To the Editors:
In their letter, Belloli et al reported their attempt to establish the presence of subclinical atherosclerosis in a series of 10 patients with spondylarthropathies, mainly PsA (n = 9), without clinically evident cardiovascular disease. Their small sample size constitutes a major limitation of their study. In this regard, a large number of patients should have been studied to establish stronger conclusions. However, data from this small series are of potential interest because they support the presence of endothelial dysfunction and a trend toward increased carotid IMT in patients with PsA.
There are some clues that may help explain the results found by the authors. First, as reported in RA, endothelial dysfunction is an early step in the atherogenesis process that may be seen soon after the onset of a chronic inflammatory rheumatic disease (1, 2). Second, as observed in RA, the increase of the carotid artery IMT and subsequently the development of carotid plaques may depend on several factors such as the patient age at the time of the study, the presence of traditional cardiovascular risk factors, and the duration and severity of the disease (3, 4). Third, Belloli et al found a higher frequency of cardiovascular events in first-degree relatives of patients compared with relatives of controls. Psoriasis, a chronic inflammatory skin disease, displays strong familial aggregation and has one of the highest heritabilities of any complex genetic disorder. Moreover, regardless of the presence of joint manifestations, the prevalence of traditional cardiovascular risk factors is increased in patients with psoriasis, particularly in those with severe cutaneous involvement (5).
Taking together all these considerations, both the genetic predisposition and the severity of cutaneous involvement with the presence of an increased inflammatory response may enhance the risk of subclinical atherosclerosis and cardiovascular events in patients with PsA.