caa a22 4500 445885629 CHVBK 20180317145558.0 cr unu---uuuuu 170323e20111001xx s 000 0 eng 10.1007/s00011-011-0358-x doi (NATIONALLICENCE)springer-10.1007/s00011-011-0358-x Influence of chronic inflammation and autoimmunity on coronary calcifications and myocardial perfusion defects in systemic lupus erythematosus patients [Elektronische Daten] [Wojciech Plazak, Mieczyslaw Pasowicz, Magdalena Kostkiewicz, Jakub Podolec, Lidia Tomkiewicz-Pajak, Jacek Musial, Piotr Podolec] Objective: Conventional risk factors for coronary artery disease fail to explain the increased frequency or cardiovascular morbidity in systemic lupus erythematosus (SLE) patients. This study was conducted to determine the possible influence of autoimmune and inflammatory phenomena markers on coronary artery calcifications and myocardial perfusion abnormalities in SLE patients. Materials and methods: Multi-detector computed tomography (MDCT)-based coronary calcium scoring and single photon emission computerized tomography (SPECT) studies (Tc-99m sestamibi) were performed in 60 SLE patients in stable clinical condition, without a prior history of coronary artery disease. Laboratory evaluation included serum C-reactive protein (CRP), complement C3c and C4 components and antiphospholipid antibodies (aPL). The latter included anticardiolipin (aCL) and anti-β2-glycoprotein I (aβ2GPI) antibodies, of both IgG and IgM classes, and lupus anticoagulant (LA) in plasma. Results: SPECT revealed persistent perfusion defects in 22 (36.7%) patients and exercise-induced defects in eight (13.3%), while MDCT revealed coronary calcifications in 15 (25%). Calcium scores ranged from 1 to 843.2 (mean 113.5±259.7). No association was found between conventional coronary artery disease risk factors (obesity, hypertension, tobacco use, hyperlipidaemia, diabetes) nor CRP, C3c or C4 levels and coronary calcifications or myocardial perfusion defects. On the contrary, in patients with these pathologies, augmented autoimmunization was found, reflected by increased aCL IgG and antiβ2GPI IgG levels. In patients with aCL IgG >20RU/ml or antiβ2GPI IgG >3RU/ml, the relative risk of coronary calcification formation was 4.1 compared to patients with normal values. Accordingly, in LA-positive patients the relative risk of coronary calcification formation was 4.4 compared to LA-negative patients. Conclusions: Conventional risk factors for coronary artery disease as well as markers of an ongoing inflammation did not show any association with perfusion defects and/or coronary artery calcifications in SLE patients. On the contrary, calcified atherosclerotic plaques and myocardial perfusion defects were observed mainly in patients with elevated levels of anticardiolipin and aβ2GPI antibodies of the IgG class. It might be speculated that coronary artery calcifications and perfusion defects are a result of antiphospholipid antibodies-induced coronary artery microthrombosis. The Author(s), 2011 Systemic lupus erythematosus nationallicence Autoimmune diseases nationallicence Coronary calcification nationallicence Atherosclerosis nationallicence MDCT nationallicence SPECT nationallicence Perfusion scintigraphy nationallicence Plazak Wojciech Department of Cardiac and Vascular Diseases, The John Paul II Hospital, Jagiellonian University Medical College, ul. Pradnicka 80, 31-202, Krakow, Poland aut Pasowicz Mieczyslaw Center for Diagnosis, Prevention and Telemedicine, The John Paul II Hospital, Jagiellonian University Medical College, Krakow, Poland aut Kostkiewicz Magdalena Department of Cardiac and Vascular Diseases, The John Paul II Hospital, Jagiellonian University Medical College, ul. Pradnicka 80, 31-202, Krakow, Poland aut Podolec Jakub Cardiovascular Intervention Center, The John Paul II Hospital, Jagiellonian University Medical College, Krakow, Poland aut Tomkiewicz-Pajak Lidia Department of Cardiac and Vascular Diseases, The John Paul II Hospital, Jagiellonian University Medical College, ul. Pradnicka 80, 31-202, Krakow, Poland aut Musial Jacek Department of Internal Medicine, Jagiellonian University Medical College, Krakow, Poland aut Podolec Piotr Department of Cardiac and Vascular Diseases, The John Paul II Hospital, Jagiellonian University Medical College, ul. Pradnicka 80, 31-202, Krakow, Poland aut Inflammation Research SP Birkhäuser Verlag Basel 60/10(2011-10-01), 973-980 1023-3830 60:10<973 2011 60 11 https://doi.org/10.1007/s00011-011-0358-x text/html Onlinezugriff via DOI 1 research-article jats NATIONALLICENCE 856 40 https://doi.org/10.1007/s00011-011-0358-x text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Plazak Wojciech Department of Cardiac and Vascular Diseases, The John Paul II Hospital, Jagiellonian University Medical College, ul. Pradnicka 80, 31-202, Krakow, Poland aut NATIONALLICENCE 700 1- Pasowicz Mieczyslaw Center for Diagnosis, Prevention and Telemedicine, The John Paul II Hospital, Jagiellonian University Medical College, Krakow, Poland aut NATIONALLICENCE 700 1- Kostkiewicz Magdalena Department of Cardiac and Vascular Diseases, The John Paul II Hospital, Jagiellonian University Medical College, ul. Pradnicka 80, 31-202, Krakow, Poland aut NATIONALLICENCE 700 1- Podolec Jakub Cardiovascular Intervention Center, The John Paul II Hospital, Jagiellonian University Medical College, Krakow, Poland aut NATIONALLICENCE 700 1- Tomkiewicz-Pajak Lidia Department of Cardiac and Vascular Diseases, The John Paul II Hospital, Jagiellonian University Medical College, ul. Pradnicka 80, 31-202, Krakow, Poland aut NATIONALLICENCE 700 1- Musial Jacek Department of Internal Medicine, Jagiellonian University Medical College, Krakow, Poland aut NATIONALLICENCE 700 1- Podolec Piotr Department of Cardiac and Vascular Diseases, The John Paul II Hospital, Jagiellonian University Medical College, ul. Pradnicka 80, 31-202, Krakow, Poland aut NATIONALLICENCE 773 0- Inflammation Research SP Birkhäuser Verlag Basel 60/10(2011-10-01), 973-980 1023-3830 60:10<973 2011 60 11 Metadata rights reserved Springer special CC-BY-NC licence nationallicence BK010053 XK010053 XK010000 NATIONALLICENCE NATIONALLICENCE NL-springer