Association between systemic lupus erythematosus and myocardial infarction subtypes - a matched cohort study in Sweden

Abstract Background Systemic lupus erythematosus (SLE) is linked to a 2- to 3-fold higher risk of myocardial infarction (MI), with accelerated coronary artery disease suggested as a key contributor. However, this hypothesis requires further investigation, as no sufficiently large study has estimated the risk of MI with obstructive coronary artery disease (MI-CAD) associated with SLE. Purpose To estimate the risk of MI-CAD and MI with non-obstructive coronary arteries (MINOCA) in individuals with SLE compared to individuals without SLE. Methods This matched cohort study linked nationwide prospectively collected Swedish registers 2006 to 2021. Individuals aged 18–80 with incident SLE were identified using the National Patient Register (NPR). SLE was defined as two visits within one year, listing ICD-10 code M32 (excluding M32.0), with at least one visit to a specialist (rheumatology, internal medicine, nephrology, dermatology, or pediatrics). Individuals with SLE were matched by age, sex, and residential location to ten general population comparators without SLE. Comparators were identified using the Total Population Register. Individuals with MI prior to start of follow-up were excluded. Follow-up started at the second SLE-coded visit or matching date and ended at the first MI diagnosis, 2021-01-01, death, or emigration, whichever came first. MI was identified via ICD codes in the NPR or the Swedish web-system for enhancement and development of evidence-based care in heart disease evaluated according to recommended therapies (SWEDEHEART). The latter was also used to determine MI subtype, i.e. MI-CAD or MINOCA. Incidence rates, rate differences, and cause-specific hazard ratios (HRs) for MI-CAD and MINOCA were calculated using Poisson and Cox regression, adjusted for age, sex, and educational level. Results The study population included 3893 individuals with SLE and 38154 comparators. Eighty-four percent were female. Mean age at start of follow-up was 47 years. Other characteristics of the study population are reported in Table 1. MI occurred in 120 individuals with SLE and 525 comparators, corresponding to incidence rates of 4.4 (95% CI 3.6 - 5.3) and 1.9 (95% CI 1.7 - 2.0) MIs per 1000 person-years, respectively. SLE was associated with a higher risk for any MI (HR 2.5; 95% CI 2.0 to 3.0) and MI-CAD (HR 2.4; 95% CI 1.9 to 3.1), but not MINOCA (HR 0.9; 95% CI 0.4 to 2.2), relative to comparators (Table 2). The risk for unspecified MI, where data from coronary angiography was missing, was also higher in individuals with SLE (HR 3.4; 95% CI 2.4 to 4.8; Table 2). Conclusion The risk of MI-CAD, but not of MINOCA, was higher in individuals with SLE compared to those without SLE, supporting the hypothesis that accelerated CAD contributes to the higher MI risk in this population. These findings underscore the need for research targeting risk factors and prevention strategies for atherosclerotic MI in SLE.