Home About us Contact
|
Home About us Contact | ||
|
|
||
Right Superior PV (right + superior_pv)
Selected AbstractsClinical Experience with a Single Catheter for Mapping and Ablation of Pulmonary Vein OstiumJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 4 2009PAOLO DE FILIPPO M.D. Introduction: The aim of this single center study is to evaluate the safety and the efficacy of performing pulmonary vein isolation (PVI) using a single high-density mesh ablator (HDMA) catheter. Methods: A total of 17 consecutive patients with paroxysmal (10 patients) or persistent atrial fibrillation (7 patients) and no heart disease were enrolled. A single transseptal puncture was performed and the HDMA was placed at each PV ostium identified with anatomic and electrophysiological mapping. Pulsed radiofrequency (RF) energy was delivered at the targeted temperature of 58°C with maximum power of 80 watts. No other ablation system was utilized. The primary objective of the study was acute isolation of the targeted PV, and the secondary objective was clinical efficacy and safety of PVI with HDMA for atrial fibrillation (AF) prevention. Patients were followed at intervals of 1, 3, 6, and 12 months. Results: PVI was attempted with HDMA in 67/67 PVs. [Correction made after online publication October 27, 2008: PVs changed from 6/67 to 67/67] Acute success rate were: 100% (16/16) for left superior PV, 100% (16/16) for left inferior PV, 100% (17/17) for right superior PV, 100% (1/1) for left common trunk and 47% (8/17) for right inferior PV. Total procedure time was 200 ± 36 minutes (range 130,240 minutes) and total fluoroscopy time was 42 ± 18 minutes (range 23,75 minutes). During a mean follow-up of 11 ± 4 months, 64% of patients remained in sinus rhythm (8/10 paroxysmal AF and 3/7 for persistent AF). No complications occurred either acutely or at follow-up. Conclusions: PV isolation with HDMA is feasible and safe. The midterm efficacy in maintaining sinus rhythm is higher in paroxysmal than in persistent patients. [source] A Single Pulmonary Vein as Electrophysiological Substrate of Paroxysmal Atrial FibrillationJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 11 2006HE HUANG M.D. Introduction: It has been demonstrated that pulmonary veins (PVs) play an important role in initiation and maintenance of paroxysmal atrial fibrillation (AF). However, it is not clearly known whether a single PV acts as electrophysiological substrate for paroxysmal AF. Methods and Results: This study included five patients with paroxysmal AF. All patients underwent complete PV isolation with continuous circular lesions (CCLs) around the ipsilateral PVs guided by a three-dimensional mapping system. Irrigated radiofrequency (RF) delivery was performed during AF on the right-sided CCLs in two patients and on the left-sided CCLs in three patients. The incomplete CCLs resulted in a change from AF to atrial tachycardia (AT), which presented with an identical atrial activation sequence and P wave morphology. Complete CCLs resulted in AF termination with persistent PV tachyarrhythmias within the isolated PV in all five patients. PV tachyarrhythmia within the isolated PV was PV fibrillation from the left common PV (LCPV) in two patients, PV tachycardia from the right superior PV (RSPV) in two patients, and from the left superior PV in one patient. All sustained PV tachyarrhythmias persisted for more than 30 minutes, needed external cardioversion for termination in four patients and a focal ablation in one patient. After the initial procedure, an AT from the RSPV occurred in a patient with PV fibrillation within the LCPV, and was successfully ablated. Conclusion: In patients with paroxysmal AF, sustained PV tachyarrhythmias from a single PV can perpetuate AF. Complete isolation of all PV may provide good clinical outcome during long-term follow-up. [source] Characterization of a New Pulmonary Vein Variant Using Magnetic Resonance Angiography:JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 5 2004Imaging, Incidence, Interventional Implications of the "Right Top Pulmonary Vein" Introduction: Catheter ablation of the pulmonary veins (PVs) for prevention of recurrent atrial fibrillation requires precise anatomic information. We describe the characteristics of a new anatomic variant of PV anatomy using magnetic resonance angiography. Methods and Results: A 1.5-T magnetic resonance imaging system with a body coil or a torso phased-array coil was used before and after gadolinium injection. Magnetic resonance angiograms were acquired with a breath-hold three-dimensional fast spoiled gradient-echo imaging sequence in the coronal plane. Three-dimensional reconstruction with maximum intensity projections and multiplanar reformations was performed. A newly described variant PV ascending from the roof of the left atrium was found in 3 of 91 subjects. The mean ostial diameter of the roof PV was 7 ± 2 mm, the mean distance from the ostium to the first branching point was 22 ± 8.5 mm, and the mean distance to the right superior PV was 3.3 ± 0.6 mm. Conclusion: We refer to the newly described variant of PV anatomy as the "right top pulmonary vein." It is important to be aware of this anatomic pattern to avoid inadvertent catheter intubation, which can result in misleading mapping results and PV stenosis. (J Cardiovasc Electrophysiol, Vol. 15, pp. 538-543, May 2004) [source] Focal Atrial Fibrillation: Experimental Evidence for a Pathophysiologic Role of the Autonomic Nervous SystemJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 5 2001PATRICK SCHAUERTE M.D. Focal AF and Autonomic Nerves.Introduction: Focal paroxysmal atrial fibrillation (AF) was shown recently to originate in the pulmonary veins (PVs) and superior vena cava (SVC). In the present study, we describe an animal model in which local high-frequency electrical stimulation produces focal atrial activation and AF/AT (atrial tachycardia) with electrogram characteristics consistent with clinical reports. Methods and Results: In 21 mongrel dogs, local high-frequency electrical stimulation was performed by delivering trains of electrical stimuli (200 Hz, impulse duration 0.1 msec) to the PVs/SVC during atrial refractoriness. Atrial premature depolarizations (APDs), AT, and AF occurred with increasing highfrequency electrical stimulation voltage. APD/AT/AF originated adjacent to the site of high-frequency electrical stimulation and were inducible in 12 of 12 dogs in the SVC and in 8 of 9 dogs in the left superior PV (left inferior PV: 7/8, right superior PV: 6/8; right inferior PV: 4/8). In the PVs, APDs occurred at 13 ± 8 V and AT/AF at 15 ± 9 V (P < 0.01; n = 25). In the SVC, APDs were elicited at 19 ± 6 V and AT/AF at 26 ± 6 V (P < 0.01; n = 12). High-frequency electrical stimulation led to local refractory period shortening in the PVs. The response to high-frequency electrical stimulation was blunted or prevented after beta-receptor blockade and abolished by atropine. In vitro, high-frequency electrical stimulation induced a heterogeneous response, with shortening of the action potential in some cells (from 89 ± 35 msec to 60 ± 22 msec; P < 0.001; n = 7) but lengthening of the action potential and development of early afterdepolarizations that triggered APD/AT in other cells. Action potential shortening was abolished by atropine. Conclusion: High-frequency electrical stimulation evokes rapid ectopic beats from the PV/SVC, which show variable degrees of conduction block to the atria and induce AF, resembling findings in patients with focal idiopathic paroxysmal AF. The occurrence of the arrhythmia in this animal model was likely due to alterations in local autonomic tone by high-frequency electrical stimulation. Further research is needed to prove absolutely that the observed effects of high-frequency electrical stimulation were caused by autonomic nerve stimulation. [source] Pulmonary Vein Internal Electrical Activity Does Not Contribute to the Maintenance of Atrial FibrillationPACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 6 2003GJIN NDREPEPA Whether the electrical activity generated in the pulmonary veins (PVs) during atrial fibrillation (AF) contributes to the maintenance of arrhythmia is not known. The study population consisted of 22 patients (mean age 58 ± 9.5 years, 16 men) with persistent (12 patients) or intermittent (10 patients) AF. Mapping of the left atrium (LA) was performed with a 64-electrode basket catheter. PVs were mapped simultaneously with the LA with a quadripolar catheter. PV were defined as arrhythmogenic (if frequent ectopic activity induced AF) or nonarrhythmogenic (if no ectopic activity was observed during the procedure). AF cycle lengths in arrhythmogenic and nonarrhythmogenic PV were 130 ± 50 ms and 152 ± 42 ms, respectively(P < 0.001). Both were significantly longer than simultaneous AF activity recorded from the posterior wall of the LA(116 ± 49 ms, P < 0.001). AF cycle lengths in arrhythmogenic PVs as compared to nonarrhythmogenic PVs were: right superior PV 125 ± 49 ms versus 148 ± 51 ms ; left superior PV 140 ± 52 ms versus 161 ± 30 ms ; left inferior PV 127 ± 48 ms versus 147 ± 45 ms ; and right inferior PV 129 ± 38 versus 152 ± 44 ms (P < 0.001for all four comparisons). AF activity in the PV was more organized than in the posterior wall of the LA and the veins were activated in a proximal-to-distal direction during sustained AF episodes. In patients with AF not related to rheumatic heart disease, the posterior wall of the LA has faster activity than the PVs. The AF activity generated inside the PV during sustained AF episodes originates from the posterior wall of the LA rather than from focal firing. (PACE 2003; 26:1356,1362) [source] Myocardium Extending from the Left Atrium onto the Pulmonary Veins: A Comparison Between Subjects with and Without Atrial FibrillationPACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 10 2001MINORU TAGAWA TAGAWA, M., et al.: Myocardium Extending from the Left Atrium onto the Pulmonary Veins: A Comparison Between Subjects with and Without Atrial Fibrillation. Rapid discharges from the myocardium extending from the left atrium onto the pulmonary vein (PV) have been shown to initiate AF, and AF may be eradicated by the catheter ablation within the PV. However, if there is any difference in the distribution patterns of the myocardial sleeve onto the PV between the subjects with and without AF is to be determined. Twenty-one autopsied hearts were examined. Eleven patients previously had AF before death and another 10 patients had normal sinus rhythm as confirmed from the medical records including ECGs before death. After exposing the heart, the distance to the peripheral end of the myocardium was measured from the PV-atrial junction in each PV. Then, the PVs were sectioned and stained and the distal end of myocardium and the distribution pattern were studied. The anteroposterior diameter of the left atrium was also measured. In 74 of 84 PVs, the myocardium extended beyond the PV-atrial junction. The myocardium was localized surrounding the vascular smooth muscle layer forming a myocardial sleeve. The peripheral end of the myocardial sleeve was irregular and the maximal and minimal distances were measured in each PV. The myocardium extended most distally in the superior PVs compared to the inferior ones and the maximal distance to the peripheral end was similar between the AF and non-AF subjects (8.4 ± 2.8 vs 8.7 ± 4.4 mm for the left superior and 6.5 ± 3.5 vs 5.1 ± 3.9 mm for the right superior PV, respectively). A significant difference was found in the maximal distance in the inferior PVs: 7.3 ± 4.6 vs 3.3 ± 2.8 mm for the left (P < 0.05) and 5.7 ± 2.4 vs 1.7 ± 1.9 mm for the right inferior PV (P < 0.001) in the subjects with and without AF, respectively. The diameter of left atrium was slightly dilated in AF patients but insignificantly (4.1 ± 0.1 vs 3.6 ± 0.1 cm, P > 0.07). The myocytes on the PV were less uniform and surrounded by more fibrosis in patients with AF compared to those without AF. In conclusion, the myocardium extended beyond the atrium-vein junction onto the PVs. The distribution patterns of the myocardium was almost similar between subjects with and without AF, but the histology suggested variable myocytes in size and fibrosis in patients with AF. [source] | ||||||||||