Background and objective: An association between coronary artery disease (CAD) and agerelated macular degeneration (ARMD) has long been postulated, but exact mechanisms remain unclear. The global prevalence of CAD and ARMD increases and early biomarkers for early diagnosis of these diseases are necessary.
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Background and objective: An association between coronary artery disease (CAD) and agerelated macular degeneration (ARMD) has long been postulated, but exact mechanisms remain unclear. The global prevalence of CAD and ARMD increases and early biomarkers for early diagnosis of these diseases are necessary. The aim of this study was to investigate the plasma level of oxidative stress biomarker CML in patients with and without angiographic findings of atherosclerosis in the coronary arteries (CADath+ and CADath, respectively) and to assess if there was an association of CAD with ARMD.
Materials and methods: The study enrolled 233 subjects. Based on cardiologic and ophthal- mologic examinations, the patients were divided into four subgroups: CADath+ARMD+, CADath+ARMD−, CADath−ARMD+, and CADath−ARMD−. The enzyme-linked immunosorbent assay was used for the measurement of plasma CML levels. Serum lipid levels were determined by an automatic analyzer using conventional enzymatic methods.
Results: CADath+ patients had higher CML concentration compared to CADath subjects (1.04 ± 0.6 vs. 0.83 ± 0.4 ng/mL,
P < 0.001). The highest mean CML level (1.12 ± 0.7 ng/mL) was found in CADath+ARMD+ patients. The mean plasma CML concentration was higher in subjects with any of the analyzed diseases compared to CADath−ARMD− subjects. A significant positive association of CADath+ (OR = 2.50, 95% CI 1.60–3.90,
P = 0.0001), ARMD (OR = 2.08, 95% CI 1.40–3.11,
P = 0.0001) and both analyzed diseases (OR = 4.67, 95% CI 2.29– 9.53,
P = 0.0001) with an increased level of plasma CML in a logistic regression model adjusting by age was identified.
Conclusions: The level of CML, an oxidative stress biomarker, reflects the presence of atherosclerosis in coronary arteries and shows a possible link between ARMD and CADath+ via oxidative status.
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