P Wave Dispersion: a valuable non-invasive marker of vulnerability to atrial arrhythmias

The prolongation of intraatrial and interatrial conduction time and the non-homogeneous propagation of sinus impulses are well known electrophysiologic characteristics in patients with atrial arrhythmias and especially paroxysmal atrial fibrillation (AF). Previous studies have demonstrated that individuals with clinical history of paroxysmal AF show a significantly increased P wave duration in 12-lead surface electrocardiograms (ECG) and signal-averaged ECG recordings. The inhomogeneous and discontinuous atrial conduction in patients with atrial arrhythmias has been studied, during the last years, with a new ECG index, P wave dispersion. P wave dispersion is defined as the difference between the longest and the shortest P wave duration recorded from multiple different surface ECG leads. Extensive clinical evaluation of P wave dispersion has been performed in the assessment of the risk for AF in patients without apparent heart disease, in hypertensive patients, in patients with coronary artery disease, in patients undergoing coronary artery bypass surgery, in patients with congenital heart diseases, as well as in other groups of patients suffering from various cardiac or non-cardiac diseases. P wave dispersion has proven to be a sensitive and specific ECG predictor of AF in the various clinical settings. However, the methodology used for the calculation of P wave dispersion has not been standardized so far and more efforts to improve the reliability and reproducibility of P wave dispersion measurements are needed. In conclusion, P wave dispersion constitutes a significant contribution to the field of non-invasive electrocardiology and seems to be quite promising in the field of AF prediction

The antihypertensive treatment effect on left ventricular diastolic function is reflected in exercise electrocardiogram

Background/Purpose: Exercise electrocardiographic hump sign is associated with uncontrolled arterial hypertension (AH), left ventricular (LV) diastolic dysfunction, and false-positive exercise testing (ET). The aim of this prospective study was to evaluate the antihypertensive treatment effect on hump and on pseudoischemic ST-segment depression and potential correlations to LV diastolic function and mass changes. Methods: The study comprised 59 non coronary artery disease patients (45.9 years; 67.8% men) with never-treated arterial hypertension (143.2/95.1 mm Hg). Treadmill ET and echocardiography were performed at baseline and 6 months after pharmaceutical blood pressure normalization. Prevalence of hump and ST depression, transmitral (E/A) and tissue Doppler imaging (E’/A’) early/late velocities ratios, E/E’ ratio, and LV mass index (LVMI) were all defined. Results: Prevalence of hump was reduced from 69.5% to 23.7% and false-positive ETs from 35.6% to 18.6% (P < .05). Significant improvement (P < .05) was found in E’/A’ ratio (0.68 vs 0.84), E/E’ ratio (9.3 vs 7.9), and LVMI (109.2 vs 99.8 g/m(2)). Changes in hump were related to ST-depression changes (r = 0.632, P < .001) and to LV diastolic indices changes; patients with hump only at first ET (54.2%) improved E/A and E’/A’ ratios, whereas patients with hump only at second ET (8.5%) worsened diastolic indices with similar changes in blood pressure and LVMI. Conclusions: Antihypertensive treatment reduces the prevalence of hump and exercise ischemic-appearing ST depression probably through LV diastolic function improvement. (C) 2012 Elsevier Inc. 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