A nationwide population-based retrospective cohort study:
Increased
risk of acute myocardial infarction in systemic lupus
erythematous patients
Chi-Hung Chou
a,1, Cheng-Li Lin
b, Shih-Ni Chang
b,c, Ming-Chia Lin
d,1,
Chia-Hung Kao
e,f,⁎
, Yi-Jia Huang
dAcute myocardial infarction (AMI) includes any condition that suddenly blocks blood fow to the heart, necrotizing a substantial portion of the myocardium. Male sex, hypertension, smoking, hyperlipidemia, and diabetes mellitus are known cardiovascular
(CV) risk factors [1,2]. Systemic lupus erythematous (SLE) is a
systemic autoimmune disease that often affects young women. A nationwide study in Sweden considered whether hospitalization for immune-mediated diseases such as SLE and rheumatoid arthritis was predictive of subsequent hospitalization for coronary artery disease
[3]. CV disease is a primary cause of both morbidity and premature
mortality among women with SLE [4–7]. The pathogenesis of
premature CV disease in women with lupus is likely multifactorial, related to underlying vascular infammation and arterial wall injuries, the adverse effects of corticosteroids, the high prevalence of renal disease and hypertension, and increased thrombosis in the setting of antiphospholipid antibodies. This study uses a large cohort representing 99% of Taiwan's population to analyze the incidence of AMI in disabled SLE patients. The resultsmay guide future care of SLE patients and AMI prevention.
This research used the Taiwan National Health Insurance Research Database (NHIRD) claim data to identify 10,954 patients diagnosed with SLE between 1998 and 2008 and 43,816 comparison patients. The risk of SLE patients developing AMI was measured using a Cox proportional hazard model. The SLE cohort included 10,954 patients and the
comparison cohort included 43,816 patients of almost the same average age (39.5 y vs 39.77, p=0.23) and sex ratio (male: 11.7%, p=0.99). The proportion of AMI associated with diabetes, hypertension, or hyperlipidemia comorbidities in the SLE cohort was much higher than that in the
comparison cohort (p b 0.0001).
10,000 person-years and was 2.66 times higher than that in the
comparison cohort (Table 1). Fig. 1 shows the Kaplan–Meier estimated
cumulative incidence curves for the two study cohorts and indicates that the SLE cohort incidence curve is signifcantly greater than that of the comparison cohort (log-rank test, p b 0.001). After adjusting for potential confounding factors, the SLE cohortwas 2.74 timesmore likely to develop AMI than the comparison cohort (HR=2.74, 95%; CI=2.09–3.06).
Table 1 also shows the demographic-specifc and comorbidityspecifc incidence of developing AMI for the two cohorts. Relative to
the comparison cohort, younger SLE patients had the highest risk of developing AMI (b34 y, HR = 12.9; 35–49 y, HR =2.78; 50–64 y, HR = 2.14; ≥65 y, HR = 2.14). Women and men in the SLE cohort were more likely to develop AMI than those in the comparison cohort
(female, HR=3.36; male, HR=2.01). In Table 2, we stratifed patients
according to comorbidities. A lack of hypertension (HR = 2.93, 95% CI = 1.86–4.63), diabetes (HR = 3.11, 95% CI = 2.23–4.33), hyperlipidemia
(HR = 2.81, 95% CI = 2.07–3.80), COPD (HR = 2.74, 95%
CI = 2.05–3.65), and proteinuria (HR = 2.69, 95% CI = 2.05–3.54) was signifcantly associated with an increased risk of AMI. However, the risk of AMI was signifcantly elevated in SLE patients who exhibited CVA (HR = 2.67, 95% CI = 1.51–4.74) or ESRD (HR = 4.44, 95% CI = 1.09–18.1).
Our study showed a signifcantly higher frequency of hypertension, diabetes mellitus, hyperlipidemia, CVA, COPD, ESRD, and proteinuria among SLE patients compared with non-SLE patients. Asians with SLE exhibited increased rates of renal involvement, and CVinvolvementwas a
leading cause of death [8]. Wells and Ward observed that nephritis was
associated with 2.8-fold increased risk of AMI among SLE patients [9]. It is
necessary to do appropriate interventions with these patients to reduce CV risk and improve longevity and quality of life.
The study has certain limitations. First, crucial data were missing from the NHIRD regarding major risk factors of AMI such as smoking habits, body mass index, socioeconomic status, and family history of systemic diseases. Second, because all benefciaries listed on the NHIRD are protected by anonymity, we could not obtain individual clinical (blood pressure), imaging, pathologic, or laboratory data (including lipid profle, fasting blood glucose, infammatory markers such as CRP or ESR, and SLE disease activity index) for each study
participant. Third, we were unable to contact the patients to inquire on the use of their most common non-steroidal anti-infammatory drugs.
Our fndings indicate that SLE patients exhibit an increased risk of AMI. Identifying subgroups that exhibit various risk levels would facilitate evaluating prognoses. To conclude, SLE patients exhibit a higher risk of AMI compared with the general population.
