Gregory T. Altemose

Inhibition of the Na+/H+ Exchanger Delays the Development of Rapid Pacing–Induced Atrial Contractile Dysfunction

Background —Atrial mechanical stunning due to atrial fibrillation may persist after restoration of sinus rhythm. Although the mechanism of rapid rate–related contractile dysfunction remains unknown, ischemia, pH changes, and calcium overload have been postulated as potential mechanisms. We hypothesized that blockade of the Na+/H+ exchanger (NHE) would alter atrial contractile dysfunction from rapid rates. Methods and Results —Twenty-three anesthetized dogs were studied and subjected to 5 hours of rapid right atrial pacing. Ten received an inhibitor of the NHE, 10 received saline, and 3 received nifedipine. All animals underwent placement of 2 sonomicrometers on the left atrium, transesophageal echocardiography, and invasive hemodynamic monitoring. All measurements were made in sinus rhythm. Except for baseline and postdrug measurements, reduction in left atrial fractional shortening was significantly less at all time points in the NHEI group than in the control and nifedipine groups (P =0.05). The percent change from baseline of left atrial function at all time intervals as assessed by left atrial appendage contraction velocity (LAACV) was significantly less in the NHEI group than in the control (P =0.05) group. LAACV was significantly preserved at all time intervals (except 300 minutes) in the NHEI group compared with the nifedipine group (P =0.05). The only significant difference in hemodynamics among the groups was between the control and the nifedipine groups at 30 minutes after drug (P =0.05). Conclusions —Treatment with HOE642 significantly blunts the decline in left atrial mechanical function from rapid atrial rates compared with both control and nifedipine-treated groups.

Atrioventricular Nodal Reentrant Tachycardia Requiring Ablation on the Mitral Annulus

Mitral Ablation for AV Nodal Reentry. We report a case of initial transient success during ablation for typical AV nodal reentrant tachycardia utilizing traditional right‐sided approaches, followed by recurrence of the same tachycardia and an ultimately successful ablation on the posteromedial mitral annulus.

MANAGEMENT OF POSTINFARCT VENTRICULAR TACHYCARDIAS

The clinical profile of patients with postinfarct VT has changed in the past two decades. Along with these changes, existing treatments have improved, and entirely new therapeutic approaches have been developed. The expanded range of treatment options has made postinfarct VT a less imposing clinical problem than it once was. Emerging therapies promise to make an even greater beneficial impact. The challenge in treating patients with postinfarct VT has changed from merely keeping patients alive to keeping up with innovations in therapy that can provide them with a better quantity and quality of life.

Catheter ablation of ventricular tachycardia in patients with structural heart disease.

Radiofrequency catheter ablation has revolutionized therapy of most forms of supraventricular tachycardia and ventricular tachycardia in the absence of structural heart disease by providing arrhythmia cure in almost 90% of patients. However, this treatment has not been nearly as successful in patients with ventricular tachycardia in the setting of structural heart disease, because of a number of factors. Some of these limitations are technical (imprecise mapping tools, multiple regions requiring ablation) although others are patient-related (hemodynamic instability during arrhythmia, progression of disease process). Because of these and other factors, the majority of patients in this group are treated with implantable defibrillators. Ablative therapy has an adjunctive role in their management, mainly to decrease the frequency of device therapy (particularly shocks). This review will discuss mapping and ablation techniques as well as patient selection and evaluation for this procedure.

Radiofrequency catheter ablation for postinfarct ventricular tachycardia.

Catheter mapping and radiofrequency ablation of postinfarct sustained ventricular tachycardia (VT) remain one of the greatest challenges for the electrophysiologist. Although there were no major breakthroughs during the past year, several refinements and clarifications of existing mapping criteria were published. In addition, initial reports appeared describing new mapping systems and ablation technologies that may significantly impact the way ablation studies are performed as well as the way in which they affect success rates. Uncertainties remain as to how effective catheter ablation will be as a longterm cure for this type of VT. For the foreseeable future, catheter ablation in postinfarct VT will remain adjunctive rather than primary therapy.

Unusual Features of Intermediate Septal Bypass Tracts

Intermediate Septal Bypass Tracts. Introduction: Intermediate septal (TS) AV bypass tracts, located along the tricuspid annulus between the His bundle and coronary sinus os, lie in close proximity to the AV node. Surgical or catheter ablation of IS bypass tracts incurs increased risk for development of complete heart block. We report additional unusual features of some IS bypass tracts that distinguish them from typical bypass tracts in other anatomic regions.