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Biomedical subjects

N S Peters

Publications and source records attributed to N S Peters.

At least 37 records · Page 2Linked to original sources
PubMed1999

Feasibility of a noncontact catheter for endocardial mapping of human ventricular tachycardia.

BACKGROUND: Catheter ablation of ventricular tachycardia (VT) is limited by difficulty in identifying suitable sites for ablation. This study assesses use of a system capable of simultaneous endocardial mapping of the human left ventricle to map and guide radiofrequency (RF) catheter ablation of VT. METHODS AND RESULTS: A catheter-mounted noncontact multielectrode array was used to reconstruct 3360 electrograms, superimposed onto a computer-simulated endocardial model. Of 24 patients studied, 20 had ischemic heart disease. Exit sites were demonstrated by the noncontact system in 80 (99%) of 81 VTs, with complete VT circuits traced in 17 (21%). In another 37 VTs, 36+/-30% (mean+/-SD) of the diastolic interval was identified. Thirty-eight VT morphologies were ablated with 154 RF energy applications. Successful ablation was achieved by 77% of RF applications to relevant diastolic activity identified by the system and was significantly more likely (P<0.0001) than by RF at the VT exit or remote from diastolic activation. Over a mean follow-up of 1.5 years, 14 patients (64%) have had no recurrence of VT, and only 2 target VTs (5.3%) have recurred. Five patients have had recurrence of other VTs. CONCLUSIONS: This noncontact mapping system identified diastolic portions of the circuit in most VTs studied and can safely map and guide ablation of human VT.

Adult↗
PubMed1999

Noncontact mapping of cardiac arrhythmias.

The development of new mapping systems is beginning to overcome some of the limitations of conventional techniques by offering percutaneous deployment, simultaneous acquisitions of data, high-resolution maps, and correlation of anatomy and electrophysiology, in addition to a catheter location system. The noncontact mapping system continues to undergo development and does not completely address all requirements for an ideal mapping system. The limitations of the system include deterioration in the quality of electrogram reconstruction with increasing distance between the MEA and the endocardium, the inability of the noncontact system to identify subendocardial activation, and problems with distinguishing noise from low-amplitude diastolic electrograms.

Arrhythmias, Cardiac↗
PubMed1999

Mapping and ablation of ventricular tachycardia with the aid of a non-contact mapping system.

OBJECTIVE: Treatment of ventricular tachycardia (VT) in coronary heart disease has to date been limited to palliative treatment with drugs or implantable defibrillators. The results of curative treatment with catheter ablation have proved disappointing because the complexity of the VT mechanism makes identification of the substrate using conventional mapping techniques difficult. The use of a mapping technology that may address some of these issues, and thus make possible a cure for VT with catheter ablation, is reported. PATIENTS AND INTERVENTION: The non-contact system, consisting of a multielectrode array catheter (MEA) and a computer mapping system, was used to map VT in 24 patients. Twenty two patients had structural heart disease, the remainder having "normal" left ventricles with either fasicular tachycardia or left ventricular ectopic tachycardia. RESULTS: Exit sites were demonstrated in 80 of 81 VT morphologies by the non-contact system, and complete VT circuits were traced in 17. In another 37 morphologies of VT 36 (30)% (mean (SD)) of the diastolic interval was identified. Thirty eight VT morphologies were ablated using 154 radiofrequency energy applications. Successful ablation was achieved by 77% of radiofrequency within diastolic activation identified by the non-contact system and was significantly more likely to ablate VT than radiofrequency at the VT exit, or remote from diastolic activation. Over a mean follow up of 1.5 years, 14 patients have had no recurrence of VT and only two target VTs have recurred. Five patients have had recurrence of either slower non-sustained, undocumented or fast non-target VT. Five patients have died, one from tamponade from a pre-existing temporary pacing wire, and four from causes unrelated to the procedure. CONCLUSION: The non-contact system can safely be used to map and ablate haemodynamically stable VT with low VT recurrence rates. It is yet to be established whether this system may be applied with equal success to patients with haemodynamically unstable VT.

Adult↗
PubMed1998

Simultaneous endocardial mapping in the human left ventricle using a noncontact catheter: comparison of contact and reconstructed electrograms during sinus rhythm.

BACKGROUND: Catheter ablation of ventricular tachycardia is limited in part by difficulty in identifying suitable sites for ablation. A noncontact multielectrode array (MEA) has been developed that allows reconstruction of 3360 electrograms, using inverse-solution mathematics, that are superimposed onto a computer-simulated model of the endocardium. This study assesses the accuracy of timing and morphology of reconstructed unipolar electrograms compared with contact unipolar electrograms from the same endocardial site. METHODS AND RESULTS: The MEA was deployed in the left ventricles of 13 patients (end-diastolic diameters, 61.7+/-8.4 mm [mean+/-SD]). We recorded contact electrograms at 76 points equatorial and 32 points nonequatorial to the MEA during sinus rhythm using a catheter-locator signal to record direction and distance from the MEA. Morphology (cross-correlation) and timing of maximum -dV/dt of contact and reconstructed electrograms were compared at different distances from the MEA center to endocardium (M-E) and from the MEA equatorial plane. For equatorial data, the M-E was 32.12+/-12.12 mm. The timing of reconstructed with respect to contact electrograms was -1.94+/-7.12 ms for M-E <34 mm and -14.16+/-19.29 ms at M-E >34 mm (P<0.001). Cross-correlation of electrograms was 0.87+/-0.12 (95% CI, 0.84 to 0.91) and 0.76+/-0.18 (95% CI, 0.69 to 0.83) for M-E <34 mm and >34 mm, respectively. Nonequatorial points were 32.33+/-10.81 mm (range, 16.9 to 55.6 mm) from the MEA equatorial plane; electrogram timing difference was -8.97+/-15.75 ms and was unrelated to this distance from the equator. CONCLUSIONS: This noncontact mapping system accurately reconstructs endocardial unipolar electrograms from the human left ventricle. At M-E distances >34 mm, timing accuracy of reconstruction decreases.

Adult↗
PubMed1998

Characteristics of the temporal and spatial excitable gap in anisotropic reentrant circuits causing sustained ventricular tachycardia.

The excitable gap of a reentrant circuit has both temporal (time during the cycle length that the circuit is excitable) and spatial (length of the circuit that is excitable at a given time) properties. We determined the temporal and spatial properties of the excitable gap in reentrant circuits caused by nonuniform anisotropy. Myocardial infarction was produced in canine hearts by ligation of the left anterior descending coronary artery. Four days later, reentrant circuits were mapped in the epicardial border zone of the infarcts with a multielectrode array during sustained ventricular tachycardia induced by programmed stimulation. During tachycardia, premature impulses were initiated by stimulation at sites around and in the reentrant circuits, and their conduction characteristics in the circuit were mapped. All circuits had a temporal excitable gap in at least part of the circuit, which allowed premature impulses to enter the circuit. Completely and partially excitable segments of the temporal gap were identified by measuring conduction velocity of the premature impulses; conduction was equal to the native reentrant wave front in completely excitable regions and slower than the reentrant wave front in partially excitable regions. In some circuits, a temporal gap existed throughout the circuit, permitting the entire circuit to be reset over a range of premature coupling intervals, although the size of the gap varied at different sites. In other circuits, the gap became so small at local sites that even though premature impulses could enter the circuit, the circuit could not be reset. Premature impulses could terminate reentry in circuits that could be reset or not. We also found a significant spatial gap, which was identified by determining the distance between the head of the circulating wave front, which could be located on the activation map, and its tail, which was the site most distal from the head as located by the site of entry of the premature wave front into the circuit. The spatial gap could also vary in different parts of the circuit. Therefore, nonuniform anisotropic reentrant circuits have both a temporal and spatial excitable gap with fully and partially excitable components that change in different parts of the circuit.

Animals↗
PubMed1998

Characteristics of sinus rhythm electrograms at sites of ablation of ventricular tachycardia relative to all other sites: a noncontact mapping study of the entire left ventricle.

INTRODUCTION: Regions of the diseased ventricle that activate abnormally during sinus rhythm (SR) may be the areas of slow and disorganized conduction that form the diastolic pathway through which reentry may occur during ventricular tachycardia (VT). METHODS AND RESULTS: We examined features of electrograms recorded during SR that might indicate a site suitable for ablation of VT using a noncontact mapping system, which enables reconstruction of > 3,000 electrograms. Preablation SR electrogram characteristics at sites of successful radiofrequency ablation (RFA) were examined in 13 patients with 53 VTs. Timing of onset, lateness of activity, electrogram duration, and number of baseline crossing events of reconstructed electrograms at the sites of successful RFA were compared with the electrograms of latest onset, latest activity, longest duration, and most baseline crossing events of all ventricular sites. Onset of activation at sites of successful RFA were 26.9+/-25.2 msec (mean +/- SD) earlier than (and 2.9+/-1.7 cm away from) the site of latest onset of SR activation. Electrogram duration at sites of successful RFA was 83%+/-14.6% of (and 4.3+/-1.8 cm away from) the longest electrogram. The baseline crossing events at sites of successful RFA were 53%+/-22% of (and 4.9+/-1.9 cm away from) the most fractionated electrogram. The latest activity at sites of successful RFA was 21.6+/-24.8 msec earlier than (and 4.3+/-1.6 cm away from) the site of latest activity. CONCLUSION: Although the site of latest onset of endocardial activation during SR proved to be the most sensitive indicator, the characteristics of SR electrograms did not usefully predict successful ablation sites.

Adult↗
PubMed1997

Mechanisms causing sustained ventricular tachycardia with multiple QRS morphologies: results of mapping studies in the infarcted canine heart.

BACKGROUND: Sustained reentrant ventricular tachycardias (VTs) with different QRS morphologies have been observed to occur spontaneously and during programmed stimulation in human hearts. We determined mechanisms that can cause tachycardias with multiple morphologies in a canine model of myocardial infarction by mapping reentrant circuits. METHODS AND RESULTS: Reentrant VT with multiple QRS morphologies was induced in 11 canine hearts with 4-day-old infarcts. Comparison of activation maps of the reentrant circuits in the epicardial border zone associated with each morphology indicated two basic mechanisms. Less frequently, VTs of different morphologies in the same heart were caused by reentrant circuits in different regions of the infarct. Most commonly, the reentrant circuits associated with different morphologies were in the same region. Three different factors caused different exit routes from circuits in the same region, leading to the multiple morphologies. (1) The reentrant wave front for each morphology rotated around the same line of block but in different directions. (2) Reentrant circuits associated with each morphology were similar, but there were small changes in the extent of the central line of block. (3) Reentrant circuits with completely different sizes and shapes caused different morphologies. CONCLUSIONS: In this canine model, tachycardias with multiple morphologies most commonly arise from reentrant circuits in the same region of the infarct, suggesting that most often only one area has electrophysiological properties necessary to sustain reentry.

Animals↗
PubMed1997

Disturbed connexin43 gap junction distribution correlates with the location of reentrant circuits in the epicardial border zone of healing canine infarcts that cause ventricular tachycardia.

BACKGROUND: Slow, nonuniform conduction caused by abnormal gap-junctional coupling of infarct-related myocardium is thought to be a component of the arrhythmogenic substrate. The hypothesis that changes in gap-junctional distribution in the epicardial border zone (EBZ) of healing canine infarcts define the locations of reentrant ventricular tachycardia (VT) circuits was tested by correlating activation maps of the surviving subepicardial myocardial layer with immunolocalization of the principal gap-junctional protein, connexin43 (Cx43). METHODS AND RESULTS: The EBZ overlying 4-day-old anterior infarcts in three dogs with inducible VT and three noninducible dogs was mapped with a high-resolution electrode array and systematically examined by standard histology and confocal immunolocalization of Cx43. The thickness of the EBZ was significantly less in the hearts with (538 +/- 257 microns) than without (840 +/- 132 microns; P < .05) VT. At the interface with the underlying necrotic cells, the EBZ myocardium showed a marked disruption of gap-junctional distribution, with Cx43 labeling abnormally arrayed longitudinally along the lateral surfaces of the cells. In the EBZ of all hearts, the disrupted Cx43 labeling extended part of the way to the epicardial surface, with the most superficial epicardial myocytes having the normal transversely orientated pattern. Only in the hearts with inducible VT did the disorganization extend through the full thickness of the surviving layer at sites correlating with the location of the central common pathways of the figure-of-8 reentrant VT circuits. CONCLUSIONS: Altered gap-junctional distribution is part of the early remodeling of myocardium after infarction, and by defining the location of the common central pathway of the reentrant VT circuits, it may be a determinant of VT susceptibility.

Animals↗
PubMed1996

17-beta-Estradiol therapy lessens angina in postmenopausal women with syndrome X.

OBJECTIVES: We sought to investigate the hypothesis that estrogen replacement therapy ameliorates symptoms in postmenopausal women with syndrome X. BACKGROUND: Syndrome X (angina pectoris, positive findings on exercise electrocardiography and normal results on coronary angiography) frequently occurs in menopausal women. This observation, in conjunction with the known vasoactive properties of estrogens, suggests that estrogen depletion may contribute to the pathogenesis of syndrome X in some women. METHODS: Twenty-five postmenopausal patients with syndrome X completed a double-blind, placebo-controlled study of the effect of 17-beta-estradiol cutaneous patches (100 micrograms/24 h) on the frequency of chest pain and on exercise tolerance. Patients were randomly assigned to receive either placebo or 17-beta-estradiol patches for 8 weeks and were then crossed over to the other treatment. RESULTS: During the placebo phase, patients had a mean of 7.3 episodes of chest pain/10 days. A reduction to 3.7 episodes/10 days was observed during the 17-beta-estradiol phase (p < 0.05). No significant differences were observed between the effects of 17-beta-estradiol and placebo on exercise duration or the results of other cardiologic investigations. CONCLUSIONS: Estrogen replacement reduces the frequency of chest pain and may be a useful new therapeutic option for treating postmenopausal women with syndrome X.

Cross-Over Studies↗
PubMed1996

New insights into myocardial arrhythmogenesis: distribution of gap-junctional coupling in normal, ischaemic and hypertrophied human hearts.

1. Ischaemic and hypertrophic heart diseases are associated with ventricular arrhythmias, in which abnormal cellular coupling is implicated as having a causative role. The aim of this series of studies was to characterize gap-junctional organization in normal human ventricular myocardium, and to investigate the hypothesis that alterations in the quantity and patterns of expression of myocardial gap junctions occur in ischaemic and hypertrophic myocardial disease. 2. An antibody raised against connexin43 was used for immunohistochemical labelling of myocardium examined by confocal laser scanning microscopy, permitting highly sensitive and quantifiable immunofluorescent imaging of gap junctions through volumes of intact cardiac tissue. 3. Connexin43 gap junctions in normal adult human ventricular myocardium are highly organized into clusters of fluorescent label confined to the intercalated disks as a peripheral ring of larger junctions, with smaller junctions centrally, and occupy a surface area of 0.005 micron2/micron3 myocyte volume. 4. Neonatal human myocardium has a punctate distribution of connexin43 over the entire surface of the ventricular myocytes, with a progressive polarization of the gap junctions towards the positions of the mature intercalated disks, reaching the adult pattern at about 6 years. 5. At the myocardial interface with the scar of a healed infarct, connexin43 gap junction distribution is grossly disturbed, being strewn in longitudinally orientated arrays along the lateral interfaces between degenerated but viable myocytes, which may be due to a redistribution of the pre-existing population of junctions. This altered distribution is present as early as 4 days after coronary occlusion in a canine model, in which it defines the location of circuits causing ventricular tachycardia. 6. Myocardium distant from infarction in patients with ischaemic heart disease has a normal pattern of connexin43 gap junction distribution, but has a 47% reduction in gap junction surface area per unit cell volume, and a 30% reduction per cell. 7. In hypertrophied myocardium from chronically pressure-loaded human left ventricles, connexin43 gap junction expression per myocyte is not significantly different from normal, but is reduced by 40% per unit volume of myocyte. 8. The early phases of the hypertrophic response of myocardium to renovascular hypertension in guinea pigs revealed a substantially increased connexin43 gap junction expression compared with controls, both when measured per cell (increased by 45%) and per unit volume of myocyte (increased by 30%), and therefore showed an alteration apparently contrary to that observed in chronically hypertrophied human ventricular myocardium. 9. In this series of studies, normal adult human ventricular myocardium and the post-natal developmental changes have been characterized with respect to connexin43 gap junction content, and the observed alterations of both distribution and quantity in ischaemic and hypertrophied hearts would be expected to influence myocardial conduction and the arrhythmogenic substrate.

Adult↗
PubMed1995

Myocardial gap junction organization in ischemia and infarction.

Ischemia causes an increase in myocardial resistivity and a decrease in conduction velocity, thereby enhancing cardiac contractile dysfunction and arrhythmic tendency. Myocardial gap junctions, as principal determinants of conduction velocity, may, therefore, be expected to be deranged in ischemia. Despite a lack of consensus, attempts at correlating gap junction ultrastructural morphology with functional state have revealed the component connexons of gap junctions in freeze-fractured myocardium to be in multiple small hexagonal arrays, tending to become randomly distributed and compacted under uncoupling conditions. Further hypoxic uncoupling causes ultrastructural damage and a reduction in gap-junctional surface area. Immunohistochemical detection of connexin43 gap junctions in chronically ischemic non-infarcted human myocardium demonstrates a reduction in junctional surface area within a normal number of intercalated disks per myocyte, and with a normal distribution of junction sizes. In healed canine infarction there are smaller and fewer gap junctions in the fibrotic myocardium adjacent to infarcts, with reductions in overall gap-junctional content and the proportion of side-to-side vs. end-to-end intercellular connections. Immunohistochemical examination of intact human ventricular myocardium shows the myocytes immediately abutting healed infarcts to have connexin43 gap junctions spread longitudinally over the cell surfaces, and not in discrete transversely orientated intercalated disks as in normal myocardium. Early after canine infarction, and before fibrotic healing, the connexin43 gap junctions in myocytes abutting the infarct show disorganization similar to that described in healed human infarcts, suggesting that this disturbance is an early pathophysiological cellular response, and not simply due to later fibrotic distortion. Such changes in gap-junctional organization in myocardial ischemia and infarction may be implicated in the elusive link between subcellular structure, contractile dysfunction and arrhythmogenesis.

Animals↗