A case of atrial tachycardia treated with ivabradine as bridge to ablation.

Ivabradine is indicated in cardiac failure and ischemia to reduce sinus rate by inhibition of the pacemaker I(f) current in sinoatrial node. We report a case of an 18-year-old woman with left atrial tachyarrhythmia resistant to several antiarrhythmic drugs and to electric cardioversion who responded only to ivabradine, which significantly reduced heart rate without abolishing the arrhythmia itself. An ectopic focus in the ostium of left pulmonary veins was found and the patient was successfully ablated. We suggest that ivabradine might be therefore useful in the treatment of supraventricular tachyarrhythmias due to an enhanced automaticity.

Unifying mechanism of sustained idiopathic atrial and ventricular annular tachycardia.

BACKGROUND: Based on the current understanding of cardiac conduction system development and the observation that arrhythmogenic foci can originate in areas near the atrioventricular annuli, we hypothesized that focal annular tachycardias, whether atrial or ventricular, share a common mechanism. We, therefore, prospectively evaluated this hypothesis in patients with sustained atrial and ventricular tachycardia originating from the peri-tricuspid and mitral annuli. METHODS AND RESULTS: Forty-nine consecutive patients with sustained, focal annular tachycardia comprised the study group. All underwent electrophysiological evaluation and the mode of tachycardia initiation, termination, sensitivity to catecholamine infusion, and response to adenosine/verapamil were evaluated. Electroanatomical activation maps identified the sites of arrhythmia origin. Tachycardias could be initiated or terminated or both with programmed stimulation in 46 of 46 patients and most (70%) were catecholamine facilitated. Of the 9 patients with sustained annular ventricular tachycardia, 3 were localized to the tricuspid annulus, and 6 to the mitral annulus. All the 9 ventricular tachycardias (100%) terminated with adenosine, 2 of 2 terminated with verapamil, and 2 of 2 terminated with Valsalva. Of the 40 patients with annular atrial tachycardia, 4 tachycardias were localized to the mitral annulus and 37 to the tricuspid annulus (including 9 para-Hisian), and all were adenosine sensitive. CONCLUSIONS: Peri-annular atrial and ventricular tissue correspond to a region enriched with arrhythmogenic foci, which may reflect a common developmental origin. Furthermore, the sensitivity of these tachycardias to adenosine provides evidence for a shared arrhythmia mechanism, consistent with intracellular calcium overload and triggered activity.

Magnesium adjunctive therapy in atrial arrhythmias.

Magnesium (Mg) is an important intracellular ion with cardiac metabolism and electrophysiologic properties. A large percentage of patients with arrhythmias have an intracellular Mg deficiency, which is out of line with serum Mg concentrations, and this may explain the rationale for Mg's benefits as an atrial antiarrhythmic agent. A current limitation of antiarrhythmic therapy is that the potential for cardiac risk offsets some of the benefits of therapy. Mg enhances the balance of benefits to harms by enhancing atrial antiarrhythmic efficacy and reducing antiarrhythmic proarrhythmia potential as well as providing direct antiarrhythmic efficacy when used as monotherapy in patients undergoing cardiothoracic surgery.

Arrhythmias (IV). Clinical approach to atrial tachycardia and atrial flutter from an understanding of the mechanisms. Electrophysiology based on anatomy.

In 2009, 2343 catheter ablation procedures were performed in Spain for focal atrial tachycardia or atrial flutter (typical and atypical), with a yearly growth rate of 8%, indicating the clinical importance of these arrhythmias. The classic categorization of atrial tachycardia and atrial flutter based on rate and morphological criteria has become almost irrelevant at a time when clinical electrophysiology may lead to curative intervention based on a definition of the mechanism, making it necessary to bring laboratory experience closer to clinical practice. In this review we outline our present understanding of atrial tachycardia mechanisms, both focal and macroreentrant, and attempt to establish the conceptual links with classic concepts that may help the clinician to make a differential diagnosis and establish therapeutic indications, including that of an electrophysiologic study. Some of the concepts may seem complex, but we thought it important to provide an overview of the electrophysiological methods that may eventually lead to the description of the anatomic bases of the arrhythmias; currently, these are easier to understand thanks to the virtual anatomic casts built using computerized navigation systems.

Focal atrial tachycardia: new insight from noncontact mapping and catheter ablation.

BACKGROUND: This study investigated the electrophysiologic characteristics, atrial activation pattern, and effects of radiofrequency (RF) catheter ablation guided by noncontact mapping system in patients with focal atrial tachycardia (AT). METHODS AND RESULTS: In 13 patients with 14 focal ATs, noncontact mapping system was used to map and guide ablation of AT. AT origins were in the crista terminalis (n=8), right atrial (RA) free wall (n=3), Koch triangle (n=1), anterior portion of RA-inferior vena cava junction (n=1), and superior portion of tricuspid annulus (n=1); breakout sites were in the crista terminalis (n=5), RA free wall (n=5), middle cavotricuspid isthmus (n=2), and RA-superior vena cava junction (n=2). ATs arose from the focal origins (11 ATs inside or at the border of low-voltage zone), with preferential conduction, breakout, and spread to the whole atrium. After applications of RF energy on the earliest activation site or the proximal portion of preferential conduction from AT origin, 13 ATs were eliminated without complication. During the follow-up period (8+/-5 months), 11 (91.7%) of the 12 patients with successful ablation were free of focal ATs. CONCLUSIONS: Focal AT originates from a small area and spreads out to the whole atrium through a preferential conduction. Application of RF energy guided by noncontact mapping system was effective and safe in eliminating focal AT.

Global distribution of atrial ectopic foci triggering recurrence of atrial tachyarrhythmia after electrical cardioversion of long-standing atrial fibrillation: a bi-atrial basket mapping study.

OBJECTIVES: The objective of this study was to assess the spatial distribution of atrial ectopic foci potentially triggering recurrent atrial tachyarrhythmias after electrical cardioversion of long-standing atrial fibrillation (AF). BACKGROUND: It remains unknown whether targeted ablation of atrial ectopic foci concentrated in the pulmonary veins is feasible in patients with long-standin

[Radiofrequency ablation in permanent ectopic left atrial tachycardia]. / Radiofrequenzablation bei permanenter ektoper linksatrialer Tachykardie.

HISTORY AND FINDINGS: A 35-year-old symptom-free woman was known since childhood to have an increased resting heart rate (130-150/min). In the ECG there was a negative P in leads I and aVL, with a shortened P-Q interval of 90 ms. Previous treatment with beta-receptor blockers and calcium antagonists had failed. Clinical examination and echocardiography, as well as levels of thyroid hormone were unremarkable. During electrophysiological studies the earliest atrial activity was localised by endocardial leads in the region of the distal coronary sinus and the arrhythmia could not be terminated by atrial over-stimulation. TREATMENT AND COURSE: After transseptal puncture the ablation catheter was introduced into the left atrium and, the exact site of the origin of the atrial tachycardia having been established, radiofrequency ablation of this point was successfully performed. Subsequently the patient was always found to be in stable sinus rhythm at around 80/min. CONCLUSION: To prevent tachycardia-induced cardiomyopathy, radiofrequency ablation can be indicated even in symptom-free patients with atrial tachycardia.