These findings suggest that endothelial function is impaired in people with SCF and that CTFC correlates well with endothelial dysfunction.

Many studies have demonstrated that cirrhosis is frequently associated with autonomic dysfunction. The aim of this study was to test autonomic dysfunction in cirrhotic patients by analyzing heart rate variability (HRV), to determine whether or not the degree of autonomic dysfunction is correlated with the severity of disease, and, also, to compare the changes of HRV between survivor and nonsurvivor groups after 2-year follow-up periods. HRV was analyzed using 24-hr ECG recording in 30 cirrhotic patients and 28 normal controls. The changes in HRV parameters including mean normal-to-normal (N-N) interbeat intervals (mean NN), standard deviation of all N-N intervals (SDNN), standard deviation of the average of N-N intervals for each 5-min period over 24 hr (SDANN), root mean square succesive differences (r-MSSD; msec), and percentage of adjacent N-N intervals that are >50 msec apart (pNN50), all as time domain parameters, were evaluated. The cirrhotic patients were also evaluated according to Child-Pugh classification scores as markers of the disease severity. The time-domain measures of HRV in cirrhotic patients were significantly reduced compared with those in the control group (for all parameters; P < 0.001). The severity of disease was associated with reduced HRV measures (for all parameters; P < 0.001). After the 2-year follow-up periods, HRV measurements in cirrhotic patients were significantly much lower in nonsurvivors than in survivors (P < 0.001 for all). We conclude that increasing severity of cirrhosis is associated with a reduction in HRV. This finding may be an indicator of poor prognosis and mortality for cirrhosis.

Currently, the number of imaging and interventional procedures that use contrast agents (CAs) is gradually increasing. Contrast-induced nephropathy (CIN) is the most important CA-related complication. Oxidative stress plays a significant role in its pathophysiology. Lycopene (LPN) is a natural substance with strong antioxidant capacity. The present study aimed to investigate the potential preventive effects of LPN against CIN. In total, 28 male Wistar albino rats were divided into 4 groups with 7 rats in each group; the groups include normal control group, LPN only group at a dose of 4 mg/kg/day for 10 days, CIN group by administering 10 mg/kg furosemide IM + 10 mg/kg indomethacin IP + 10 ml/kg iomeprol IV following 24-h dehydration, and CIN + LPN group. There were statistically significant increase in urea, creatinine, and malondialdehyde levels ( p < 0.001, for all) but a significant decrease in glutathione, superoxide dismutase, catalase, and glutathione peroxidase levels ( p < 0.001, for all) in the CIN group compared with the control group. On histological examination, a significant increase of infiltrated inflammatory cells and necrotic degenerative changes were observed in the CIN group and the immunohistochemical examination revealed a significant increase in inflammation (inducible nitric oxide synthase), autophagy (LC3/B), and apoptosis (cleaved caspase 3) in the CIN group compared with the control group ( p < 0.05, for all). Significant improvements in these unfavorable parameters were observed with CIN + LPN group compared with the CIN only group. In conclusion, the favorable effects of LPN as an anti-inflammatory, antiautophagic, and antiapoptotic agent in an experimental model of CIN have been demonstrated.

Slow coronary flow (SCF) in a normal-appearing coronary angiogram is a well-recognized clinical entity, but its etiopathogenesis remains unclear. The aim of the study was to evaluate echocardiographic features in patients with SCF. Thirty-four patients with angiographically proven SCF (group I) and 25 patients with normal coronary flow (group II) were enrolled in the study. The diagnosis of SCF was made with use of the "TIMI frame count (TFC)'' method. All patients underwent complete transthoracic echocardiographic examination (M-mode, 2-dimensional [2-D], and Doppler parameters such as color, continuous, pulsed wave). There were no significant differences with respect to systolic parameters between the 2 groups; in spite of these, group I showed impaired left ventricular diastolic patterns compared to group II. Group I patients had higher peak late diastolic filling velocities due to enhanced atrial systole (A), lower peak (E/A) diastolic filling velocity ratios, and longer isovolumetric relaxation times compared with group II, and these were statistically significant (p<0.001). In conclusion; the authors detected diastolic filling abnormalities and showed diastolic dysfunction in patients with SCF.

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