Background and Purpose-Several factors have been held responsible for the development of atherosclerosis. To avoid the masking effect of age, we evaluated correlates of carotid atherosclerosis in patients Ͻ55 years of age. Methods-Plasma lipids, oxidative resistance of low-density lipoprotein, homocysteine, inflammatory markers, plasma viscosity, and red cell deformability were measured in fasting blood samples of 100 subjects: 45 patients with Ͼ30% stenosis of the internal carotid artery, 20 patients with carotid occlusion, and 35 control subjects. Stenosis and intima-media thickness (IMT) of the carotid artery were evaluated by duplex ultrasound. Results-White blood cell (WBC) count, plasma fibrinogen, C-reactive protein (CRP), and lipoprotein(a) levels were significantly higher in patients than in control subjects, and patients had increased IMT (PϽ0.01 for all comparisons). There was a tendency for higher homocysteine levels in patients. Smokers had higher WBC, fibrinogen, and CRP levels. After the effect of smoking was controlled for, WBC count, natural logarithmic transform of homocysteine, and online-measured IMT remained significantly higher in patients than in control subjects. WBC, fibrinogen, and CRP levels were highest in the highest IMT quartile (Pϭ0.012, Pϭ0.007, and Pϭ0.036, respectively). Conclusions-Inflammatory markers and homocysteine have a more important role than lipid factors in early-onset carotid atherosclerosis. We cannot recommend the measurement of low-density lipoprotein peroxidation as a routine screening test to identify high-risk patients for early-onset carotid atherosclerosis. The confounding effect of smoking on inflammatory markers should be considered in studies on atherosclerosis.

Vascular and endothelial functions were investigated in long term survivors of childhood cancer exposed to anthracycline treatment. We enrolled 96 long-term survivors (57 males and 39 females, mean age 14.9 ± 5.3 year) of different childhood cancers and 72 age-, sex-, bodyweight- and blood pressure matched controls (39 males and 33 females, mean age 13.7 ± 4.9 year). Aortic stiffness was characterized by echocardiography. Brachial artery endothelial function was assessed by flow-mediated dilatation (FMD%) and nitrate-mediated dilatation (NTG%). Results were compared between three subgroups: anthracycline treated, only chemotherapy treated and control subgroups. The cumulative anthracycline dose was less than 350 mg/m². The healthy control subgroup had a significantly greater FMD response (13.13 ± 2.40 %), and lower stiffness index (2.08 ± 0.6) than both the anthracycline (7.12 ± 6.28 % and 6.45 ± 3.25, respectively) and only chemotherapy treated (10.17 ± 4.23 % and 4.12 ± 2.32, respectively) subgroups. In the anthracycline treated subgroup a significantly (p < 0.01) lower FMD% response, and higher stiffness index were detected than in the only chemotherapy treated subgroup. Higher triglyceride level, higher cumulative anthracycline dose and lower age at the start of treatment were found to be associated independently with impairment of FMD% response and aortic stiffness. We found a significant negative correlation between FMD and aortic stiffness (p < 0.001) and a positive correlation between FMD and distensibility (p < 0.0001). Childhood cancer long term survivors exposed to anthracycline treatment exhibit a marked preclinical vasculopathy, characterized by endothelial dysfunction and increased arterial stiffness, contributing to a deteriorated cardiovascular function.

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Background: QT interval (QT) and QT dispersion (QTd) are electrocardiograph (ECG) parameters for the evaluation of myocardial repolarization. The inhomogeneity of ventricular repolarization is associated with ventricular arrhythmias. An increased QT, QTd, and increased incidence of nocturnal cardiac rhythm disturbances have been described in patients with obstructive sleep apnea (OSA), while other investigators did not find a relationship between ventricular arrhythmias and OSA. Hypothesis: The aim of this study was to examine the occurrence of ventricular arrhythmias and to measure QT parameters in patients with untreated OSA using an ambulatory Holter-ECG. Methods: A total of 25 patients with untreated OSA were studied. After routine biochemical investigation and 2-dimensional, M-mode echocardiography, a 24-hour Holter-ECG was recorded to detect cardiac arrhythmias and QT parameters. QT parameters were measured by the QT Guard system. Results: Only the QT interval increased significantly during the nighttime period (nocturnal QT interval: 423.1 ± 34.6 ms, daytime QT interval: 381.6 ± 33.8 ms, 24-hour QT interval: 394.7 ± 31.1 ms). However, during the nighttime QT interval (422.8 ± 14.9 ms), QTd (31.2 ± 11.0 ms) and QT dispersion (30.5 ± 10.2 ms) did not show any change compared to 24-hour (QTc interval: 423.7 ± 14.2 ms, QTd: 28.8 ± 9.4 ms, QTcd: 30.5 ± 9.43 ms) and daytime levels (QTc interval: 423.9 ± 14.3 ms, QTd: 27.3 ± 10.7 ms, QTcd: 29.9 ± 11.1 ms). None of the patients had ventricular arrhythmias. Conclusions: QTd and QTcd did not increase during the nighttime period. Our study did not show an increased risk of ventricular arrhythmias in this population during the monitoring period.