosclerosis in PAPS as they temporally appeared in the scientific literature, and will discuss how these reports support the concept of atherosclerosis as a low grade inflammatory and immune process.…”