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Nicholas S Peters

Publications and source records attributed to Nicholas S Peters.

33 records · Page 2Linked to original sources
PubMed2004

Percutaneous pulmonary vein cryoablation to treat atrial fibrillation.

BACKGROUND: Cryothermic tissue injury, unlike hyperthermic tissue injury, preserves tissue architecture and causes less thrombus formation, and thus may prevent venous stenosis and stroke in ablating pulmonary veins (PVs) to treat patients with atrial fibrillation (AF). We investigate the feasibility, efficacy, safety and clinical outcome of using percutaneous cryoablation to treat such patients. METHODS: Thirty-one patients who had drug refractory paroxysmal (20) or persistent (11) AF underwent 37 PV ablative procedures using a 4 mm- or 6 mm-tipped 7F cryoablation catheter (CryoCath Technologies Inc., Quebec, Canada). Segmental isolation at the veno-atrial junction was guided by a distal circumferential mapping catheter. RESULTS: A total of 47 PV were ablated, of which 35/47 (74%) were electrically isolated and the remaining 12/47 had attenuation of PV electrograms, altered activation sequence, and marked slowing of left atrial-PV conduction. There was no change in PV diameter, either immediately following cryoablation (21 +/- 5 versus 22 +/- 6, p = 0.69), or at 18 +/- 9 months follow-up (22 +/- 5 versus 22 +/- 5 mm, p = 0.23). There was no clinical thromboembolic event. The duration of cryoablation for each treated PV and procedural duration was 65 +/- 39 and 290 +/- 101 min, respectively. Following cryoablation, 5/30 (6%) were free from AF and 12/30 (43%) showed improvement from previously ineffective antiarrhythmic drug therapy. 13/30 (43%) patients were unchanged by cryoablation. CONCLUSIONS: Cryothermic ablation shows great promise in reducing the risks of PV stenosis and thrombo-embolism associated with PV isolative procedures. However, cryoablation of these veins with linear catheters is time consuming, and the clinical outcomes are disappointing. Alternative catheter designs are required to overcome these difficulties.

Analysis of Variance↗
PubMed2004

Localization of the isthmus in reentrant circuits by analysis of electrograms derived from clinical noncontact mapping during sinus rhythm and ventricular tachycardia.

INTRODUCTION: New methods for electrogram analysis accurately estimated reentrant circuit isthmus location and shape in a canine model. It was hypothesized that these methods also would locate reentrant circuits causing clinical ventricular tachycardia (VT). METHODS AND RESULTS: Intracardiac electrogram recordings, obtained with a noncontact mapping system, were analyzed retrospectively from 14 patients with reentrant VT who had undergone successful radiofrequency ablation for prevention of VT initiation. Unipolar electrograms from 256 uniformly distributed endocardial sites were reconstructed by mathematical transformation. Twenty-seven tachycardias were mapped; 15 (in 11 patients) had a complete endocardial reentrant circuit with a figure-of-eight conduction pattern. During sinus rhythm, the location and axis of the slowest and most uniform conduction in the region of latest endocardial activation (the primary axis), the limits of which were defined as boundaries with >15 ms difference in electrogram duration between contiguous recordings, identified the location and shape of the reentrant circuit isthmus with a mean sensitivity compared with activation mapping of 79.3% and a mean specificity of 97.6%. The midpoint of a theoretical "estimated best ablation line" drawn perpendicular to the primary axis of activation, spanning the estimated isthmus location was within 1.3 +/- 0.2 cm (mean distance +/- SD) of the actual ablation site that terminated tachycardia. Analysis of VT electrograms, based on time shifts in the far-field component of the local electrogram when cycle length changed (piecewise linear adaptive template matching [PLATM] method) in 5 of the cases, accurately estimated the time interval between activation at the recording site and the circuit isthmus slow conduction zone where the effective ablation lesion had been placed, which is proportional to the distance between the two locations (mean difference compared with activation mapping: +/-37.3 ms). CONCLUSION: In selected patients with VT who have a complete endocardial circuit, isthmus location and shape can be discerned by analysis of sinus rhythm or tachycardia electrograms, and an effective ablation site can be predicted without the need to construct activation maps of reentrant circuits.

Algorithms↗
PubMed2004

Relationship between connexins and atrial activation during human atrial fibrillation.

INTRODUCTION: Gap junctional connexin proteins (connexin40 [Cx40], connexin43 [Cx43]) are a determinant of myocardial conduction and are implicated in the development of atrial fibrillation (AF). We hypothesized that atrial activation pattern during AF is related to connexin expression and that this relationship is altered by AF-induced remodeling in the fibrillating atria of chronic AF. METHODS AND RESULTS: Isochronal activation mapping was performed during cardiac surgery on the right atria of patients in chronic AF (n = 13) using an epicardial electrode array. The atrial activation pattern was categorized using a complexity score based on the number of propagating wavefronts of activation and by grouping atria into those capable of uniform planar activation (simple) and those that were not (complex). The activation pattern was correlated with the levels of Cx43 and Cx40 signal measured by immunoconfocal quantification of biopsies from the mapped region. We studied the impact of electrical remodeling by comparing these findings with the unremodeled atria of patients in sinus rhythm during pacing-induced sustained AF (n = 17). In chronic AF, atria with complex activation had lower Cx40 signal than atria showing simple activation (0.013 +/- 0.006 microm(2)/microm(2) vs 0.027 +/- 0.009 microm(2)/microm(2), P < 0.02), with the relative connexin signal (Cx40/Cx40+Cx43) correlating with complexity score (P = 0.01, r =-0.74). This relationship did not occur in the unremodeled atria, and increased heterogeneity of distribution of Cx40 labeling in chronic AF was the only evidence of connexin remodeling that we detected in the overall group. CONCLUSION: The pattern of atrial activation is related to immunoconfocal connexin signal only in the fully remodeled atria of chronic AF. This suggests that intercellular coupling and pattern of atrial activation are interrelated, but only in conjunction with the remodeling of atrial electrophysiology that occurs in chronic AF.

Adult↗
PubMed2004

Percutaneous isolation of multiple pulmonary veins using an expandable circular cryoablation catheter.

Although radiofrequency pulmonary vein (PV) ablation is effective in the treatment of atrial fibrillation (AF), it is associated with small but significant risks of PV stenosis and systemic thromboembolism. The characteristics of cryothermic tissue injury may reduce the likelihood of such complications, but using conventionally tipped cryoablation catheters can be time consuming and may, thus, not permit isolation of all PVs during a single procedure. We describe a case of rapid and effective isolation of all electrically connected PVs in a patient with paroxysmal AF, using a percutaneous self-expanding circular-tipped cryoablation catheter.

Adult↗
PubMed2003

Characterization of left atrial activation in the intact human heart.

BACKGROUND: The patterns of activation of the human left atrium (LA), how they relate to atrial myocardial architecture, and their role in arrhythmogenesis remain largely unknown. METHODS AND RESULTS: Left atrial endocardial activation was mapped in 19 patients with a percutaneous noncontact mapping system. Earliest endocardial breakthrough during sinus rhythm (SR) occurred more frequently in the septal (63%, principally posteroseptal) than anterosuperior (37%) LA and varied little with isoproterenol or high right atrial pacing rate. Regardless of site of breakthrough, LA activation was characterized in all patients by propagation around a variably complete line of functional conduction block, descending on the posterior wall from the roof, passing between the ostia of the superior and then inferior pulmonary veins (PVs) before turning septally, passing below the oval fossa, and merging further anteriorly with the septal mitral annulus. Examination of the myocardial architecture in 10 normal adult postmortem hearts revealed an abrupt change in subendocardial fiber orientation along a line following the same course. During episodes of focal initiation of atrial fibrillation (AF), interaction was observed between wavefronts entering the LA from PVs and this functional line of conduction block that resulted in LA macroreentry or formation of daughter wavefronts. CONCLUSIONS: The LA endocardium has complex but characteristic patterns of activation during sinus rhythm, pacing, and AF initiation by PV ectopy that are determined largely by the functional properties of atrial musculature. These findings have important implications for both pacing and ablative strategies for the prevention of initiation of AF.

Adult↗
PubMed2003

Remodeling of gap junctional channel function in epicardial border zone of healing canine infarcts.

The epicardial border zone (EBZ) of canine infarcts has increased anisotropy because of transverse conduction slowing. It remains unknown whether changes in gap junctional conductance (Gj) accompany the increased anisotropy. Ventricular cell pairs were isolated from EBZ and normal hearts (NZ). Dual patch clamp was used to quantify Gj. At a transjunctional voltage (Vj) of +10 mV, side-to-side Gj of EBZ pairs (9.2+/-3.4 nS, n=16) was reduced compared with NZ side-to-side Gj (109.4+/-23.6 nS, n=14, P<0.001). Gj of end-to-end coupled cells was not reduced in EBZ. Steady-state Gj of both NZ and EBZ showed voltage dependence, described by a two-way Boltzmann function. Half-maximal activation voltage in EBZ was shifted to higher Vj in positive and negative directions. Immunoconfocal planimetry and quantification showed no change in connexin43 per unit cell volume or surface area in EBZ. Decreased side-to-side coupling occurs in EBZ myocytes, independent of reduced connexin43 expression, and is hypothesized to contribute to increased anisotropy and reentrant arrhythmias.

Animals↗
PubMed2002

Effects of pinacidil on electrophysiological properties of epicardial border zone of healing canine infarcts: possible effects of K(ATP) channel activation.

BACKGROUND: K(ATP) channels, activated by ischemia, participate in the arrhythmogenic response to acute coronary occlusion. The function of these channels in border zones of healing infarcts, where arrhythmias also arise, has not been investigated. Do these channels remain maximally activated during infarct healing, or do they downregulate after a period of time? Both might preclude further activation. METHODS AND RESULTS: Myocardial infarction was produced in dogs by ligation of the left anterior descending coronary artery. Impulse propagation in the epicardial border zone (EBZ) of 4-day-old healing infarcts was mapped during administration of pinacidil, a K(ATP) channel activator, directly into the EBZ coronary blood supply. Pinacidil restored conduction and excitability when the EBZ was initially inexcitable and had large regions of block (6 of 8 experiments). This allowed reentrant circuits to form in the EBZ, causing tachycardia (4 of 8 experiments). In hearts with an initially excitable EBZ, pinacidil shortened the effective refractory period and abolished conduction block at short cycle lengths (7 experiments). This effect prevented initiation of reentry (1 of 2 experiments). CONCLUSIONS: The response to pinacidil indicates that K(ATP) channels in the EBZ remain functional and can be activated to influence electrophysiological properties and arrhythmogenesis.

Animals↗
PubMed2002

Characteristics of wavefront propagation in reentrant circuits causing human ventricular tachycardia.

BACKGROUND: We investigated the relationship between wavefront curvature and slowing of conduction both within and outside the diastolic pathway of circuits causing ventricular tachycardia (VT) in the infarcted human heart. METHODS AND RESULTS: Propagation was determined around the reentrant circuits of 11 VT (cycle length, 348+/-75 ms) in 8 patients undergoing high-resolution noncontact mapping. The diastolic pathway had a mean wavefront velocity of 0.82+/-0.49 m/s and occupied 68+/-7% of VT cycle length. Significant changes (>5 degrees/mm) in trajectory of propagation occurred in 8 diastolic pathway segments (10.1+/-3 degrees/mm) in which wavefront propagation slowed to 0.41+/-0.11 m/s compared with the segments immediately preceding (0.91+/-0.16 m/s, P< 0.05) and following (1.07+/-0.33, P<0.05) the change in trajectory. At the turning points of entry (9.3+/-3.9 degrees/mm) and exit (9.0+/-4.8 degrees/mm) of the diastolic pathway propagation, velocity slowed at entry from 1.23+/-0.4 to 0.6+/-0.26 ms (P<0.001) and was more rapid at exit turning points (0.8+/-0.25 m/s) (P<0.05). There was an inverse relationship between wavefront curvature and velocity, both within and outside the diastolic pathway (r=0.46, P=0.0001), and VT cycle length correlated with total curvature multiplied by length of the diastolic pathway (P< 0.01). CONCLUSIONS: Slowing of propagation in circuits causing VT in the infarcted human heart occurs over regions of wavefront turning, with an inverse relationship between wavefront curvature and velocity, both within and outside the diastolic pathway. Conduction is slower at entry than exit turning points of the diastolic pathway but is slowest during turns within the diastolic pathway.

Aged↗
PubMed2002

Atrial fibrillation: strategies to control, combat, and cure.

Atrial fibrillation is the commonest clinical arrhythmia, is increasing in incidence and prevalence, and is associated with substantial morbidity and mortality. The arrhythmia may be paroxysmal (self-limiting), persistent (amenable to cardioversion), or permanent. Especially in its paroxysmal form, atrial fibrillation may be initiated by rapidly firing foci, generally located in the proximal pulmonary veins. Sustained atrial fibrillation is maintained by an atrial tissue substrate capable of accommodating many meandering wavelets. With continuing arrhythmia, the electrophysiological properties of the atria change and further facilitate continuing fibrillation. Treatment is aimed at prevention of thromboembolic complications, restoration and maintenance of sinus rhythm, and control of ventricular rate during atrial fibrillation. With greater understanding of the arrhythmia mechanisms, it is becoming possible to offer targeted curative treatments to more and more patients.

Aged↗
PubMed2002

Relative expression of immunolocalized connexins 40 and 43 correlates with human atrial conduction properties.

OBJECTIVES: The aim of this study was to determine the relationship between immunolocalized gap-junctional proteins and human atrial conduction. BACKGROUND: As a determinant of intercellular conductance, gap-junctional coupling is considered to influence myocardial conduction velocity. This study tested the hypothesis that the quantity of immunodetectable atrial gap-junctional proteins, connexin40 (Cx40) and connexin43 (Cx43), are related to atrial conduction velocity in humans. METHODS: Epicardial mapping was performed on 16 patients undergoing cardiac surgery using an array of 56 unipolar electrodes. The conduction velocity was measured over the right atrial free wall during sinus rhythm and at a paced cycle length 500 ms. A biopsy from this region was excised for quantitative confocal immunodetection of Cx40 and Cx43. RESULTS: There was no correlation between conduction velocity and Cx43 signal or total connexin signal (Cx40 + Cx43). Connexin40 signal was inversely correlated with conduction velocity (p = 0.036). However, the relative quantity of connexin immunolabeling (expressed as Cx40/[Cx40+Cx43] or the inverse equivalent Cx43/[Cx40+Cx43]) was strongly associated with conduction velocity during sinus rhythm, such that, as the proportion of Cx40 signal increased (and that for Cx43 decreased), the conduction velocity decreased (p < 0.005, r = -0.66). Furthermore, with paced atrial activation at 500 ms cycle length, the relative quantity of connexin labeling (Cx40/[Cx40+Cx43]) correlated with the rate-related change in atrial conduction velocity (p < 0.02, r = 0.59). CONCLUSIONS: In human right atrium, conduction velocity is inversely related to immunodetectable Cx40 levels. The relative level of connexins 40 and 43 signal is strongly associated with atrial conduction properties, suggesting that interactions between the two connexins may result in novel coupling properties.

Adult↗
PubMed2002

Mechanisms underlying the development of atrial arrhythmias in heart failure.

There is an important association between heart failure and the development of atrial arrhythmias. Although most often associated with atrial fibrillation, there is some evidence to suggest an association between heart failure and other atrial arrhythmias and, in particular, atrial flutter and atrial tachycardia. The mechanisms by which these common atrial arrhythmias may arise in patients with heart failure are discussed.

Aged↗