D-dimer (r = 0.315, p = 0.003) and troponin I (r = 0.300, p = 0.004) and inversely correlated with arterial oxygen saturations (r = -0.533, p < 0001). When the correlation of copeptin with right ventricular dysfunction parameters was investigated, it was significantly inversely correlated with the tricuspid annular plane systolic excursion (r = -0.521, p < 0.001) and positively cor related with right to left ventricle ratio (r = 0.329, p = 0.024). Copeptin (OR 1.836, p = 0.008) (Cardiol J 2016; 23, 1: 42-50)

These results suggest that a high-admission BNP level is associated with an increased risk of AKI development and 6-month all-cause mortality in patients with STEMI undergoing primary PCI.

Subclinical hypothyroidism (SH) is characterized by normal serum free T4 (FT4), free T3 (FT3) levels and increased serum thyroid-stimulating hormone (TSH) levels. Endothelial dysfunction, which is an early step of atherosclerosis, has been reported in patients with subclinical hypothyroidism. The aim of this study is to evaluate endothelial functions and the effect of L-thyroxin (L-T4) therapy on endothelial functions in SH. Twenty-seven patients with SH and 22 healthy controls were evaluated in terms of endothelial functions, using brachial artery Doppler ultrasonography. After restorating euthyroidism, measurements were repeated. Baseline and nitroglycerin induced diameter (NID) of brachial artery were similar in patients with SH and the control group. Compared to the control group, the patients with SH showed significantly reduced flow-mediated diameter (FMD). Baseline and NID values were significantly higher after LT4 therapy in SH group. FMD also significantly increased after LT4 therapy. Hypothyroidism accelerates atherogenesis through modification of atherosclerotic risk factors and direct effects on the blood vessels. In this study, we observed marked improvement in endothelial functions after L-T4 therapy in SH patients. We suggest that thyroid hormone replacement therapy may help to prevent atherosclerosis in this group of patients.

IntroductionNowadays, clopidogrel and acetylsalicylic acid (ASA) have become routinely applied therapies in percutaneous coronary interventions (PCI) with stenting.AimNumerous variables can interfere with antiplatelet responsiveness, so we aimed to investigate the role of different variables associated with ASA or clopidogrel resistance in stable coronary artery disease.Material and methodsA total of 207 patients undergoing elective PCI were included in the analysis. All patients received a loading dose of clopidogrel and ASA during PCI procedure and followed by dual antiplatelet therapy. Clopidogrel and ASA resistance were measured by impedance aggregometry method.ResultsOf the patients, 19.8% had clopidogrel resistance, 18.8% had ASA resistance, 9.2% had both clopidogrel and ASA resistance, and 71.5% were responsive to both drugs. In multivariate analysis, platelet count, angiotensin receptor blocker (ARB) use, and ASA resistance were independent variables associated with clopidogrel resistance, and clopidogrel resistance was the only variable associated with ASA resistance. In differentiating whether clopidogrel resistance exists or not, optimum ASA aggregometry response cut-off values were specified, and in differentiating whether ASA resistance exists or not, optimum clopidogrel aggregometry response cut-off values were specified.ConclusionsIn this study, there was a higher incidence of low responsiveness to ASA when there was a low response to clopidogrel, and vice versa. Angiotensin receptor blocker use, platelet count, and ASA resistance were independent variables associated with clopidogrel resistance. Clopidogrel resistance was the only independent variable associated with ASA resistance. Angiotensin receptor blocker use seems to an independent risk factor for clopidogrel resistance in this study, but this result needs to be verified in other studies.

Our data suggest that SH is associated with biventricular systolic and diastolic dysfunction.