Our study provides novel and preliminary observations--n-3 PUFA supplementation reveals additional decreasing effects on depressive and anxiety symptoms in early post-MI patients.
Standard-dose anthracycline chemotherapy is associated with LV dilatation and diastolic dysfunction, regardless of the preserved global systolic function. It coexists with negative structural arterial remodelling.
Aims. We sought to investigate whether enhanced oxidation contributes to unfavorable fibrin clot properties in patients with diabetes. Methods. We assessed plasma fibrin clot permeation (K
s, a measure of the pore size in fibrin networks) and clot lysis time induced by recombinant tissue plasminogen activator (CLT) in 163 consecutive type 2 diabetic patients (92 men and 71 women) aged 65 ± 8.8 years with a mean glycated hemoglobin (HbA1c) of 6.8%. We also measured oxidative stress markers, including nitrotyrosine, the soluble form of receptor for advanced glycation end products (sRAGE), 8-iso-prostaglandin F2α (8-iso-PGF2α), oxidized low-density lipoprotein (oxLDL), and advanced glycation end products (AGE). Results. There were inverse correlations between K
s and nitrotyrosine, sRAGE, 8-iso-PGF2α, and oxLDL. CLT showed a positive correlation with oxLDL and nitrotyrosine but not with other oxidation markers. All these associations remained significant for K
s after adjustment for fibrinogen, disease duration, and HbA1c (all P < 0.05), while oxLDL was the only independent predictor of CLT. Conclusions. Our study shows that enhanced oxidative stress adversely affects plasma fibrin clot properties in type 2 diabetic patients, regardless of disease duration and glycemia control.
Copeptin is a new biomarker of cardiovascular diseases. Its diagnostic value in degenerative aortic valve stenosis (AS) with preserved left ventricle systolic function is unknown. We aimed to assess the association of serum copeptin levels with AS severity and coexistence of coronary artery disease (CAD). Sixty-four patients with AS and preserved left ventricle systolic function including 40 with severe degenerative AS (group sAS, effective orifice area EOA = 0.67 cm(2)) and 24 with moderate degenerative AS (group mAS, EOA = 1.40 cm(2)) were enrolled into the study. Twenty-three patients without AS and heart failure, matched for age, sex, and CAD occurrence served as the control group (group C). Serum levels of copeptin and N-terminal pro-brain natriuretic peptide (NT-proBNP) were measured using enzyme-linked immunosorbent assay. The mean serum copeptin concentrations were significantly higher in patients with AS: sAS (405 pg/ml) and mAS (351 pg/ml; sAS vs mAS P< 0.05), compared with group C (302 pg/ml, P < 0.05). Serum copeptin levels correlated inversely with EOA (r = -0.55; P < 0.001) in AS patients. There was no correlation between copeptin and NT-proBNP or association with the coexisting CAD. Receiver-operating characteristics analysis showed that copeptin was a good marker of severe/moderate AS (sensitivity 71 %; specificity 87 %), with the optimized cut-off value of 354 pg/ml. Serum copeptin concentration constitutes a novel biomarker of degenerative AS. Coexisting CAD does not interfere with copeptin level.
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