Abstract

To the Editor: It was with great interest we read the report by Cipollone et al1 on the role of transforming growth factor-β1 (TGF-β1) in the process of plaque stabilization. The authors demonstrate that TGF-β mRNA levels are increased up to 3-fold in asymptomatic as compared with symptomatic plaques, with a parallel increase in protein expression at immunocytochemistry and Western blot analyses.1 In addition, TGF-β1 expression was associated with a comparable increase in plaque procollagen and collagen content, thus providing a tangible mechanism of plaque stabilization.1 As Cipollone et al acknowledge in their discussion, one important issue would be to measure systemic levels of TGF-β1 to verify whether a correlation exist between the localized expression and circulating levels of this cytokine; this correlation would suggest a systemic process in these patients rather than a local phenomenon, and probably might add prognostic information to the management of patients with carotid plaques. We have only recently completed reviewing the data collected in a 10-year prospective study of the incidence of major cardiovascular events in 42 patients with asymptomatic low-grade carotid stenosis. Patients were consecutively enrolled over a 1-year period from those presenting at the Department of Internal Medicine of the Palermo University Hospital for ultrasound evaluation (high-resolution B-mode ultrasonography using a 7.5-MHz duplex-type probe; Toshiba) of carotid atherosclerotic involvement because of the presence of at least 1 cardiovascular risk factor. Percent carotid lumen stenosis was graded as low-grade lumen stenosis because of plaque >15% but <50% (intima-media thickness …

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