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Enhanced oxidative stress in coronary heart disease and chronic heart failure as indicated by an increased 8‐epi‐PGF 2α
Author(s) -
Wolfram Roswitha,
Oguogho Anthony,
Palumbo Barbara,
Sinzinger Helmut
Publication year - 2005
Publication title -
european journal of heart failure
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.149
H-Index - 133
eISSN - 1879-0844
pISSN - 1388-9842
DOI - 10.1016/j.ejheart.2004.05.007
Subject(s) - medicine , ejection fraction , heart failure , cardiology , oxidative stress , pathogenesis , pathophysiology , cardiomyopathy , isoprostane , lipid peroxidation
The role of oxidation injury as an important factor in the pathophysiology of cardiomyopathy (CMP) has recently gained increasing interest. Semiquantitative analysis for isoprostane, 8‐epi‐prostaglandin F 2α (8‐epi‐PGF 2α ), and oxidised low‐density lipoprotein (ox‐LDL) of coronary vascular tissue samples derived from CMP patients revealed an increased extent and intensity of uptake as compared to the respective controls. To evaluate oxidative stress in vivo, we examined plasma, serum, salivary, and urinary 8‐epi‐PGF 2α in patients with dilated CMP ( n =20) and ischemic CMP ( n =20) with decreased left ventricular ejection fraction (LVEF). Patients with coronary heart disease (CHD) ( n =20) and 20 healthy, age‐matched, and sex‐matched controls were investigated in parallel. 8‐Epi‐PGF 2α levels were correlated with the functional severity of heart failure [New York Heart Association (NYHA) classification] and LVEF. 8‐Epi‐PGF 2α levels were matched according to risk factors (smoking and hypercholesterolemia) and were significantly higher in patients with CMP as compared to healthy controls and patients with CHD in all investigated compartments. A positive correlation between NYHA stages and 8‐epi‐PGF 2α , as well as a negative correlation to LVEF, could be demonstrated in a subgroup analysis. These findings reflect the enhanced oxidation injury in patients with CMP and, to a lesser extent, in CHD as compared to healthy controls, thus highly indicating the relevance of oxidative stress for the pathogenesis and progression of cardiovascular disease.