No abstract

Combined prophylactic therapy with amiodarone and MgSO(4) at the early postoperative period without a maintenance phase is an effective, simple, well-tolerated, and possibly cost-effective regimen to prevent POAF in normomagnesemic, high-risk patients.

No abstract

QT dispersion defined as interlead QT variability in a 12-lead electrocardiogram was proposed by Day and associates as a simple method to evaluate the repolarization heterogenicity of the ventricular myocardium. The frequency of onset of myocardial infarction and sudden death has been reported to have a circadian variation, with a peak incidence in the early morning hours. The authors investigated whether there is diurnal variation of QT interval and QT interval dispersion in healthy subjects and in patients with coronary artery disease. The study population consisted of two groups. Group I consisted of 62 subjects without coronary artery disease and group II consisted of 82 patients with coronary artery disease. Twelve-lead ECG was recorded for each patient in the morning (between 7 AM and 8 AM), afternoon (between 3 PM and 5 PM) and at night (between 11 PM and 1 AM), on the day after performance of coronary angiography. QTc dispersion was significantly higher in patients with coronary artery disease than in healthy subjects in the morning hours and afternoon (p<0.001). Although the differences were much prominent in group I than group II, both QTc dispersion of morning and afternoon were significantly greater than those at night. There were no statistically significant differences between group I and group II at nighttime with respect to maximum QTc, minimum QTc intervals, and QTc dispersion (p>0.05). In conclusion, QT dispersion shows diurnal variation with an increase in the morning hours in both patients with coronary artery disease and subjects without coronary artery disease. The mechanism of diurnal variation of QT dispersion in patients with coronary artery disease is quite different from that of healthy subjects.

This study demonstrated for the first time that the high level of lipoprotein (a) negatively affects the formation of coronary collateral vessels in human beings. Reduced production or bioactivity of vascular endothelial cell growth factor caused by high levels of lipoprotein (a) may be the possible responsible mechanisms of hyperlipoprotein (a)-related poor collateral formation.