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Myocardial Infarction in Systemic Lupus Erythematosus: Incidence and Coronary Angiography Findings.

ABSTRACT: An association between acute myocardial infarction (AMI) and systemic lupus erythematosus (SLE) has been suggested. The cause of AMI is presumed to be atherothrombosis. In the present study, the primary objective was to assess incident AMI cases and the secondary objective was to estimate the proportion of myocardial infarction with nonobstructive coronary arteries (MINOCA) in patients with SLE. All Swedish patients with SLE without AMI before 1996 (n = 4192) were followed for 20 years in the national patient registry. For each SLE patient, 10 age- and sex-matched controls without SLE and AMI before 1996 (n = 41 892) were identified. Data from patients and controls with AMI after 1996 were linked with the Swedish coronary angiography and angioplasty register; 549 (13%) and 3352 (8%) first AMIs occurred in patients with SLE and controls, respectively. The incidence of AMI was 9.6 (95% CI: 8.9-10.5) and 4.9 (95% CI: 4.8-5.1) events/1000 person-years in patients with SLE and controls, respectively. The proportion of MINOCA was 10.8% in patients with SLE and 13.8% in controls (P = .261), respectively. In conclusion, the incidence of AMI is increased in a European population of patients with SLE but there is no indication that the proportion of MINOCA is increased in these patients.

SUBMITTER: Tornvall P

PROVIDER: S-EPMC8044619 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:ObjectiveSystemic lupus erythematosus (SLE) is a multisystem-involved, highly heterogeneous autoimmune disease with diverse clinical manifestations. We report an extremely rare case of SLE with severe diffuse myocardial hypertrophy.MethodsThe patient's echocardiography and cardiac magnetic resonance imaging (CMR) results indicated diffuse myocardial hypertrophy. After excluding coronary atherosclerosis, hypertensive cardiomyopathy, drug toxicity, and other causes, the patient was diagnosed with SLE-specific cardiomyopathy. Medications such as hormones, antimalarials, immunosuppressants, and biologics were administered.ResultsAncillary test results were as follows: hs-cTnI: 0.054 ng/mL (0-0.016); NTproBNP: 1594.0 pg/mL (<150); A contrast-enhanced CMR revealed the diffuse thickening of the left ventricular wall with multiple abnormal enhancements, reduced left ventricular systolic and diastolic function, and moderate amount of pericardial effusion. Endomyocardial myocardial biopsy was performed, showing cardiomyocyte hypertrophy and degeneration, and no changes in myocarditis or amyloidosis. The pathology viewed by electron microscopy showed increased intracellular glycogen in the myocardium, and no hydroxychloroquine-associated damage in the myocardium. The 24-h ambulatory blood pressure and contrast-enhanced computed tomography of coronary arteries were normal. The diagnosis of SLE-specific cardiomyopathy was clear. The myocardial hypertrophy showed reversible alleviation following treatment with high-dose corticosteroids. CMR results before and after treatment were as follows: interventricular septum, pretreatment (28) versus post-treatment (22) mm; left ventricular inferior wall, pretreatment (18-21) versus post-treatment (12-14) mm; left ventricular lateral wall, pretreatment (17-18) versus post-treatment (10-12) mm; pericardial effusion (left ventricular lateral wall), pretreatment (25) versus post-treatment (12) mm; left ventricular ejection fraction, pretreatment (38.9%) versus post-treatment (66%).ConclusionMyocardial hypertrophy may be an important sign of active and prognostic assessment in SLE diagnosis and management. Similarly, when encountering cases of myocardial hypertrophy, the possibility of autoimmune disease should be considered in addition to common causes.

Project description:BackgroundThe risk of acute myocardial infarction (AMI) is elevated in patients with systemic lupus erythematosus (SLE), and it is of great clinical value to identify potential molecular mechanisms and diagnostic markers of AMI associated with SLE by analyzing public database data and transcriptome sequencing data.MethodsAMI and SLE-related sequencing datasets GSE62646, GSE60993, GSE50772 and GSE81622 were downloaded from the Gene Expression Omnibus (GEO) database and divided into prediction and validation cohorts. To identify the key genes associated with AMI related to SLE, WGCNA and DEGs analysis were performed for the prediction and validation cohorts, respectively. The related signaling pathways were identified by GO/KEGG enrichment analysis. Peripheral blood mononuclear cells (PBMCs) from patients with AMI were collected for transcriptome sequencing to validate the expression of key genes in patients with AMI. Least absolute shrinkage and selection operator (LASSO) regression analysis was applied to screen diagnostic biomarkers. The diagnostic efficacy of biomarkers was validated by ROC analysis, and the CIBERSORTx platform was used to analyze the composition of immune cells in AMI and SLE.ResultsA total of 108 genes closely related to AMI and SLE were identified in the prediction cohort, and GO/KEGG analysis showed significantly enriched signaling pathways. The results of differential analysis in validation cohort were consistent with them. By transcriptional sequencing of PBMCs from peripheral blood of AMI patients, combined with the results of prediction and validation cohort analysis, seven genes were finally screened out. LASSO analysis finally identifies DYSF, LRG1 and CSF3R as diagnostic biomarkers of SLE-related-AMI. CIBERSORTx analysis revealed that the biomarkers were highly correlated with neutrophils.ConclusionNeutrophil degranulation and NETs formation play important roles in SLE-related AMI, and DYSF, LRG1 and CSF3R were identified as important diagnostic markers for the development and progression of SLE-related AMI.

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Myocardial Infarction in Systemic Lupus Erythematosus: Incidence and Coronary Angiography Findings.

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