Page 107 - THE EVOLUTION OF EARLY ARTHRITIS AND CARDIOVASCULAR RISK Samina A. Turk

THE RELATION BETWEEN CARDIAC CONDUCTION TIMES
time was prolonged in only 0.4% of the patients, a level comparable to the general population(8;19). Unfortunately, the 2 patients with a prolonged QTc time at baseline did not have an ECG after 1 year of treatment. Five patients (2.0%) developed a prolonged QTc time after 1 year. Of those patients, only 1 reached a good EULAR response.
Multiple factors affect the functioning of ion channels in myocardial cells and therefore conduction times: genetic abnormality, a cardiac disease (such as MI, owing to transmural ischemia), electrolyte levels and some medications(28). Another important
factor is reactive oxygen species which affects the ion channels on the cardiac myocytes and is stimulated by cytokines such as tumor necrosis factor-α (TNF-α) and interleukine-6 (IL-6)(29). However, in our study conduction times were not associated
with disease and inflammation markers (DAS28, EULAR response, ESR, or CRP levels).
Although disease activity improved during 1 year of antiinflammatory treatment, this
did not translate into a significant effect on conduction times. Because inflammation
is considered the major pathophysiological link between arthritis and conduction 5 disorders, the studied population might explain this difference. Patients with early
arthritis have been exposed to inflammatory activity for a shorter period of time, which in our study was a median symptom duration of 6 months, compared with established chronic arthritis. However, it could also be that patients with established RA have prolonged exposure to more traditional CV risk factors, particularly dyslipidemia, which is already present in patients with early arthritis(30;31). This is important because of the association between traditional CV risk factors and conduction disorders; we found that a high total cholesterol at baseline was associated with a prolonged QRS time. However, this association disappeared after 1 year of treatment. After correction for RBBB, because RBBB can be physiologic, the same results were obtained. However, Kurl, et al. found that QRS duration is an independent predictor of the risk of SCD, where each 10-ms increase in QRS duration was associated with a 27% higher risk for SCD(32). In our present study this would mean that the 4.4-ms increased mean in QRS time in the patients with a high TChol resembles a 11.9% higher risk for SCD, compared with the patients with a normal TChol. It has been suggested that TNF-α, Interferon-γ, and IL-1 can stimulate the production of ceramide. Ceramide are lipid molecules that partly consist of fatty acids, they downregulate ion channels in cardiac myocytes and can affect conduction times(29). Therefore, both CV risk management as well as disease control are important and should be performed in all patients with arthritis(33). Our study strengthens the notion that antiinflammatory treatment, in an early stage of the disease, leads to a significant improvement in several important CV risk factors, including the TChol:HDL ratio and blood pressure(34;35). Interestingly, patients with early arthritis with lower inflammation markers had a lower heart rate compared with those with high inflammation markers. In the general population heart rate is positively associated with CRP, as demonstrated by Nanchen, et al. who found, in 4084 adults with a known CV risk factor, that an increased heart rate was associated with systemic inflammation(36). In patients with RA, the association between inflammation and heart rate has not been previously described, particularly not the improvement in inflammation and the
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