Article first published online: 28 DEC 2007
Copyright © 2008 by the American College of Rheumatology
Arthritis & Rheumatism
Volume 58, Issue 1, page 331, January 2008
How to Cite
Hirata, K., Homma, S., Choy, A. and Lang, C. C. (2008), Reply. Arthritis & Rheumatism, 58: 331. doi: 10.1002/art.23233
- Issue published online: 28 DEC 2007
- Article first published online: 28 DEC 2007
To the Editor:
We appreciate the comments and information presented by Dr. Korkmaz in reference to our report on altered coronary vasomotor function in patients with SLE. Dr. Korkmaz drew attention to the potential deleterious effects of cyclosporin A on endothelial function, highlighting the study by Petrakopoulou and colleagues, who reported a greater deterioration of microvascular endothelial function during followup over 12 months in heart transplant recipients randomized to cyclosporin A versus tacrolimus (1).
The vascular toxicity of cyclosprin A is well described (2). Besides microvascular thromboses (3), impairment of vascular reactivity to vasodilator stimuli may represent a principal cause of the vasculotoxic effect of cyclosporin A (4, 5). Experimental studies suggest that cyclopsorin A has an impact on both endothelial and smooth muscle function (4, 5). In our study, adenosine was used to produce maximal coronary vasodilatation. In this respect, cyclosprin A has been reported to impair vascular relaxations elicited by adenosine analogs (6). Therefore, we agree with Dr. Korkmaz that cyclosprin A may have been a contributory factor in our study findings. However, as mentioned in our report, our small study sample did not allow us to fully define the role of cyclosporin A in the pathophysiology of vascular dysfunction in SLE. We do not have full details of the duration of cyclosporin A treatment in our study population. Clearly, the potential effects of cyclosporin A on atherogenesis in the SLE population should be studied.
We agree with Dr. Korkmaz that it would have been useful to have a disease control group in our study to fully define whether our observed findings were indeed specific to young patients with SLE. Such disease control groups would include patients with inflammatory disorders such as systemic sclerosis or rheumatoid arthritis. It should, however, be noted that these patient groups are also associated with potential confounding variables including the use of disease-modifying drugs, renal dysfunction, and comorbid conditions.
The recent literature review article by Dr. Korkmaz and associates (7) described a shorter lag time between the onset of SLE and the occurrence of MI in patients with apparently normal coronary arteries/coronary thrombosis than in patients with coronary arteritis/aneurysm or coronary atherosclerosis. His suggestion that altered coronary vasomotor function in a subgroup of patients with apparently normal coronary arteries may be at risk of early myocardial infarction is interesting but can only be speculative. With respect to coronary vasomotor function and normal coronary arteries, it should be noted that coronary flow studies have been used to evaluate patients with chest pain syndrome and angiographically normal coronary arteries. These patients have a heterogeneous prognosis. Coronary flow reserve has been shown to be related to the pattern of exercise-induced ST change on electrocardiograms during exercise testing (8) and to be an independent predictor of the long-term prognosis for these patients in terms of atherosclerosis (9). Clearly, further research with followup of patients with SLE who have low coronary flow velocity reserve is needed.
Kumiko Hirata MD*, Shunichi Homma MD, FACC*, AnnaMaria Choy MD, FACC, Chim C. Lang MD, FRCP, FACC, * Columbia University, New York, NY, Ninewells Hospital and Medical School, Dundee, UK.