Association of the 894G>T polymorphism in the endothelial nitric oxide synthase gene with risk of acute myocardial infarction

Background: This study was designed to investigate the association of the 894G>T polymorphism in the eNOS gene with risk of acute myocardial infarction (AMI), extent of coronary artery disease (CAD) on coronary angiography, and in-hospital mortality after AMI. Methods: We studied 1602 consecutive patients who were enrolled in the GEMIG study. The control group was comprised by 727 individuals, who were randomly selected from the general adult population. Results: The prevalence of the Asp298 variant of eNOS was not found to be significantly and independently associated with risk of AMI (RR = 1.08, 95%CI = 0.77–1.51, P = 0.663), extent of CAD on angiography (OR = 1.18, 95%CI = 0.63–2.23, P = 0.605) and in-hospital mortality (RR = 1.08, 95%CI = 0.29–4.04, P = 0.908). Conclusion: In contrast to previous reports, homozygosity for the Asp298 variant of the 894G>T polymorphism in the eNOS gene was not found to be associated with risk of AMI, extent of CAD and in-hospital mortality after AM

Determinants of electrocardiographic and spatial vectorcardiographic descriptors of ventricular repolarization in normal subjects

he link between the dispersion of ventricular recovery times and arrhythmias has previously been demonstrated.(1) QT dispersion has been used to quantify the dispersion of ventricular refractoriness from the standard 12-lead electrocardiogram.(2) However, not only the accuracy and reproducibility of the "dispersion " indexes,(3) but also the presence of a direct link between the heterogeneity of ventricular repolarization and QT dispersion(4) has been challenged recently. Several studies have now focused on the spatial T-loop morphology features as a more accurate measure of the repolarization heterogeneity.(4-7) Although the correlation between QT dispersion and the T-loop morphology features has previously been evaluated,(8) there are no adequate data on the determinants of the spatial vectorcardiographic (VCG) descriptors of ventricular repolarization in normal subjects. The objective of the present study was to assess the clinical determinants of the electrocardiographic (ECG) and spatial VCG descriptors of ventricular repolarization in a population of young, healthy men

Spatial aspects of ventricular repolarization in postinfarction patients

QT dispersion has been proposed to reflect the heterogeneity of ventricular repolarization, but a poor reproducibility limits its clinical usefulness. Spatial vectorcardiographic descriptors constitute a novel approach to quantify ventricular repolarization. To test the ability of vectorcardiographic descriptors to discriminate among different subsets of postinfarction patients, 50 consecutively recruited patients with acute MI, 50 patients with history of an old (> 6 months) MI and 50 healthy controls were evaluated. The maxim um and minim um QT and JT intervals and QT and JT dispersion were manually measured from a digitally recorded 12-lead EGG. X, Y, and Z leads were reconstructed from the 12-lead EGG. The amplitude of the maximum spatial T vector (spatial T amplitude), the angle between the maximum spatial QRS and T vectors (spatial QRS-T angle), and the frontal plane QRS-T angle were automatically calculated The spatial T amplitude and the spatial QRS-T angle did nor differ between patients with a recent and those with an old MI (P = 1). QT dispersion was significantly lower in patients with an old MI than in patients with a recent one (P = 0.002). The spatial repolarization descriptors showed better short-term reproducibility than the dispersion indices. In conclusion, the spatial T amplitude and the spatial QRS-T angle are accurate measures of ventricular repolarization that do not differ between patients with recent and those with old MI. The different QT dispersion values observed in this study between the two post-MI groups should be considered cautiously because of the low accuracy of the manual measurements

Assessment of ventricular repolarization alterations in subjects with early repolarization

Background: Although the electrocardiographic (ECG) features of early repolarization (ER) have been studied extensively, no systematic quantification of ventricular repolarization in subjects with ER has been conducted so far. Methods: The objective of the present study was to evaluate ECG and spatial vectorcardiographic (VCG) descriptors of ventricular repolarization in ER subjects and to associate them with the respective indices of ventricular depolarization. A digital 12-lead surface ECG was obtained from 108 young, healthy men with ER and 108 age-matched healthy controls. The maximum Q-onset-T-end interval (QT maximum), the maximum Q-onset-T-peak interval (QTp maximum), the respective QT dispersion values (QT maximum-QT minimum), the rate-corrected QTC maximum and QTpC maximum, the QRS duration, and the VCG markers spatial T amplitude, spatial QRS amplitude and spatial QRS- Tangle, were evaluated in ER subjects and controls. Results: QT maximum (P=0.05) and QTp maximum (P=0.003) were higher in ER subjects than in controls, while QTC maximum (P<0.0001)and QTpC maximum (P=0.002) were lower in ER subjects than in controls. The QRS duration (P=0.013), as well as the spatial T amplitude, the spatial QRS amplitude, and the spatial QRS-T angle were higher in ER subjects than in controls (P<0.0001). The spatial T amplitude was not associated with the indices of ventricular depolarization neither in ER subjects, nor in controls. Conclusions: Ventricular repolarization, as well as depolarization, is altered in young, healthy males with ER compared to age-matched healthy controls. Ventricular depolarization and repolarization indices in ER subjects are not associated to each other. (C) 2003 Elsevier Ireland Ltd. All rights reserved

and of Hemoglobin Filter Cigarettes on Autonomic Cardiac Control

T he adverse effects of smoking onthe cardiovascular system have beenstudied both in extensive epidemio-logical studies and on a basic research le-vel. The conclusions of these studies are in such close agreement that smoking has been identified by the American Heart Association (AHA) as the most signifi-cant modifiable risk factor of coronary artery disease in the USA1. One of the mechanisms by which smoking impairs the cardiovascular fun-ction is its effect on Autonomic Nervous System (ANS) control2-4. Out of all the biologically active substances detected in cigarettes and tobacco products, nicotine, tar and carbon monoxide have been most widely studied. Nicotine acts as an ago-nist of nicotine receptors in the central and peripheral nervous system exerting a ganglioplegic effect and causing suppres-sion of vagal (predominantly) and sympa-thetic control. However in the latter the-re seems to be a direct enhancing effect at the central nuclei level resulting in an overall increase of sympathetic tone. In addition, nicotine affects the chemore-ceptors of the aorta and the carotid thu

Jean-Baptiste de Sénac's (1693-1770) Important Work on Cardiology and Valvular Disorders.

In the 18(th) century clinical cardiology was based on pulse examination and auscultation by placing the ear directly on the patient's chest, while diagnosis of heart diseases was done in postmortem examination. In 1749, Jean-Baptiste de Sénac, physician of King Louis XV, published his work on the heart Traité de la structure du coeur, de son action et de ses maladies. It was the result of years of anatomical and physiological study, in an attempt to illuminate heart and its functions. Sénac recognized among several heart disorders, aortic regurgitation, mitral calcification, and mitral regurgitation. His work remained a landmark in valvular pathology and cardiology until the early 19(th) century