Rheumatoid arthritis (RA) affects the entire body, including the cardiovascular (CV) system. Independent of other risk factors, RA increases the risk of CV disease (CVD). Collaborative care between rheumatologists, cardiologists, and primary care doctors is crucial for managing CV risks in patients with RA, as is the careful selection of RA therapeutics that may impact CV health.

In the last decade, the heart has been extensively studied in patients with RA. RA is a multiorgan disease with a significant risk of CVD that can be independent of other risk factors such as hypertension, smoking, and diabetes, although those factors certainly also increase the risk. The first approach to mitigating the risk of CVD is to control the RA.

Several retrospective studies and meta-analyses have reported a decreased risk of heart failure, myocardial infarction, and mortality with methotrexate therapy in patients with RA. However, the large randomized CIRT study of patients with type 2 diabetes or metabolic syndrome with prior myocardial infarction or multivessel coronary disease was stopped prematurely because there was no difference in the rate of nonfatal myocardial infarction, nonfatal stroke, or CV death with methotrexate vs placebo. The earlier CANTOS study found that IL-1β inhibition reduced the risk of heart attacks vs placebo in patients with a history of myocardial infarction and a C-reactive protein (CRP) blood level of at least 2 mg/L. Patients in CANTOS were required to have this elevated CRP level for enrollment. Since the CIRT study did not require elevated CRP levels for enrollment, it did not select for patients with systemic inflammation who may benefit the most from treatment, which may help explain why the study failed.

The TARGET study randomized 159 patients with active RA despite receiving methotrexate to have adalimumab or etanercept added (anti-TNF therapy) or sulfasalazine and hydroxychloroquine added (triple therapy). The clinical effects were similar, but there was no difference in degree of arterial inflammation with anti-TNF therapy vs triple therapy according to fluorodeoxyglucose positron emission tomography/computed tomography scans, which surprised a lot of us.

Rheumatologists are being pulled into the discussion of making sure that patients are controlling their CVD risk factors, and maybe appropriately so. Because of the increased scrutiny regarding the potential CV effects of JAK inhibitors, we need to look at CV risk factors in patients who are receiving them. We have become much more aggressive in getting our patients screened and sending them to a preventive cardiologist, and I think that this is really important. For hypertension and smoking cessation, we advocate for patients to engage with their primary care doctors about treatments. The issue is with dyslipidemia management; many rheumatologists are initiating statins and notifying the patients’ primary care doctors because patients may be seeing us more frequently than their primary care doctors. If a patient has a primary care doctor who is willing to become a part of the RA management team in this way, that is great, but it does not always work out that way for our patients. Finally, if you have a patient with class I heart failure who is taking an anti-TNF drug, they really need to be monitored to make sure that their heart failure does not progress, because there is a risk of it worsening with anti-TNF therapy.