Transmural “Scar-to-Scar” Reentrant Ventricular Tachycardia

We describe a scar-related reentrant ventricular tachycardia circuit with a proximal segment in an endocardial basal septal scar and an exit in a region of slow conduction in a non-overlapping region of epicardial basal lateral scar. The 12-lead EKG demonstrates criteria for a basal lateral epicardial VT, however the same morphology could be produced with a longer stim-latency with pace mapping or VT induction from the endocardial septal region of scar. A significant segment of myocardium demonstrated no endocardial or epicardial scar on electroanatomic mapping, suggesting the presence of a mid-myocardial isthmus. Further evidence was provided by assessment of unipolar settings. The epicardial VT that initially appeared to originate from the basal lateral epicardial region, was successfully treated with radiofrequency ablation of the lateral aspect of the endocardial septal scar.     

Substrate Based Ablation of Ventricular Tachycardia Through An Epicardial Approach

Ventricular tachycardia (VT) occurring late after myocardial infarction is often due to reentry circuit in the peri-infarct zone. The circuit is usually located in the sub-endocardium, though subepicardial substrates are known. Activation mapping during VT to identify target regions for ablation can be difficult if VT is non inducible or poorly tolerated. In the latter, a substrate based approach of mapping during sinus rhythm in conjunction with pace mapping helps to define the reentry circuit and select target sites for ablation in majority of patients with hemodynamically unstable VT. Percutaneous epicardial catheter ablation has been attempted as an approach where ablation by a conventional endocardial access has been unsuccessful. We report a case of post myocardial infarction scar VT which could be successfully ablated with a substrate based approach from the epicardial aspect.     

Structural Heterogeneity Modulates Effective Refractory Period: A Mechanism of Focal Arrhythmia Initiation

Reductions in electrotonic loading around regions of structural and electrophysiological heterogeneity may facilitate capture of focal triggered activity, initiating reentrant arrhythmias. How electrotonic loading, refractoriness and capture of focal ectopics depend upon the intricate nature of physiological structural anatomy, as well as pathological tissue remodelling, however, is not well understood. In this study, we performed computational bidomain simulations with anatomically-detailed models representing the rabbit left ventricle. We used these models to quantify the relationship between local structural anatomy and spatial heterogeneity in action potential (AP) characteristics, electrotonic currents and effective refractory periods (ERPs) under pacing and restitution protocols. Regions surrounding vessel cavities, in addition to tissue surfaces, had significantly lower peak downstream electrotonic currents than well coupled myocardium ( vs A/cm²), with faster maximum AP upstroke velocities ( vs mV/ms), although noticeably very similar APDs ( vs ms) and AP restitution properties. Despite similarities in APDs, ERPs in regions of low electrotonic load in the vicinity of surfaces, intramural vessel cavities and endocardial structures were up to ms shorter compared to neighbouring well-coupled tissue, leading to regions of sharp ERP gradients. Consequently, focal extra-stimuli timed within this window of ERP heterogeneity between neighbouring regions readily induced uni-directional block, inducing reentry. Most effective induction sites were within channels of low ERPs between large vessels and epicardium. Significant differences in ERP driven by reductions in electrotonic loading due to fine-scale physiological structural heterogeneity provides an important mechanism of capture of focal activity and reentry induction. Application to pathological ventricles, particularly myocardial infarction, will have important implications in anti-arrhythmia therapy.     

Premature excitation and onset of reentrant ventricular tachycardia

It was hypothesized that quantitative sinus rhythm electrogram measurements could be used to predict conduction events that result from premature stimulation and reentrant ventricular tachycardia inducibility. Sinus rhythm activation and electrogram-duration maps were constructed from bipolar electrograms acquired at 196-312 sites in the epicardial border zone of 43 canine hearts (25 with and 18 without reentrant ventricular tachycardia inducible by premature stimulation). From these maps, lines of electrical discontinuity, where blocks would occur during premature excitation, were estimated. The mean error in distance between the estimated and actual block lines of premature excitation was 0.97 +/- 0.49 cm. Based on the quantitative characteristics of the activation and electrogram-duration maps and the longest block line that formed during premature excitation, it was possible to predict whether reentry would occur (sensitivity, 94.7%; specificity, 79.6%). In reentry experiments, the breakthrough-point location along the unidirectional arc of the block that initiated reentry was also predictable (mean error, 0.79 +/- 0.19 cm). Sinus rhythm measurements are useful to predict conduction events that result from premature stimulation and reentry inducibility.     

Left ventricular endocardial or triventricular pacing to optimize cardiac resynchronization therapy in a chronic canine model of ischemic heart failure

Cardiac resynchronization therapy (CRT) is a proven treatment for heart failure but ~30% of patients appear to not benefit from the therapy. Left ventricular (LV) endocardial and multisite epicardial [triventricular (TriV)] pacing have been proposed as alternatives to traditional LV transvenous epicardial pacing, but no study has directly compared the hemodynamic effects of these approaches. Left bundle branch block ablation and repeated microembolizations were performed in dogs to induce electrical dysynchrony and to reduce LV ejection fraction to <35%. LVdP/dt(max) and other hemodynamic indexes were measured with a conductance catheter during LV epicardial, LV endocardial, biventricular (BiV) epicardial, BiV endocardial, and TriV pacing performed at three atrioventricular delays. LV endocardial pacing was obtained with a clinically available pacing system. The optimal site was defined as the site that increased dP/dt(max) by the largest percentage. Implantation of the endocardial lead was feasible in all canines (n = 8) without increased mitral regurgitation seen with transesophageal echocardiography and with full access to the different LV endocardial pacing sites. BiV endocardial pacing increased dP/dt(max) more than BiV epicardial and TriV pacing on average (P < 0.01) and at the optimal site (P < 0.01). There were no significant differences between BiV epicardial and TriV pacing. BiV endocardial pacing was superior to BiV epicardial and to TriV pacing in terms of acute hemodynamic response. Further investigation is needed to confirm the chronic benefit of this approach in humans.     

Low Energy Defibrillation in Human Cardiac Tissue: A Simulation Study

We aim to assess the effectiveness of feedback-controlled resonant drift pacing as a method for low energy defibrillation. Antitachycardia pacing is the only low energy defibrillation approach to have gained clinical significance, but it is still suboptimal. Low energy defibrillation would avoid adverse side effects associated with high voltage shocks and allow the application of implantable cardioverter defibrillator (ICD) therapy, in cases where such therapy is not tolerated today. We present results of computer simulations of a bidomain model of cardiac tissue with human atrial ionic kinetics. Reentry was initiated and low energy shocks were applied with the same period as the reentry, using feedback to maintain resonance. We demonstrate that such stimulation can move the core of reentrant patterns, in the direction that depends on the location of the electrodes and the time delay in the feedback. Termination of reentry is achieved with shock strength one-order-of-magnitude weaker than in conventional single-shock defibrillation. We conclude that resonant drift pacing can terminate reentry at a fraction of the shock strength currently used for defibrillation and can potentially work where antitachycardia pacing fails, due to the feedback mechanisms. Success depends on a number of details that these numerical simulations have uncovered.     

Transmural reentry during acute global ischemia and reperfusion in canine ventricular muscle

Coronary occlusion and reperfusion produce tachyarrhythmias. We tested the hypothesis that variations in transmural activation after global ischemia and reperfusion were responsible for arrhythmias. We arterially perfused 36 isolated transmural wedges from canine left ventricular free walls. After > or =100 min of stabilization, the artery was occluded for 25 min, followed by reperfusion at various flow rates. We recorded 256 channels of fluorescent action potentials on transmural surfaces from preocclusion to >15 min after reperfusion. During endocardial pacing at 300 ms, ischemia of > or =570 +/- 165 s (n = 34) produced 1:1 endocardial conduction and then 2:1 and 4:1 block as the wave fronts conducted toward epicardium. Transmural reentry appeared after 535 +/- 146 s of ischemia (n = 31). Further ischemia caused epicardial inactivation and eliminated reentry (n = 24). During reperfusion, tissues progressed through sequences of epicardial inactivation and reappearance of activation with 1:1, 2:1, and 4:1 conduction; both sustained and nonsustained reentry occurred. We conclude that heterogeneous activation responses to endocardial pacing during acute ischemia provide the substrate for initiating reentry, suppressed reentry during further ischemia, and caused reentry during reperfusion.     

QTc dispersion as a novel marker in identifying patients requiring an epicardial approach for ablation of scar mediated ventricular tachycardia

IntroductionEpicardial exit sites of ventricular tachycardia (VT) are frequently encountered during VT ablation requiring an epicardial ablation approach for successful elimination of VT. We sought to assess the utility of repolarization markers in identifying individuals requiring an epicardial ablation approach in addition to an endocardial approach.Methods32 patients who underwent successful ablation for scar mediated VT were included in the study. Fourteen patients who required a combined endocardial and epicardial VT ablation were defined as epicardial VT group (Epi) whereas 18 patients who were successfully ablated from the endocardium alone constituted the endocardial VT group (Endo). Repolarization markers during sinus rhythm were compared between the two groups.ResultsA higher QTc max and QTc dispersion were seen in the Epi group compared to Endo group (479 ± 34 vs 449 ± 20, p = 0.008 and 63 ± 13 vs 38 ± 8, p = 0.001, respectively). Ts-p and Ts-p/Tp-e were higher in the Epi group (166 ± 23 vs 143 ± 23, p = 0.008 and 1.55 ± 0.26 vs 1.3 ± 0.21, p < 0.005). On multivariate regression, QTc dispersion was an independent predictor of the need for an epicardial approach to ablation. A QTc dispersion more than 51.5 msec identified individuals requiring a combined epicardial and endocardial approach to ablation with a sensitivity of 92.9% and a specificity of 100%.ConclusionsPatients requiring an epicardial ablation have a higher QTc dispersion. A value greater than 51.5 msec reliably differentiates between the two groups with high sensitivity and specificity.     

Vulnerability in simulated ischemic ventricular transmural tissues

Vulnerability is an effective index to evaluate increased risk for unidirectional conduction block and reentry in hearts. Recent reports in animal experiments have indicated an opposite characteristics of the vulnerability in normal and ischemic transmural tissues. In order to clarify the differences and to investigate the mechanisms, a computer simulation method was used in this study to investigate the vulnerability relative to the premature pacing sites in normal and ischemic transmural tissues. Endo-, mid- and epi-cardial myocytes incorporating different severities of ischemia were developed across a tissue strand. The sodium channel inactivation gating variable h was calculated to provide the degree of sodium current recovery preceding the premature pacing. In the normal tissue, the measured vulnerable window was demonstrated to be wider by delivering an endocardial premature beat than that by applying an epicardial premature pacing. On the contrary, during ischemia the epicardium showed a wider vulnerable window than the endocardium. The results illustrated that during ischemia h decreased with accumulation of [K?]o, and action potential duration dispersion was obviously altered due to anoxia. In contrast, the elevated [K?]o was suggested to play an important role in the difference of the location-dependent vulnerability in normal and ischemic tissues.     

What are the post-ablation insular residual electrograms in the posterior left pulmonary veins electrically connected to?

A 67-year-old man underwent a third ablation procedure for a recurrent atrial tachycardia (AT) after an extensive pulmonary vein (PV) isolation, linear ablation along the left atrial (LA) roof and posterolateral mitral isthmus (MI), and defragmentation of persistent atrial fibrillation and an induced perimitral AT. High-resolution mapping during the clinical AT using the Rhythmia system (Boston Scientific) suggested that the AT was a ridge-related reentrant AT and exhibited a reconnection of the left PVs (LPVs). The residual electrograms in the posterior LPVs were surrounded by endocardial scar, which was like an island consisting of residual LPV electrograms. Retrograde venography of the vein of Marshall (VOM) demonstrated that the VOM reached the posterior left superior PV through the ridge between the LA appendage and left inferior PV and then the LPV carina. An ethanol infusion into the VOM resulted in a simultaneous AT termination and complete electrical isolation of the LPVs, that is, the disappearance of the residual LPV electrograms. The insular residual LPV electrograms in the present case did not appear to be endocardially connected to the LA, because the LPV electrograms were surrounded by endocardial scar and there was a large time gap between the earliest activation in the posterior LPVs and activation in the surrounding area. The VOM course on the venography and elimination of the residual LPV electrograms with an ethanol infusion into the VOM suggested that the insular residual LPV electrograms were electrically connected to the posterolateral LA via the VOM and its branches.     

Three-dimensional endocardial impedance mapping: a new approach for myocardial infarction assessment

Precise identification of infarcted myocardial tissue is of importance in diagnostic and interventional cardiology. A three-dimensional, catheter-based endocardial electromechanical mapping technique was used to assess the ability of local endocardial impedance in delineating the exact location, size, and border of canine myocardial infarction. Electromechanical mapping of the left ventricle was performed in a control group (n = 10) and 4 wk after left anterior descending coronary artery ligation (n = 10). Impedance, bipolar electrogram amplitude, and endocardial local shortening (LS) were quantified. The infarcted area was compared with the corresponding regions in controls, revealing a significant reduction in impedance values [infarcted vs. controls: 168.8 +/- 11. 7 and 240.7 +/- 22.3 Omega, respectively (means +/- SE), P < 0.05] bipolar electrogram amplitude (1.8 +/- 0.2 mV, 4.4 +/- 0.7 mV, P < 0. 05), and LS (-2.36 +/- 1.6%, 11.9 +/- 0.9%, P < 0.05). The accuracy of the impedance maps in delineating the location and extent of the infarcted region was demonstrated by the high correlation with the infarct area (Pearson's correlation coefficient = 0.942) and the accurate identification of the infarct borders in pathology. By accurately defining myocardial infarction and its borders, endocardial impedance mapping may become a clinically useful tool in differentiating healthy from necrotic myocardial tissue.     

Haemodynamic evaluation of alternative left ventricular endocardial pacing sites in clinical non-responders to cardiac resynchronisation therapy

Introduction

Non response to cardiac resynchronisation therapy (CRT) may be related to the position of the coronary sinus lead.

Methods

We studied the acute haemodynamic response (AHR) from alternative left ventricular (LV) endocardial pacing sites in clinical non-responders to CRT. AHR and the interval from QRS onset to LV sensing (Q-LV interval) from four different endocardial pacing sites were evaluated in 24 clinical non-responders. A rise in LVdP/dtmax ≥ 15 % from baseline was considered a positive AHR. We also compared the AHR from endocardial with the corresponding epicardial lead position.

Results

The implanted system showed an AHR ≥ 15 % in 5 patients. In 9 of the 19 remaining patients, AHR could be elevated to ≥ 15 % by endocardial LV pacing. The optimal endocardial pacing site was posterolateral. There was no significant difference in AHR between the epicardial and the corresponding endocardial position. The longest Q-LV interval corresponded with the best AHR in 12 out of the 14 patients with a positive AHR, with an average Q-LV/QRS width ratio of 90 %.

Conclusions

Acute haemodynamic testing may indicate an alternative endocardial pacing site with a positive AHR in clinical non-responders. The Q-LV interval is a strongly correlated with the optimal endocardial pacing site. Endocardial pacing opposite epicardial sites does not result in a better AHR.     

Epicardial and intramural excitation during ventricular pacing: effect of myocardial structure

Published studies show that ventricular pacing in canine hearts produces three distinct patterns of epicardial excitation: elliptical isochrones near an epicardial pacing site, with asymmetric bulges; areas with high propagation velocity, up to 2 or 3 m/s and numerous breakthrough sites; and lower velocity areas (<1 m/s), where excitation moves across the epicardial projection of the septum. With increasing pacing depth, the magnitude of epicardial potential maxima becomes asymmetric. The electrophysiological mechanisms that generate the distinct patterns have not been fully elucidated. In this study, we investigated those mechanisms experimentally. Under pentobarbital anesthesia, epicardial and intramural excitation isochrone and potential maps have been recorded from 22 exposed or isolated dog hearts, by means of epicardial electrode arrays and transmural plunge electrodes. In five experiments, a ventricular cavity was perfused with diluted Lugol solution. The epicardial bulges result from electrotonic attraction from the helically shaped subepicardial portions of the wave front. The high-velocity patterns and the associated multiple breakthroughs are due to involvement of the Purkinje network. The low velocity at the septum crossing is due to the missing Purkinje involvement in that area. The asymmetric magnitude of the epicardial potential maxima and the shift of the breakthrough sites provoked by deep stimulation are a consequence of the epi-endocardial obliqueness of the intramural fibers. These results improve our understanding of intramural and epicardial propagation during premature ventricular contractions and paced beats. This can be useful for interpreting epicardial maps recorded at surgery or inversely computed from body surface ECGs.     

Virtual Electrophysiological Study of Atrial Fibrillation in Fibrotic Remodeling

Research has indicated that atrial fibrillation (AF) ablation failure is related to the presence of atrial fibrosis. However it remains unclear whether this information can be successfully used in predicting the optimal ablation targets for AF termination. We aimed to provide a proof-of-concept that patient-specific virtual electrophysiological study that combines i) atrial structure and fibrosis distribution from clinical MRI and ii) modeling of atrial electrophysiology, could be used to predict: (1) how fibrosis distribution determines the locations from which paced beats degrade into AF; (2) the dynamic behavior of persistent AF rotors; and (3) the optimal ablation targets in each patient. Four MRI-based patient-specific models of fibrotic left atria were generated, ranging in fibrosis amount. Virtual electrophysiological studies were performed in these models, and where AF was inducible, the dynamics of AF were used to determine the ablation locations that render AF non-inducible. In 2 of the 4 models patient-specific models AF was induced; in these models the distance between a given pacing location and the closest fibrotic region determined whether AF was inducible from that particular location, with only the mid-range distances resulting in arrhythmia. Phase singularities of persistent rotors were found to move within restricted regions of tissue, which were independent of the pacing location from which AF was induced. Electrophysiological sensitivity analysis demonstrated that these regions changed little with variations in electrophysiological parameters. Patient-specific distribution of fibrosis was thus found to be a critical component of AF initiation and maintenance. When the restricted regions encompassing the meander of the persistent phase singularities were modeled as ablation lesions, AF could no longer be induced. The study demonstrates that a patient-specific modeling approach to identify non-invasively AF ablation targets prior to the clinical procedure is feasible.     

Computer simulation of the reentrant cardiac arrhythmias in ischemic myocardium

Computer simulation was performed to determine how reentrant activity could occur due to the spatial heterogeneity in refractoriness induced by the regional ischemia. Two regional ischemic models were developed by decreasing the intracellular ATP concentration, reducing conductance of the inward Na+ current and increasing the extracellular K+ concentration on the two-dimensional sheet. Operator splitting method was used to integrate the models. The vulnerability to reentry was estimated from the timings of premature stimuli on the constructed models, which could result in unidirectionally propagating action potentials. Two kinds of sustained spiral waves and their Pseudo-Electroscardiograms were observed in numerical simulation. The results showed that the dispersion of refractory period increased with ischemic aggravation, and led to augment of the vulnerable window. A permature stimulation within the vulnerable window could easily induce spiral reentry. The Pseudo-Electrocardiograms of the spiral waves exhibited monomorphic tachycardiac waveforms. Thus, the spatial heterogeneity in refractoriness could be a substrate for reentrant ventricular tachyarrhythmias on the regional ischemic tissue.     

经食道心房调搏术及食道心电图在心律失常中的应用

目的:分析经食道心房调搏术(TEAP)及食道内心电图(EECG)在心律失常中的应用价值。方法:选取2018年6月至2019年12月于我院行食道心电图及经食道调搏的患者189例,其中男80例,女109例,年龄11~83岁。结果:54例为房室结折返性心动过速(AVNRT),34例为房室折返性心动过速(AVRT),8例为房性心动过速(AT),4例为心房扑动(AF),6例为心房颤动(Af),5例为室性心过速,78例为室早或其他。共105例心律失常患者拟行食道心房调搏终止心动过速,所有AVNRT和AVRT患者及17例AT患者经食道心房调搏S1S1成功转为窦律,50例AVNRT、32例AVRT、6例AT、3例AF及2例VT患者通过射频消融术成功根治。其中1例11岁AT患者因无法耐受食道调搏,未能转为窦律,患者经静推普罗帕酮后次日转为窦律。共97例患者拟行食道心房调搏诱发,共49例诱发出心动过速,1例左后分支型室速经静滴异丙肾上腺素后诱发心动过速,且仍需静滴异丙肾上腺素后经心房食道调博终止心动过速,后经射频消融术成功根治。结论:TEAP及EECG可用于复杂心律失常的诊断及治疗,是一种相对安全、临床容易掌握的技术,值得推广。     

Clinical Experience with the Elema Vario Pacemaker

Early problems after implantation of an endocardial electrode for permanent pacing occur in many patients. Difficulties can be anticipated in many of these patients and their management made much easier by a knowledge of the daily endocardial threshold obtained in patients with an implanted Elema Verio pacing unit by a simple non-invasive technique using a magnet and electrocardiogram. Twenty patients are described in whom permanent pacing with an Elema Vario unit was undertaken. The practical advantages of this unit can be readily seen in the patient who developes exit block or in the patient with obstructive airways disease, in whom frequent coughing or right ventricular hypertrophy may make stable electrode placement difficult. The chief advantage of the Elema Vario pacemaker is the extreme simplicity with which knowledge of the endocardial threshold can be obtained.     

Electrotonic myofibroblast-to-myocyte coupling increases propensity to reentrant arrhythmias in two-dimensional cardiac monolayers

In pathological conditions such as ischemic cardiomyopathy and heart failure, differentiation of fibroblasts into myofibroblasts may result in myocyte-fibroblast electrical coupling via gap junctions. We hypothesized that myofibroblast proliferation and increased heterocellular coupling significantly alter two-dimensional cardiac wave propagation and reentry dynamics. Co-cultures of myocytes and myofibroblasts from neonatal rat ventricles were optically mapped using a voltage-sensitive dye during pacing and sustained reentry. The myofibroblast/myocyte ratio was changed systematically, and junctional coupling of the myofibroblasts was reduced or increased using silencing RNAi or adenoviral overexpression of Cx43, respectively. Numerical simulations in two-dimensional models were used to quantify the effects of heterocellular coupling on conduction velocity (CV) and reentry dynamics. In both simulations and experiments, reentry frequency and CV diminished with larger myofibroblast/myocyte area ratios; complexity of propagation increased, resulting in wave fractionation and reentry multiplication. The relationship between CV and coupling was biphasic: an initial decrease in CV was followed by an increase as heterocellular coupling increased. Low heterocellular coupling resulted in fragmented and wavy wavefronts; at high coupling wavefronts became smoother. Heterocellular coupling alters conduction velocity, reentry stability, and complexity of wave propagation. The results provide novel insight into the mechanisms whereby electrical myocyte-myofibroblast interactions modify wave propagation and the propensity to reentrant arrhythmias.     

Noninvasive three-dimensional electrocardiographic imaging of ventricular activation sequence

Imaging the myocardial activation sequence is critical for improved diagnosis and treatment of life-threatening cardiac arrhythmias. It is desirable to reveal the underlying cardiac electrical activity throughout the three-dimensional (3-D) myocardium (rather than just the endocardial or epicardial surface) from noninvasive body surface potential measurements. A new 3-D electrocardiographic imaging technique (3-DEIT) based on the boundary element method (BEM) and multiobjective nonlinear optimization has been applied to reconstruct the cardiac activation sequences from body surface potential maps. Ultrafast computerized tomography scanning was performed for subsequent construction of the torso and heart models. Experimental studies were then conducted, during left and right ventricular pacing, in which noninvasive assessment of ventricular activation sequence by means of 3-DEIT was performed simultaneously with 3-D intracardiac mapping (up to 200 intramural sites) using specially designed plunge-needle electrodes in closed-chest rabbits. Estimated activation sequences from 3-DEIT were in good agreement with those constructed from simultaneously recorded intracardiac electrograms in the same animals. Averaged over 100 paced beats (from a total of 10 pacing sites), total activation times were comparable (53.3 +/- 8.1 vs. 49.8 +/- 5.2 ms), the localization error of site of initiation of activation was 5.73 +/- 1.77 mm, and the relative error between the estimated and measured activation sequences was 0.32 +/- 0.06. The present experimental results demonstrate that the 3-D paced ventricular activation sequence can be reconstructed by using noninvasive multisite body surface electrocardiographic measurements and imaging of heart-torso geometry. This new 3-D electrocardiographic imaging modality has the potential to guide catheter-based ablative interventions for the treatment of life-threatening cardiac arrhythmias.     

Use of endogenous NADH fluorescence for real-time in situ visualization of epicardial radiofrequency ablation lesions and gaps

Radiofrequency ablation (RFA) aims to produce lesions that interrupt reentrant circuits or block the spread of electrical activation from sites of abnormal activity. Today, there are limited means for real-time visualization of cardiac muscle tissue injury during RFA procedures. We hypothesized that the fluorescence of endogenous NADH could be used as a marker of cardiac muscle injury during epicardial RFA procedures. Studies were conducted in blood-free and blood-perfused hearts from healthy adult Sprague-Dawley rats and New Zealand rabbits. Radiofrequency was applied to the epicardial surface of the heart using a 4-mm standard blazer ablation catheter. A dual camera optical mapping system was used to monitor NADH fluorescence upon ultraviolet illumination of the epicardial surface and to record optical action potentials using the voltage-sensitive probe RH237. Epicardial lesions were seen as areas of low NADH fluorescence. The lesions appeared immediately after ablation and remained stable for several hours. Real-time monitoring of NADH fluorescence allowed visualization of viable tissue between the RFA lesions. Dual recordings of NADH and epicardial electrical activity linked the gaps between lesions to postablation reentries. We found that the fluorescence of endogenous NADH aids the visualization of injured epicardial tissue caused by RFA. This was true for both blood-free and blood-perfused preparations. Gaps between NADH-negative regions revealed unablated tissue, which may promote postablation reentry or provide pathways for the conduction of abnormal electrical activity.