Response to 'Ramipril attenuates lipid peroxidation and cardiac fibrosis in an experimental model of rheumatoid arthritis'

Abstract

We read with great interest the recent issue of Arthritis Research & Th erapy i n which Shi and colleagues [1] investi gated the eff ects of ramipril on oxidative stress and fi brosis in the heart of rat s with adjuvant arthritis. Th e authors concluded that ramipril reversed arthritis scoring and decreased markers of oxidative stress, infl ammation, and tissue fi brosis. Undoubtedly, their fi ndings will promote the attempt to diminish the cardiovascular risk of patients with rheumatoid arthritis (RA) by using angio tensin-converting enzyme inhibitors (ACEIs) or angiotensin receptor blockers (ARBs) or both. However, several important aspects should be considered in the interpretation of this study. As described by the authors, adjuvant arthritis was induced successfully in female rats with a 100% incidence rate, but actually the male rats were use d in most cases [2-4]. Th ere fore, we speculate that this discrepancy may be related to th e impact of arthritis on cardiac fi brosis and oxidative stress status in the heart o f rats with adjuvant arthritis. In addition, the dosage of ramipril is a matter of debate. In a randomized and double-blind clinical study, treatment with 10 mg/day ramipril eff ectively improved endothelial function in patients with RA [5]. Intriguingly, how was the ramipril dosage (10 mg/kg per day) used in this animal study calculated? Unlike previous reports focusing on the eff ect of ramipril and ARBs on vascular function with RA and experimental models [2,5], the article by Shi and colleagues reported that ramipril improved c ardiac function in rats with adjuvant arthritis. Although we list some methodological issues here, we believe that the authors’ fi ndings strongly suggest a promising therapeutic role of ACEIs and ARBs on both card iovascular risk and arthritis in patients with RA.