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RA and Cardiac Co-Morbidities

Nov 05, 2017 9:30 pm

We know that cardiovascular disease (CVD) is the leading cause of death in RA and that traditional risk factors do not fully account for increased risk. It is also recognised that RA patients have fewer warning symptoms prior to major event and also have a higher case fatality rates for stroke and cardiac events. 

In RA Clinical Aspects I Cardiac Co-Morbidities (abstracts 867-72) we heard data addressing risk stratification and mechanisms behind these observations.

Two studies assessed the predictive value of high sensitivity troponin I (hsTnI) and cardiovascular outcomes in RA.

Karpouzas et al (abstract 867) studied 150 established RA patients and found that hsTnI levels were associated with subclinical coronary plaque and calcification on cardiac CT. Over the follow-up period, 11 patients had a CVD event. hsTnI levels were associated with an increased risk of CVD events: adjusted hazard ratio (95%CI) = 5.4 (1.1, 25.9). Patients with a low hsTnI were 80% less likely to have a CVD event.

In the Norfolk Arthritis Register, Skeoch et al (abstract 868) measured hsTnI in 1022 patients with early inflammatory arthritis. Baseline hsTnI were associated with a number of classic CVD risk factors including hypertension, TC/HDL ratio and diabetes but were not associated with CRP concentrations. Over a median follow-up of 11 years, 27 patients suffered a CVD-related death. In a model adjusting for classic CVD risk factors and inflammatory arthritis related factors, log hsTnI remained significantly associated with CVD death (adjusted HR = 1.83 [1.08, 3.10]). Comparing those in the highest vs lowest tertile of hsTnI found a HR =5.42 (2.48, 11.85) for CVD-related mortality.

A third abstract in this session Liao et al (abstract 871) assessed coronary flow reserve (CFR) in 49 RA patients compared to patients with diabetes mellitus (DM) undergoing cardiac PET imaging to assess for coronary perfusion defects. In the subset with no coronary perfusion defects approximately 50% of RA patients had impaired CFR, which is similar to what is seen in DM. Over a median 5.4 yrs follow-up, 25.6% RA patients with low CFR died compared to 13.6% with normal CFR. A trend that was similar to that seen in DM patients.

Two other abstracts showed preliminary data that treating RA patients towards remission may improve cardiac MR abnormalities in RA patients, especially those with established RA (abstract 872) and that assessment of carotid IMT may also provide additional risk stratification in RA when added to Framingham Risk scores (abstract 871).

Taken together, it is clear that CVD risk in RA is poorly predicted by standard approaches and better risk stratification is needed. Biomarkers such as hsTnI may be a readily available additional risk stratifier. Also a better understanding of coronary flow reserve (reflecting microvascular dysfunction) may also provide important mechanistic insights into the excess CVD mortality in RA.


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