Bibliographic record
Abstract
With its first description published in 1976 the bimodal mortality pattern in systemic lupus erythematosus (SLE) described early mortality as usually being due to lupus disease itself or infection, and a late mortality often being due to atherosclerotic vascular events (AVE). 1 This concept has undergone a dramatic evolution in my lifetime as a lupus physician. We now deal with the recognized clinical presentations of atherosclerotic events, with subclinical and even preclinical diagnosis and have made important developments in their successful prevention and treatment.It is now recognized that the prevalence of AVE is between 6% and 17%,2–4 and women with SLE have a 5–50-fold increase in their risk for coronary artery disease (CAD).5 The mortality attributable to CAD is between 3.5% and 36.4% and is now the second leading cause of death. These findings led to an intensification of the investigations to detect atherosclerotic disease before clinical presentation. Subclinical investigations including carotid ultrasound studies, myocardial perfusion studies and brachial artery flow mediated dilatation studies all revealed subclinical disease in patients with SLE.6 In addition, the 2017 American College of Cardiology and the American Heart Association guidelines defined hypertension at a new threshold of ≥130/80 mmHg instead of ≥140/90 mm Hg.7 This revealed a further subset of SLE patients with hypertension at risk for AVE. At the same time, we were able to describe that myocardial infarction events may occur even several years prior to the diagnosis of lupus.8 This resulted in the alert lesson that if a female in her 40s or 50s presents with a myocardial infarction, investigations for an autoimmune disease such as lupus should be considered. All these findings have led to an earlier intensification of therapy for CAD risk factors, while new improved therapies have been implemented for SLE itself. Thus, when we compared the incidence of AVEs in our cohort during the years of 1975–1987 compared to 1999–2011, the incidence per 100 person years decreased from 1.8 to 0.44 (a four-fold decrease).9References Urowitz MB, Bookman AA, Koehler BE, et al. The bimodal mortality pattern of systemic lupus erythematosus. Am J Med. 1976;60(2):221–5. doi: 10.1016/0002-9343(76)90431-9.Zeller CB, Appenzeller S. Cardiovascular disease in systemic lupus erythematosus: The role of traditional and lupus related risk factors. Curr Cardiol Rev. 2008;4(2):116–22. doi: 10.2174/157340308784245775.McMahon M, Hahn BH, Skaggs BJ. Systemic lupus erythematosus and cardiovascular disease: Prediction and potential for therapeutic intervention. Expert Rev Clin Immunol. 2011;7(2):227–41. doi: 10.1586/eci.10.98.Katz G, Smilowitz NR, Blazer A, et al. Systemic lupus erythematosus and increased prevalence of atherosclerotic cardiovascular disease in hospitalized patients. Mayo Clin Proc. 2019;94(8):1436–43. doi: 10.1016/j.mayocp.2019.01.044.Tselios K, Urowitz MB. Cardiovascular and pulmonary manifestations of systemic lupus erythematosus. Curr Rheumatol Rev. 2017;13(3):206–18. doi: 10.2174/1573397113666170704102444.Teixeira V, Tam LS. Novel insights in systemic lupus erythematosus and atherosclerosis. Front Med (Lausanne). 2017;4:262. doi: 10.3389/fmed.2017.00262.Muntner P, Carey RM, Gidding S, et al. Potential us population impact of the 2017 ACC/AHA high blood pressure guideline. Circulation. 2018;137(2):109–18. doi: 10.1161/circulationaha.117.032582.Urowitz MB, Gladman DD, Anderson NM, et al. Cardiovascular events prior to or early after diagnosis of systemic lupus erythematosus in the systemic lupus international collaborating clinics cohort. Lupus Sci Med. 2016;3(1):e000143. doi: 10.1136/lupus-2015-000143.Urowitz MB, Su J, Gladman DD. Atherosclerotic vascular events in systemic lupus erythematosus: An evolving story. J Rheumatol. 2020;47(1):66–71. doi: 10.3899/jrheum.180986.Learning Objectives At the end of this presentation participants will be able to:Discuss the nature of AVEs and their impact in patients with SLEExplain the importance of investigating subclinical atherosclerosis to institute preventive measuresDescribe the success of the use preventive measures to decrease the development of AVEs in patients with lupus
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How this classification was reachedexpand
Full frame machine prediction
Teacher imitationNot calibrated prevalence, not ground truth. Human validation pending. The Gemma side is a direct model label for every work in the frame, read from the title-only record. The Codex side is a classifier learned from the 10,348 direct Codex labels and calibrated to design-weighted sample rates; fields without enough sample support carry no Codex call. Candidate is the union of the two sides; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels.
Distilled classifier scores by category (both heads)
| Category | Codex | Gemma |
|---|---|---|
| Metaresearch | 0.004 | 0.016 |
| Meta-epidemiology (narrow) | 0.001 | 0.000 |
| Meta-epidemiology (broad) | 0.001 | 0.001 |
| Bibliometrics | 0.003 | 0.001 |
| Science and technology studies | 0.005 | 0.002 |
| Scholarly communication | 0.011 | 0.006 |
| Open science | 0.001 | 0.005 |
| Research integrity | 0.004 | 0.006 |
| Insufficient payload (model declined to judge) | 0.070 | 0.034 |
Machine scores (provisional)
The two teacher heads of the student model, read on this work. A score orders the frame for review; it never asserts a category, and the validation status ships verbatim with every row.
Baseline scores from an immature model (maturity gate not passed, 7 training rounds). Scores rank; they never assert a category.
score_only:v0-immature-baseline · verbatim from the scoring run: score_only means the number may rank works, and no category label ships from itClassification
machine, unvalidatedMachine predicted; a candidate call from one source (direct Gemma or distilled Codex), not a consensus.
How this classification was reached, model by model and score by score, is at the end of the page under "How this classification was reached".