Coronary artery disease plus RA exacerbates risk for adverse CV events, mortality
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Among patients with coronary artery disease, rheumatoid arthritis was significantly associated with an elevated risk for myocardial infarction, major adverse cardiovascular events and all-cause mortality, according to data.
“Risk stratification and strategies to prevent cardiovascular events in patients with RA — such as treating hypertension, encouraging patients to stop smoking and reinforcing statin therapy — may be especially important, regardless of whether they have a history of coronary artery disease, because their risk for adverse cardiovascular outcomes is significantly greater than for patients who have neither RA nor coronary artery disease (CAD),” Brian Bridal Løgstrup, MD, PhD, of Aarhus University Hospital, in Denmark, told Healio Rheumatology.
“Our study makes a significant contribution to the literature in reporting on the additive risk of RA and CAD,” he added.
To examine the impact of RA on the risk for adverse cardiovascular events among patients with and without coronary artery disease, Løgstrup and colleagues assembled a population-based cohort of individuals in the Western Denmark Heart Registry. According to the researchers, this registry includes information regarding all cardiac procedures performed in Western Denmark since 1999, covering a population of approximately 3.5million people. For their study, the researchers included patients who underwent coronary angiography between 2003 and 2016. These patients were then stratified by the presence of RA and coronary artery disease.
Løgstrup and colleagues included 125,331 patients from the registry, of whom 1,732 had RA. Endpoints included myocardial infarction, major adverse cardiovascular events such as ischemic stroke and cardiac death, and all-cause mortality. The median follow-up was 5.2 years.
According to the researchers, compared with patients with neither RA nor coronary artery disease, who had a cumulative myocardial incidence of 2.7%, the 10-year risk for myocardial infarction for those with RA alone was higher, at 3.8% (IRR = 1.63; 95% CI, 1.04-2.54). The 10-year risk for myocardial infarction was also higher among patients with coronary artery disease alone, with a cumulative incidence of 9.9% (IRR = 3.35; 95%CI, 3.1-3.62).
However, the 10-year risk was highest among patients with both RA and coronary artery disease, with a cumulative incidence of 12.2% (IRR = 4.53; 95% CI, 3.66-5.59). Similar links were reported for major adverse cardiovascular events and all-cause mortality.
“Our study makes a significant contribution to the literature in reporting on the additive risk of RA and coronary artery disease,” Løgstrup said. “Among patients with coronary artery disease, RA was associated with an increased risk of acute myocardial infarction, major adverse cardiovascular events, cardiac death and all-cause mortality.”
“These findings indicate that RA may have a potential impact for precipitating cardiovascular events beyond coronary artery disease and, even more importantly, that RA seems to exacerbate the clinical risk of cardiovascular events in the presence of coronary artery disease,” he added. “The results of our study could result in more aggressive risk stratification among patients with RA, by presence or absence of documented coronary artery disease, which may allow for a more personalized treatment strategy.”
Perspective
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This study further cements the association between RA and a higher risk of cardiac disease. It clearly identifies the highest-risk patients — those with both known CAD and RA — which offers rheumatologists and their physician colleagues a potentially actionable treatment focus in terms of employing more aggressive cardiac risk monitoring and risk reduction strategies to mitigate adverse cardiovascular outcomes. Obviously, baseline invasive testing for CAD would not be an appropriate screening tool for asymptomatic RA patients, but other tools such as coronary CT angiography as suggested by the authors could be employed.
Given the recognition of biologic therapy to potentially reduce the risk of cardiac events in patients with RA, it would have been greatly informative if the authors had been able to identify and provide information on the specific therapeutic agents employed in the RA/negative CAD and RA/positive CAD groups.
The generalizability of the dataset to asymptomatic RA patients is somewhat limited as all patients included in the study were referred for coronary angiography due to clinical suspicion of cardiac disease. Additionally, a significant proportion of patients including those without CAD were already on aspirin, a vitamin K antagonist or a statin. Finally, the RA diagnosis itself was based on registry data as opposed to independent confirmation which may have some impact on the study’s findings.
Potential future studies might look at the wider asymptomatic RA population and employ noninvasive screening tools to identify higher-risk patients and attempt more individualized risk reduction strategies.
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