Atherosclerosis predominantly affects systemic arteries as compared to pulmonary arteries; however, the reasons for this differential predilection are not clear. Oxidative damage caused by free radicals is a key initiating event in atherogenesis and the lungs are able to produce large quantities of free radicals even under physiological conditions. The present study investigated whether pulmonary venous blood reaching the aorta contained greater quantities of lipid peroxides, a marker of oxidative stress, compared to the pulmonary artery. Aortic and pulmonary artery blood samples were collected at the time of cardiac catheterization from 45 consecutive patients (38% female) without acute coronary event and free of other medical disorders, who were scheduled to undergo coronary angiography for anginal chest pain. Lipid peroxides were measured in terms of malondialdehyde (MDA). MDA levels were significantly higher in the aorta compared to the pulmonary artery (4.93±1.97 vs. 3.36±1.14 nmol/ml; P<0.001); the difference was significant in patients with angiographic coronary artery disease (CAD) (P<0.001) compared to the patients without CAD (P=0.071). Higher aortic MDA levels were associated with the presence of CAD even following adjustment for major risk factors. The results of the present study demonstrate that aortic blood contains significantly greater levels of lipid peroxides compared to pulmonary artery. This differential oxidative stress between systemic and pulmonary arteries could provide a mechanistic explanation for their difference in the propensity to develop atherosclerosis.
Keywords: aorta; atherosclerosis; free radicals; lipid peroxidation; oxidant stress; pulmonary artery.