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Risk of ischaemic and non-ischaemic heart failure in patients with systemic sclerosis: a population-based study
Majd Bairkdar1, Jonas Faxén2,3, Elizabeth V Arkema1
1Clinical Epidemiology Division, Department of Medicine Solna, Karolinska Institutet, Stockholm, Sweden.
Insights
Systemic sclerosis (SSc) significantly increases the risk of heart failure (HF), both ischemic and non-ischemic. This risk is highest early after SSc diagnosis, highlighting non-ischemic mechanisms beyond just reduced blood flow.
Area of Science:
- Cardiology
- Rheumatology
- Epidemiology
Background:
- Systemic sclerosis (SSc) is a complex autoimmune disease with known cardiovascular implications.
- Heart failure (HF) is a significant complication, but its specific types and risk factors in SSc require further elucidation.
Purpose of the Study:
- To determine the risk of incident ischemic and non-ischemic heart failure (HF) in patients with systemic sclerosis (SSc).
- To compare HF incidence in SSc patients against a matched general population cohort.
Main Methods:
- A population-based cohort study using Swedish nationwide registers from 2004-2019.
- 1,598 SSc patients were matched 1:10 with general population comparators.
- Flexible parametric models were used to estimate hazard ratios (HR) for HF over time.
Main Results:
- Patients with SSc had a significantly higher risk of developing HF (6% vs 2%).
- The relative risk of overall, ischemic, and non-ischemic HF was highest within the first year post-SSc diagnosis.
- Hazard ratios at one year were 5.7 for overall HF, 6.7 for ischemic HF, and 5.8 for non-ischemic HF.
Conclusions:
- Systemic sclerosis is strongly associated with both ischemic and non-ischemic heart failure.
- Mechanisms beyond ischemia, including myocyte dysfunction, fibrosis, and microvascular impairment, are crucial in SSc-related HF development.
Objectives:
To investigate the risk of incident ischaemic and non-ischaemic heart failure (HF) in a population-based cohort of all patients with SSc in Sweden compared with the general population.
Methods:
We identified patients with incident SSc 2004-19 using nationwide Swedish registers and age- and sex-matched comparators from the general population (1:10). We started follow-up from the date of SSc diagnosis, the same date was assigned to the respective comparators. Our primary outcome was incident HF [International Statistical Classification of Diseases and Related Health Problems (ICD)-10: I50] as main diagnosis stratified into ischaemic and non-ischaemic HF depending on whether a visit listing ischaemic heart disease (ICD-10: I20-I25) was recorded before HF diagnosis or not. We used flexible parametric models to estimate hazard ratios (HRs) over time since SSc diagnosis.
Results:
The study cohort comprised 1598 patients with SSc and 16 616 comparators. During follow-up, 101 (6%) patients with SSc developed HF compared with 378 (2%) of the comparators. Ischaemic HF represented 35% and non-ischaemic HF represented 65% of all HF cases in both groups. The relative risk of HF overall, ischaemic HF and non-ischaemic HF was highest soon after SSc diagnosis. HR at the end of the first year of follow-up was 5.7 (95% CI 4.2-7.9) for HF overall, 6.7 (95% CI 3.5-13.0) for ischaemic HF and 5.8 (95% CI 4.0-8.3) for non-ischaemic HF.
Conclusion:
SSc is associated with both ischaemic and non-ischaemic HF, emphasizing the role of other mechanisms than ischaemia, such as myocyte dysfunction, myocardial fibrosis and microvascular impairment, in the development of HF in SSc.
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