Thoracic Vein Arrhythmias: Mechanisms and Treatment

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Asirvatham S.

Atrial Arrhythmias

Supraventricular tachycardia: diagnosis and treatment. Mayo Clinic Cardiology: Concise Textbook. Fluoroscopic cardiac anatomy for catheter ablation of tachycardia. Pacing Clin Electrophysiol. The dimensions of the triangle of Koch in children. Am J Cardiol. Radiofrequency ablation of accessory pathways associated with congenital heart disease. Prospective evaluation of the coronary sinus anatomy in patients undergoing electrophysiologic study. Clin Cardiol.

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Catheter ablation of accessory atrioventricular pathways Wolff-Parkinson-White syndrome by radiofrequency current. Thoracic vein arrhythmias: Mechanisms and treatment. Does atrial myocardium extend into the superior vena cava and azygous vein?


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Circulation ; 17 Suppl :II. Journal of Cardiovascular Electrophysiology. Wellens H.

The preexcitation syndrome. Baltimore: University Park Press; The nodoventricular Mahaim pathway: an endangered concept? Mahaim I, Winston M. Recherches d'anatomie comparee et de pathologie experimental su les connexions hautes du faisceau de His-Tawara. Outcomes of radiofrequency catheter ablation of atrioventricular reciprocating tachycardia in patients with congenital heart disease. Heart Rhythm. Topographic anatomy of the inferior pyramidal space: relevance to radiofrequency catheter ablation. J Cardiovasc Electrophysiol.

Involvement of a nodofascicular connection in supraventricular tachycardia with VA dissociation.

Okishige K, Friedman PL. New observations on decremental atriofascicular and nodofascicular fibers: implications for catheter ablation. Anatomy of the left atrium: implications for radiofrequency ablation of atrial fibrillation. Effect of isthmus anatomy and ablation catheter on radiofrequency catheter ablation of the cavotricuspid isthmus.

Management of perioperative arrhythmias Dua N, Kumra V P - Indian J Anaesth

Progressive isthmus delay during atrial flutter ablation: the critical importance of isthmus spanning electrodes for distinguishing pseudoblock from block. Europace ;3 Suppl A :A Syncope is uncommon, but some patients experience serious psychologic distress. SVTs are often recurrent, occasionally persistent, and are a frequent cause of emergency room ER and primary care physician PCP visits. After restoration of sinus rhythm, the twelve-lead ECG should be examined for the presence of delta waves, which indicate an accessory pathway.

Most SVTs depend on the AV node for maintenance of the re-entry circuit and can be interrupted by vagal maneuvers or pharmacological agents, which slow AV nodal conduction, the first-line pharmacological agent being adenosine. For patients in whom SVT recurs, preventive therapy is generally warranted if there are frequent, prolonged, or highly symptomatic episodes that cannot easily be terminated by the patient using vagal maneuvers. Options for long-term treatment include medication and ablation therapy. Referral to an electrophysiologist is warranted for patients with syncope, severe symptoms, or pre-excitation syndrome.

These agents decrease the frequency of the episodes and the severity of symptoms in a number of patients, but complete suppression of SVT is uncommon. Long-term therapy with class IC or III drugs is generally not recommended because of their potential adverse effects. Verapamil and digoxin are contraindicated in patients with WPW syndrome, unless the AP has been shown to have a long refractory period msec or more , because these drugs may increase the risk of rapid ventricular response causing ventricular fibrillation in case of atrial fibrillation.

Although catheter ablation is considered the treatment of choice in these patients, both flecainide and propafenone are effective and have been approved for the prevention of paroxysmal SVTs mediated by an accessory pathway. Medical treatment of SVT with antiarrhythmic drugs has limited efficacy.

In addition, these drugs can produce significant side effects or may be inconvenient for a number of patients. Catheter ablation has been increasingly used in the management of SVT, based on its observed efficacy and overall safety in experienced centers. Generally, radiofrequency ablation is recommended as primary therapy for patients with pre-excitation syndrome or hemodynamic instability during their arrhythmia. Moreover, catheter ablation is recommended for the patients with arrhythmias refractory to AV node blocking agents.

Finally, catheter ablation can also be proposed for patients who experience adverse effects or find it inconvenient to take medication. Indeed, many patients, informed of the risks and benefits of catheter ablation, prefer this approach than a long-term antiarrhythmic drug therapy.

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Catheter ablation of SVT can be performed as a one-day out-patient procedure, or it may require overnight hospitalization. One to four catheter electrodes are introduced into the heart cavities through femoral or, alternatively, internal jugular or subclavian venous access after local anesthesia is administered. For left-sided accessory pathways, a retrograde approach through the femoral artery and the aortic valve can be used, or a transseptal puncture can be performed to gain access to the left atrium.

This was highlighted in an interesting study of 32 patients without clinical recurrence of AF in which a repeat electrophysiological study was performed. In this study recovery of pulmonary vein conduction was observed in In fact, In further support of the lack of pulmonary vein isolation impact on those patients without symptomatic recurrences a recent study compared contrast MRI scar imaging with scar that was predicted by the 3D voltage maps during the ablation procedure In this study, the mean percentage of scar quantified by electroanatomic mapping was There are several mechanisms that may be behind these discrepant findings.

First, electroanatomic maps are dependent on ideal catheter-tip and atrial wall contact. In the absence of adequate contact, local electrical signal strength can be lost or diminished and appear erroneously as scar. Second, electroanatomic maps are dependent on sampling. Point-by-point area samples are then integrated to project a 3D image with algorithmic delineation of tissue characteristics such as scar. If one or more of these points is misclassified, then the region is also prone to misclassification error. Errors are typically a product of points sampled, since intra-point automated interpolation is smaller.

Overview of Arrhythmias

Thereby, dense maps containing multiple sampling sites with good catheter tip to tissue contact will be more accurate than less dense maps. Third, delivery of ablative energy does not correlate with a transmural lesion and definitive scar formation. In this case the electroanatomic map may be correct, but the durable injury per lesion marker is less than anticipated.

Means to improve transmural lesion formation will be discussed subsequently the topic how to improve durable pulmonary vein isolation is developed. In regards to the trial that found significant discord between electroanatomic map based scar quantification and that observe by cardiac MRI, the authors did not report their long-term arrhythmia-free success rates. However, a contemporary article from the same institution of patients that underwent an AF ablation and received a cardiac MRI reported a 1-year survival free of atrial arrhythmia rate post ablation of Summarizing these two trials it is reasonable to assume patients with very little scar post ablation around the pulmonary veins had no symptomatic recurrence.

These studies raise some very important questions about our assumptions of pulmonary vein antral isolation with catheter ablation. First, is the amount of myocardial tissue injury necessary to produce acute pulmonary vein isolation adequate to produce durable scar. If not, what markers other than acute pulmonary vein isolation can be used to suggest that adequate ablation has been performed to produce durable scar around the antra of the pulmonary veins.

Based on the findings of these studies it seems that the amount of durable scar produced during the majority of pulmonary vein antral isolation is much less than predicted. Also, continuous transmural lesions around the pulmonary veins seem to be rare. As such, pulmonary vein isolation confirmed by exit and entrance block is likely an insufficient guide. Finally, the lack of MRI identified scar and lack of durable pulmonary vein isolation did not seem to affect the outcomes.

Central Venous Catheter-Induced Cardiac Arrhythmias in Neonates

Therefore is pulmonary vein isolation the cornerstone of ablation procedures or it some other mechanism targeted during the ablation the driver of success? This is particularly important in that we have mechanistic evidence of pulmonary vein triggers in patients with paroxysmal AF Figure 1. Currently, there are no proven ways to improve long-term durable pulmonary vein isolation, largely because we are just beginning to realize the frequency of reconnection in patients without recurrence of arrhythmia.

Thereby our understanding of reconnection rates and their significance has been primarily derived from patients with a failed prior ablation that present for a subsequent electrophysiology study.

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