Risk for cardiovascular events, including stroke, atrial fibrillation (AF), and congestive heart failure, were higher in patients with vs without antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV), with the highest risk in the first year after AAV diagnosis, according to study data published in Clinical Kidney Journal.
In a retrospective cohort study, the researchers collected medical records data from the Institute for Clinical Evaluative Sciences in Ontario, Canada. Adult residents of Ontario who received a diagnosis of AAV between 2007 and 2017 were eligible for inclusion in the analysis. Patients with AAV were defined as any individual with a hospital or emergency room visit with a diagnostic code for AAV. Individuals with AAV were matched 1:4 with control participants based on age, sex, estimated glomerular filtration rate, income quintile, rurality status, and number of hospitalizations in the 3 years prior to study entry.
The study outcomes of interest were major cardiovascular event (MACE), AF, and congestive heart failure, identified using the associated diagnostic codes. MACE was defined as a composite of myocardial infarction (MI), stroke/transient ischemic attack (TIA), and cardiovascular death. Incidence rates were calculated for each cardiovascular event. Subdistribution hazard ratios (sHRs) were estimated to compare outcomes between patients with AAV and control participants.
The study cohort included 1520 patients with AAV, among whom 50.5% were women. Mean age at index date was 60.8±17.4 years; mean follow-up time was 3.8 years. The control cohort included 5834 individuals. Demographic characteristics were similar between groups.
Among patients with AAV, the cumulative incidence rates for cardiovascular outcomes were 15.4% for MACE, 6.6% for MI, 7.0% for stroke/TIA, 4.1% for cardiovascular death, 16.4% for AF, and 20.8% for congestive heart failure. Compared with control participants, individuals with AAV had significantly elevated risk for stroke/TIA (sHR, 1.49; 95% CI, 1.10-2.02), AF (sHR, 1.51; 95% CI, 1.30-1.75), and congestive heart failure (sHR, 1.41; 95% CI, 1.22-1.62), but not for MACE, MI, or cardiovascular death.
In analyses limited to the first 365 days after AAV diagnosis, patients were at particularly elevated risk for cardiovascular events. During this time period, patients were much more likely than control participants to experience MACE (sHR, 1.31; 95% CI, 1.07-1.62), MI (sHR, 1.52; 95% CI, 1.10-2.10), stroke/TIA (sHR, 1.87; 95% CI, 1.25-2.80), AF (sHR, 2.06; 95% CI, 1.71-2.48), and congestive heart failure (sHR, 1.75; 95% CI, 1.48-2.07). Risks were further elevated in the first 90 days after diagnosis, during which a 3.3-fold risk for AF and 2.7-fold risk for congestive heart failure were observed. These risks attenuated over time, reducing substantially at 1 year post-diagnosis, and further, during all follow-up.
Results from this study underlined the cardiovascular risks associated with AAV. Patients with vs without AAV were more likely to experience cardiovascular events, particularly within the first 3 months after diagnosis.
Study limitations included that fact that because patients with AAV were identified based on diagnostic codes at hospitalization, results may not be generalizable to patients diagnosed in the outpatient setting.
“Our study demonstrates a key ‘high-risk window’ that should prompt careful monitoring for CV disease and aggressive risk factor reduction,” the researchers wrote. “This study highlights the complexity of caring for patients with AAV and additional benefits which may be derived from focused, multidisciplinary care in specialty clinics.”
Disclosure: One study author declared affiliations with biotech, pharmaceutical, and/or device companies. Please see the original reference for a full list of disclosures.
David Massicotte-Azarniouch, William Petrcich, Michael Walsh, et al. Association of ANCA-associated vasculitis and cardiovascular events: a population-based cohort study. Clinical Kidney Journal. Published online November 24, 2021. doi:10.1093/ckj/sfab229
This article originally appeared on Rheumatology Advisor