Using the 12-Lead ECG to Localize the Origin of Atrial and Ventricular Tachycardias: Part 2—Ventricular Tachycardia

Monomorphic ventricular tachycardia (VT) can arise from multiple different ventricular locations in the context of several different underlying myocardial substrates. Despite this variability, the surface 12-lead electrocardiograph (ECG) has proven to be a robust and reproducible initial mapping tool that can provide useful information in localizing the origin of both focal and reentrant forms of VT. The second part of this review series will look at the use of the ECG in mapping the various forms of VT encountered in clinical practice.     

Electrophysiological Studies on Cardiac Catheter Ablation

Clinical and animal investigations have pointed out that high energy electrical shocks are associated with the development of cardiac arrhythmias and with variable success in permanent ablation. The effects of electrode configuration and location on the size of the recorded electrogram was investigated to help explain variable catheter ablation results. We analyzed the cellular effects of catheter ablation shocks and found depression of resting potential, action potential amplitude, dV/dt and action potential duration. The most severe effects were noted with high current densities in tissues located between the cathode and anode. Damage was worse nearest the cathode. Similar cellular studies were completed using argon laser photoablation. Again, there was a decrease in resting potential, action potential amplitude and dV/dt. Laser energy led to a more focal region of myocardium void of action potentials and the border zone of injury was smaller. We also investigated the effects of lower energy shocks)1 to 10 joule) on cardiac tissues. Using microelectrodes, we observed that the membrane potential can "hang up" at the depolarized levels for varying periods of time and that conduction is altered during this membrane "hang-up" period. The duration and membrane hang-up level correlated with shock intensity and shock duration. Sequential shocks resulted in additive membrane "hang-up". We believe that membrane hang-up may be associated with brief arrhythmias observed following catheter ablation since conduction, refractoriness and excitability are all altered.     

Vagal Paroxysmal Atrial Fibrillation: Prevalence and Ablation Outcome in Patients Without Structural Heart Disease

Prevalence of Vagal Paroxysmal Atrial Fibrillation . Introduction: The prevalence of vagal and adrenergic atrial fibrillation (AF) and the success rate of pulmonary vein isolation (PVI) are not well defined. We investigated the prevalence of vagal and adrenergic AF and the ablation success rate of antral pulmonary vein isolation (APVI) in patients with these triggers compared with patients with random AF. Methods and Results: Two hundred and nine consecutive patients underwent APVI due to symptomatic drug refractory paroxysmal AF. Patients were diagnosed as vagal or adrenergic AF if >90% of AF episodes were related to vagal or adrenergic triggers; otherwise, a diagnosis of random AF was made. Clinical, electrocardiogram (ECG), and Holter follow‐up was every 3 months in the first year and every 6 months afterward and for symptoms. Of 209 patients, 57 (27%) had vagal AF, 14 (7%) adrenergic AF, and 138 (66%) random AF. Vagal triggers were sleep (96.4%), postprandial (96.4%), late post‐exercise (51%), cold stimulus (20%), coughing (7%), and swallowing (2%). At APVI, 94.3% of patients had isolation of all veins. Twenty‐five (12%) patients had a second APVI. At a follow‐up of 21 ± 15 months, the percentage of patients free of AF was 75% in the vagal group, 86% in the adrenergic group, and 82% for random AF (P = 0.51). Conclusion: In patients with PAF and no structural heart disease referred for APVI, vagal AF is present in approximately one quarter. APVI is equally effective in patients with vagal AF as in adrenergic and random AF. (J Cardiovasc Electrophysiol, Vol. 21, pp. 489‐493, May 2010)     

Early white-matter abnormalities of the ventral frontostriatal pathway in fragile X syndrome

Aim  Fragile X syndrome is associated with cognitive deficits in inhibitory control and with abnormal neuronal morphology and development.
Method  In this study, we used a diffusion tensor imaging (DTI) tractography approach to reconstruct white-matter fibers in the ventral frontostriatal pathway in young males with fragile X syndrome ( n =17; mean age 2y 9mo, SD 7mo, range 1y 7mo–3y 10mo), and two age-matched comparison groups: (1) typically developing ( n =13; mean age 2y 3mo, SD 7mo, range 1y 7mo–3y 6mo) and (2) developmentally delayed ( n =8; mean age 3y, SD 4mo, range 2y 9mo–3y 8mo).
Results  We observed that young males with fragile X syndrome exhibited increased density of DTI reconstructed fibers than those in the typically developing ( p =0.001) and developmentally delayed ( p =0.001) groups. Aberrant white-matter structure was localized in the left ventral frontostriatal pathway. Greater relative fiber density was found to be associated with lower IQ (Mullen composite scores) in the typically developing group ( p =0.008).
Interpretation  These data suggest that diminished or absent fragile X mental retardation 1 protein expression can selectively alter white-matter anatomy during early brain development and, in particular, neural pathways. The results also point to an early neurobiological marker for an important component of cognitive dysfunction associated with fragile X syndrome.     

The role of histidine in human epidermis

Incorporation of radioactively-labelled histidine into half-thickness skin and into the major protein fraction extracted from epidermis by urea (protein Fraction A) has been measured and compared with the amount of labelled urocanic acid appearing in the same specimen. After a short lag period, incorporation into half-thickness skin and into protein Fraction A was found to be linear up to 23 h of the study. Histidine appeared to be initially preferentially deaminated to urocanic acid. The somewhat erratic presence of urocanic acid at later periods is attributed to its high instability and solubility.     

Effects of Sustained Ventricular Pacing During Cardioplegic Arrest on Global and Regional Postischemic Left Ventricular Performance

Although coronary artery bypass graft surgery is frequently performed in patiejits with permanent ventricular pacemakers, the effects of pacemaker generator stimuli during cardioplegic arrest are unknown. This study was undertaken to detennine whether, during cardioplegic arrest in the presentee of a coronary occlusion, pacemaker stimuli accentuate postischemic LV damage.
Twelve pigs were placed on cardiopulmonary bypass and subjected to 80 min ofischemic arrest with multiple doses of crystalloid potassium crystalloid caidioplegia supplemented with topical and systemic (28C) hypothermia. During arrest, the mid LAD was occluded with a snare that was released upon reperfusion. In all animals, epicardial ventricular pacing wires were placed and capture was confirmed. In 6 pigs, pacing was instituted prior to ischemic arrest and continued throughout the ischemic and postischemic periods. Six other pigs were not paced and served as controls.
Pacemaker stimuli during arrest had no effect on LV temperature. There was no difference in postischemic Lt mass, compliance curves, wall-motion scores, or stroke xvork itidex between the paced and nonpaced hearts.
We conclude that sustained pacemaker stimuli during cardioplegic arrest does not impair global and regional postischemic LV function.