Cardiovascular disease represents an important cause of morbidity and mortality in patients with a diagnosis of systemic lupus erythematosus (SLE), due to a complex interplay between traditional risk factors and disregulation of autoimmunity but uncertainty is still present about the most important predictors of cardiovascular events. The aim of our work was to perform a collaborative systematic review on the main predictors of cardiovascular events in SLE patients. PubMed and Cochrane were systematically searched for eligible studies on SLE and cardiovascular events between January 2008 and December 2012. Study features, patient characteristics and incidence of stent thrombosis were abstracted and pooled, when appropriate, with random-effect methods (point estimate – 95% confidence intervals) and consistency of predictors was formally appraised. A total of 17,187 patients was included; of those, 93.1% were female and the median age was 39 years. After a median follow-up period of 8 years, cardiovascular events presented in 25.4%, including acute myocardial infarction (4.1%) and stroke (7.3%). The most important predictors may be divided into traditional risk factors, such as male gender (OR 6.2, CI 95% 1.49–25), hyperlipidaemia (OR 3.9, CI 95% 1.57–9.71), familiar history of cardiac disease (OR 3.6, CI 95% 1.15–11.32) and hypertension (OR 3.5, CI 95% 1.65–7.54), and SLE-related features, such as the presence of auto-antibodies (OR 5.8 and 5.0, CI 95% 3.28–7.78) and neurological disorders (OR 5.2, CI 95% 2.0–13.9). A low correlation was shown for the importance of organ damage and SLE activity (respectively OR 1.4, CI 95% 1.09–4.44 and OR 1.2, CI 95% 1.2–1.2), as well as for age at diagnosis (OR 1.1, CI 95% 1.07–1.17). Cardiovascular events in SLE patients are caused by a multifactorial mechanism, including both traditional and disease-specific risk factors. A global valuation with an individual risk stratification based on both these features is important to correctly manage these patients in order to reduce negative outcomes.

Background: Accuracy of high sensitive troponin (hs-cTn) to detect coronary artery disease (CAD) in patients with renal insufficiency is not established. The aim of this study was to evaluate the prognostic role of hs-cTn T and I in patients with chronic kidney disease (CKD). Methods: All consecutive patients with chest pain, renal insufficiency (eGFR < 60 mL/min/1.73 m2) and high sensitive troponin level were included. The predictive value of baseline and interval troponin (hs-cTnT and hs-cTnI) for the presence of CAD was assessed. Results: One hundred and thirteen patients with troponin I and 534 with troponin T were included, with 95 (84%) and 463 (87%) diagnosis of CAD respectively. There were no differences in clinical, procedural and outcomes between the two assays. For both, baseline hs-cTn values did not differ be­tween patients with/without CAD showing low area under the curve (AUC). For interval levels, hs-cTnI was significantly higher for patients with CAD (0.2 ± 0.8 vs. 8.9 ± 4.6 ng/mL; p = 0.04) and AUC was more accurate for troponin I than hs-cTnT (AUC 0.85 vs. 0.69). Peak level was greater for hs-cTnI in patients with CAD or thrombus (0.4 ± 0.6 vs. 15 ± 20 ng/mL; p = 0.02; AUC 0.87: 0.79–0.93); no differences were found for troponin T assays (0.8 ± 1.5 vs. 2.2 ± 3.6 ng/mL; p = 1.7), with lower AUC (0.73: 0.69–0.77). Peak troponin levels (both T and I) independently predicted all cause death at 30 days. Conclusions: Patients with CKD presenting with altered troponin are at high risk of coronary disease. Peak level of both troponin assays predicts events at 30 days, with troponin I being more accurate than troponin T. (Cardiol J 2017; 24, 2: 139–150) Background: Accuracy of high sensitive troponin (hs-cTn) to detect coronary artery disease (CAD) in patients with renal insufficiency is not established. The aim of this study was to evaluate the prognostic role of hs-cTn T and I in patients with chronic kidney disease (CKD). Methods: All consecutive patients with chest pain, renal insufficiency (eGFR < 60 mL/min/1.73 m2) and high sensitive troponin level were included. The predictive value of baseline and interval troponin (hs-cTnT and hs-cTnI) for the presence of CAD was assessed. Results: One hundred and thirteen patients with troponin I and 534 with troponin T were included, with 95 (84%) and 463 (87%) diagnosis of CAD respectively. There were no differences in clinical, procedural and outcomes between the two assays. For both, baseline hs-cTn values did not differ be­tween patients with/without CAD showing low area under the curve (AUC). For interval levels, hs-cTnI was significantly higher for patients with CAD (0.2 ± 0.8 vs. 8.9 ± 4.6 ng/mL; p = 0.04) and AUC was more accurate for troponin I than hs-cTnT (AUC 0.85 vs. 0.69). Peak level was greater for hs-cTnI in patients with CAD or thrombus (0.4 ± 0.6 vs. 15 ± 20 ng/mL; p = 0.02; AUC 0.87: 0.79–0.93); no differences were found for troponin T assays (0.8 ± 1.5 vs. 2.2 ± 3.6 ng/mL; p = 1.7), with lower AUC (0.73: 0.69–0.77). Peak troponin levels (both T and I) independently predicted all cause death at 30 days. Conclusions: Patients with CKD presenting with altered troponin are at high risk of coronary disease. Peak level of both troponin assays predicts events at 30 days, with troponin I being more accurate than troponin T. (Cardiol J 2017; 24, 2: 139–150)