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Metabolic syndrome (MS) is a constellation of metabolic derangements associated with vascular endothelial dysfunction and oxidative stress and is widely regarded as an inflammatory condition, accompanied by an increased risk for cardiovascular disease. The present study tried to investigate the implications of telomerase activity with inflammation and impaired endothelial function in patients with metabolic syndrome. Telomerase activity in circulating peripheral blood mononuclear cells (PBMC), TNF-α, IL-6 and ADMA were monitored in 39 patients with MS and 20 age and sex-matched healthy volunteers. Telomerase activity in PBMC, TNF-α, IL-6 and ADMA were all significantly elevated in patients with MS compared to healthy volunteers. PBMC telomerase was negatively correlated with HDL and positively correlated with ADMA, while no association between TNF-α and IL-6 was observed. IL-6 was increasing with increasing systolic pressure both in the patients with MS and in the healthy volunteers, while smoking and diabetes were positively correlated with IL-6 only in the patients' group. In conclusion, in patients with MS characterised by a strong dyslipidemic profile and low diabetes prevalence, significant telomerase activity was detected in circulating PBMC, along with elevated markers of inflammation and endothelial dysfunction. These findings suggest a prolonged activity of inflammatory cells in the studied state of this metabolic disorder that could represent a contributory pathway in the pathogenesis of atherosclerosis.

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The pattern of left ventricular filling was assessed by Doppler echocardiography in 38 adult beta-thalassaemia major patients; 28 with normal (age 25.2 +/- 5.3 years) and 10 with abnormal (age 24.5 +/- 8.8 years) left ventricular systolic function. The findings were compared with those obtained from 38 age and sex matched normal individuals. In patients with normal left ventricular systolic function, peak flow velocity in early diastole was higher than in the controls (94 +/- 16 vs 79 +/- 12 cm.s-1, P < 0.001). The peak flow velocity in late diastole was also greater (60 +/- 18 vs 46 +/- 9 cm.s-1, P < 0.001), but the ratio between the early and late (atrial) peaks was approximately the same in both groups (1.74 +/- 0.72 vs 1.70 +/- 0.30). There was no difference in deceleration time and rate between the two groups (152 +/- 32 vs 151 +/- 21 ms and 504 +/- 93 vs 508 +/- 115 cm.s-2 respectively). None of the patients had atrial predominant left ventricular inflow pattern. In patients with congestive heart failure the peak flow velocity in early diastole was greater than in the controls (96 +/- 10 vs 79 +/- 2 cm.s-1 P < 0.001) while in late diastole it was smaller (39 +/- 6 vs 44 +/- 2 cm.s-1, P < 0.05). The ratio between the early and late peaks was greater in the patients than in the controls (2.5 +/- 0.35 vs 1.8 +/- 0.08, P < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Cigarette smoking increases coronary resistance in patients with coronary artery disease, causing profound disturbances in myocardial perfusion. The acute effects of smoking a single cigarette on left ventricular diastolic function were studied in 20 smokers with typical angina pectoris and angiographically documented coronary artery disease. Twenty healthy smokers served as a control group. We used simultaneous M-mode echocardiography of the mitral and aortic valves to measure isovolumic relaxation time, and pulsed Doppler echocardiography of transmitral blood flow was recorded to evaluate left ventricular filling before and immediately after smoking. In the patients with coronary artery disease, systemic blood pressure and heart rate significantly increased after smoking. The isovolumic relaxation time, the deceleration time as well as peak A velocity remained unchanged. The peak E velocity decreased by 0.06 m.s-1 (P = 0.02) and the peak E/A velocity ratio by 0.17 m.s-1 (P = 0.01). There were no significant changes in left ventricular diastolic function indexes in the controls. These results indicate that in patients with coronary artery disease, each cigarette provokes disturbances of left ventricular diastolic function.

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Oxidative stress is linked to coronary artery disease and is a major mechanism in contrast-induced nephropathy. Trans-radial approach in coronary angiography (CA) with minimized peri-procedural bleeding is expected to reduce acute kidney injury incidence. In the present study, oxidative stress patterns observed in radial CA and their associations with early manifestations of kidney injury are described. A total of 20 stable coronary disease patients submitted to CA and 17 sex-matched patients undergoing computed tomography for myoskeletal reasons were enrolled. Reduced glutathione, catalase, thiobarbituric acid reactive species (TBARS) levels and total anti-oxidant status were measured at various time points postangiography. In ischemic patients baseline TBARS levels were 2-fold lower compared to controls, while carbonyls levels were 35% higher. Glutathione was almost 4-fold lower than the control group. Glutathione and lipid peroxidation in ischemic patients gradually increased after contrast medium administration and reached 180% (P<0.001) and 20% (P=0.021) after 4–6 h, respectively. Four patients presented early evidence of contrast-induced nephropathy postangiography, while no control patient developed acute kidney injury. In the multiple logistic regression analysis, only the creatinine levels at baseline influenced the frequency of early contrast-induced nephropathy development (β =0.36, 95% CI: 0.285–0.438, P=0.01). Glutathione low levels were dominant in the baseline values of ischemic patients who developed contrast-induced nephropathy. Glutathione levels rapidly increased while protein oxidation decreased at the expense of lipid peroxidation. In conclusion, early oxidative stress changes occur in trans-radial CA patients with a mild profile, sufficient to mobilize patient antioxidant defenses.