Abstract

We read with deep interest the recent study of Dogan et al 1 entitled “Relationship Between Neutrophil-to-Lymphocyte Ratio and Saphenous Vein Graft Disease in Patients With Coronary Bypass.” The authors 1 aimed to evaluate the relationship between neutrophil-to-lymphocyte ratio and saphenous vein graft disease (SVGD) regarding the inflammatory process in atherosclerosis. We would like to comment on their methodology.
A multipronged strategy aimed at prevention of SVGD is emerging, elements of which include continued improvements in surgical technique; more effective antiplatelet drugs; increasingly intensive risk factor modification, in particular early and aggressive lipid-lowering drug therapy; and a number of evolving therapies. Besides this, most of the authors think that reducing the atherosclerotic process in which white blood cells and its subtypes are involved would reduce the adverse outcomes after coronary artery bypass grafting surgery. Endothelial dysfunction, triggered by irritative stimuli such as hyperlipidemia, high shear, and proinflammatory cytokines, is considered to be the initial stage of atherosclerosis and it is possible that inflammation triggered by neutrophils and facilitated by sustained overproduction of C-reactive protein (CRP) may accelerate atherosclerosis in some patients with low-grade inflammatory disorders. 2 –5
Atherosclerosis due to inflammation is a quite complicated process that takes different periods of time depending on several factors. Although the investigators 1 collected only 1 blood sample for each patient just 1 week before coronary angiography, it would be better to analyze repetitive complete blood count tests in order to reveal and screen the ongoing inflammatory process.
The importance of inflammation in the pathogenesis of atherosclerosis is now well established, 4,5 and highly sensitive CRP (hs-CRP) has emerged as a solid indicator of this inflammatory process. If the repetitive blood analysis including the hs-CRP test had been carried out, it would bring a better comprehensive perspective regarding the inflammatory process and SVGD.
In addition, the authors 1 did not analyze the angiologic studies in order to determine the exact localization of the saphenous vein graft atheromas. Giving the exact localization of the lesions would provide an opinion whether the graft disease depends on surgical technique, flow competition, graft varicosity, and/or wall thickness.
Previous multivariate risk factor analyses based on morphological and angiographic studies 6,7 have consistently implicated cigarette smoking as an important risk factor for the development of vein graft atheroma. Therefore, in order to homogenize the study group, there is an obvious need to consider smoking as a risk factor or exclusion criteria.
Our letter suggests that there are a few drawbacks of methodology detailed previously. In addition, the present results need to be confirmed by an adequately designed prospective study with an appropriate multivariate analysis taking into account the classical well-defined factors related to correlation between inflammation and atherosclerosis. 2,3
