The Relationship between Proliferative Scars and Endothelial Function in Surgically Revascularized Patients

Abstract

Background: Proliferative scars are benign fibrotic proliferations which demonstrate abnormal wound healing in response to skin injuries. As postulated in the “response to injury hypothesis”, atherosclerosis is also triggered by an endothelial injury. Keloid and atherosclerotic processes have many pathophysiological and cytological features in common. Aims: In this study, we investigated the relationship between proliferative scars and endothelial function in surgically revascularized patients. We aimed to test the hypothesis that atherosclerosis is a wound healing abnormality. Study Design: Cross-sectional study. Methods: Consecutive patients who were admitted to the cardiology outpatient clinic with a history of coronary artery bypass grafting operation were evaluated. Thirty-three patients with proliferative scars at the median sternotomy site formed the keloid group, and 36 age- and sex-matched patients with no proliferative scar at the median sternotomy site formed the control group. Endothelial function was evaluated by flow-mediated vasodilatation of the brachial artery via ultrasonograhic examination. Results: There is no signicant difference according to the demographic data, biochemical parameters, clinical parameters and number of grafts between keloid and control groups. Endothelial-dependent vasodilatory response was lower in the keloid group than the control group (9.30±3.5 and 18.68±8.2, respectively; p=0.001). Conclusion: This study showed that endothalial dysfunction, which is strongly correlated with atherosclerosis, was more prominent in patients with proliferative scars. As proliferative scars and atherosclerosis have many features in common, we might conclude that atherosclerosis is a wound healing abnormality.

Keywords

• Endothelium, keloid, cicatrix, wound healing

References

1. 1. Ross R. Atherosclerosis--an inflammatory disease. N Engl J Med 1999;340:115-26. [CrossRef]
2. 2. Schillinger M, Exner M, Mlekusch W, Sabeti S, Amighi J, Nikowitsch R, et al. Inflammation and carotid artery risk for atherosclerosis study (ICARAS). Circulation 2005;111:2203-9. [CrossRef]
3. 3. Tedgui A, Mallat Z. Cytokines in atherosclerosis: pathogenic and regulatory pathways. Physiol Rev 2006;86:515-81. [CrossRef]
4. 4. Schroeder S, Kopp AF, Baumbach A, Meisner C, Kuettner A, Georg C, et al. Noninvasive detection and evaluation of atheroscleotic coronary plaques with multislice computed tomography. J Am Coll Cardiol 2001;37:1430-5. [CrossRef]
5. 5. Mathers CD, Loncar D. Projections of global mortality and burden of disease from 2002 to 2030. PLoS Med 2006;3:e442. [CrossRef]
6. 6. Caplan BA, Schwartz CJ. Increased endothelial cell turnover in areas of in vivo Evans blue uptake in the pig aorta. Atherosclerosis 1973;17:401-17. [CrossRef]
7. 7. Sprague EA, Steinbach BL, Nerem RM, Schwartz CJ. Influence of a laminar steady-state fluid-imposed wall shear stress on the binding, internalization, and degradation of low-density lipoproteins by cultured arterial endothelium. Circulation 1987;76:648- 56. [CrossRef]
8. 8. Ross R. The pathogenesis of atherosclerosis--an update. N Engl J Med 1986;314:488-500. [CrossRef]

9. 9. Park JH, Park TH, Chang CH. Earring embedded within earlobe keloids. Arch Plast Surg 2013;40:466-7. [CrossRef]
10. 10. Köse O, Waseem A. Keloids and Hypertrophic Scars: Are they two different sides of the same coin? Dermatol Surg 2008;34:336-46. [CrossRef]