Plasma levels of copeptin in patients with coronary heart disease.

The present study was undertaken to investigate alteration in plasma levels of copeptin, a stable fragment derived from provasopressin, in patients with coronary heart disease. We measured plasma level of copeptin in 21 patients with coronary heart disease (CHD) and 12 age-matched healthy subjects by radioimmunoassay (RIA). Chi-square test, Student's t-test and one-way analysis of variance were used for statistical analyses. Correlations between variables were tested by simple linear regression analysis. The plasma level of copeptin was significantly increased in patients (43.07 +/- 17.08 vs 11.13 +/- 5.73 pmol/l in controls, P < 0.01) and was further increased, by 60%, to 68.71 +/- 16.81 pmol/l on day 1 after therapy with percutaneous transluminal coronary angioplasty (PTCA) and stent (P < 0.05). On days 3 and 7 after therapy, the levels were greatly decreased, to 38.82 +/- 19.00 and 32.10 +/- 14.00 pmol/l, respectively, from that before therapy (all P < 0.05) but were higher, by 249% and 188%, respectively, than that of controls (all P < 0.01). The results suggest that the vasopressin system is activated in patients with CHD as indicated by changes in copeptin level, especially after PTCA and stent therapy. As a potential risk factor for CHD, plasma copeptin activation might have important clinical significance in terms of early intervention in patients with CHD.

Plasma level of mitochondrial coupling factor 6 increases in patients with coronary heart disease.

BACKGROUND: The aim of the present study was to investigate alterations in the plasma level of coupling factor 6 (CF6), a novel endogenous inhibitor of prostacyclin, in patients with coronary heart disease. METHODS AND RESULTS: In total, 35 patients with coronary heart disease and 20 age-matched healthy subjects were examined. Plasma levels of CF6 and 6-keto-prostaglandin (PG)F(1a) (a stable metabolite of prostacyclin) were measured using radioimmunoassay. The plasma level of CF6 was significantly increased in patients (254.1+/-29.8 pg/ml vs 219.4 +/-36.7 pg/ml in controls, p<0.0001), whereas that of 6-keto-PGF(1a) was significantly decreased (23.4 +/-2.3 pg/ml vs 26.1+/-4.5 pg/ml in controls, p=0.001). Moreover, after percutaneous transluminal coronary angioplasty (PTCA) and stent therapy, the level of CF6 was further increased by 30% to 330.4+/-26.0 pg/ml, and that of 6-keto-PGF (1a) was decreased by 42% to 13.5+/-2.0 pg/ml, compared with baseline (all p<0.01). Univariate analysis showed a significant result that the plasma level of CF6 was inversely correlated with that of 6-keto-PGF(1a) in the patients. The plasma ratio of CF6 to 6-keto-PGF(1a) was 8.4 in the control group and that in patients with coronary heart disease was increased to 24.4 after the therapy from 10.9 before therapy. CONCLUSIONS: The results suggest that an increased CF6 level may be responsible in part for the decreased prostacyclin level observed in patients with coronary heart disease, in particular after PTCA and stent therapy. As a potential risk factor for coronary heart disease, CF6 might have important clinical significance.