Epicardial Electrograms Research Articles

Comparative Evaluation of Methodologies for T-Wave Alternans Mapping in Electrograms

Electrograms (EGM) recorded from the surface of the myocardium are becoming more and more accessible. T-wave alternans (TWA) is associated with increased vulnerability to ventricular tachycardia/fibrillation and it occurs before the onset of ventricular arrhythmias. Thus, accurate methodologies for time-varying alternans estimation/detection in EGM are needed. In this paper, we perform a simulation study based on epicardial EGM recorded in vivo in humans to compare the accuracy of four methodologies: the spectral method (SM), modified moving average method, laplacian likelihood ratio method (LLR), and a novel method based on time-frequency distributions. A variety of effects are considered, which include the presence of wide band noise, respiration, and impulse artifacts. We found that 1) EGM-TWA can be detected accurately when the standard deviation of wide-band noise is equal or smaller than ten times the magnitude of EGM-TWA. 2) Respiration can be critical for EGM-TWA analysis, even at typical respiratory rates. 3) Impulse noise strongly reduces the accuracy of all methods, except LLR. 4) If depolarization time is used as a fiducial point, the localization of the T-wave is not critical for the accuracy of EGM-TWA detection. 5) According to this study, all methodologies provided accurate EGM-TWA detection/quantification in ideal conditions, while LLR was the most robust, providing better detection-rates in noisy conditions. Application on epicardial mapping of the in vivo human heart shows that EGM-TWA has heterogeneous spatio-temporal distribution.

Arrhythmia susceptibility in senescent rat hearts

Cardiovascular disease increases with age as well as alterations of cardiac electrophysiological properties, but a detailed knowledge about changes in cardiac electrophysiology relevant to arrhythmogenesis in the elderly is relatively lacking. The aim of this study was to determine specific age-related changes in electrophysiological properties of the ventricles which can be related to a structural-functional arrhythmogenic substrate. Multiple epicardial electrograms were recorded on the ventricular surface of in vivo control and aged rats, while arrhythmia vulnerability was investigated by premature stimulation protocols. Single or multiple ectopic beats and sustained ventricular arrhythmias were frequently induced in aged but not in control hearts. Abnormal ventricular activation patterns during sinus rhythm and unchanged conduction velocity during point stimulation in aged hearts suggest the occurrence of impaired impulse conduction through the distal Purkinje system that might create a potential reentry substrate.

Cardiac Arrythmias: Multimodal Assessment Integrating Body Surface ECG Mapping into Cardiac Imaging

To demonstrate the feasibility of comprehensive assessment of cardiac arrhythmias by combining body surface electrocardiographic (ECG) mapping (BSM) and imaging. This study was approved by the institutional review board, and all patients gave written informed consent. Twenty-seven patients referred for electrophysiologic procedures in the context of ventricular tachycardia (VT) (n = 9), Wolff-Parkinson-White (WPW) syndrome (n = 2), atrial fibrillation (AF) (n = 13), or scar-related ventricular fibrillation (VF) (n = 3) were examined. Patients underwent BSM and imaging with multidetector computed tomography (CT) (n = 12) and/or delayed enhanced magnetic resonance (MR) imaging (n = 23). BSM was performed by using a 252-electrode vest that enabled the computation of epicardial electrograms from body surface potentials. The epicardial geometry used for BSM was registered to the epicardial geometry segmented from imaging data by using an automatic algorithm. The output was a three-dimensional cardiac model that integrated cardiac anatomy, myocardial substrate, and epicardial activation. Acquisition, segmentation, and registration were feasible in all patients. In VT, this enabled a noninvasive assessment of the arrhythmia mechanism and its location with respect to the myocardial substrate, coronary vessels, and phrenic nerve. In WPW syndrome, this enabled understanding of complex accessory pathways resistant to previous ablation. In AF and VF, this enabled the noninvasive assessment of arrhythmia mechanisms and the analysis of rotor trajectories with respect to the myocardial substrate. In all patients, models were successfully integrated in navigation systems and used to guide mapping and ablation. By combining information on anatomy, substrate, and electrical activation, the fusion of BSM and imaging enables comprehensive noninvasive assessment of cardiac arrhythmias, with potential applications for diagnosis, prognosis, and ablation targeting. Online supplemental material is available for this article.

Left ventricular epicardial electrogram recordings in idiopathic ventricular fibrillation with inferior and lateral early repolarization

Introduction Early repolarization syndrome (ERS) is a primary electrical disease characterized by early repolarization (ER) in the surface ECG and an increased risk of sudden cardiac death because of VF. Experimental studies have suggested that a prominent transient outward current-mediated action potential notch in epicardial cells creates a transmural voltage gradient that results in ER in ERS. Ghosh et al studied 2 patients with idiopathic VF and ER by using noninvasive electrocardiographic imaging and demonstrated that their depolarization was normal (homogeneous) but their repolarization was indeed “early” (premature) in some areas that were adjacent to normal repolarizing zones. However, no clinical study has yet been reported that has directly recorded and examined an epicardial electrogram of the LV in patients with ERS. We observed that patients with Brugada syndrome (BrS) have a prominent potential after the QRS complex and have prolonged repolarization in the epicardium at the right ventricular outflow tract (RVOT), but not in the endocardium. Here, we report the first EPS of ERS in which LV epicardial electrogram recording was performed.

Direct Comparison of Adjacent Endocardial and Epicardial Electrograms: Implications for Substrate Mapping

BackgroundAnalysis of unipolar voltage maps has been used to detect epicardial scar, but data to define optimal parameters to identify scar remote from the recording site is limited. This study compares the characteristics of electrograms at endocardial sites adjacent to abnormal epicardial sites.Methods and ResultsData obtained from endocardial and epicardial electroanatomical maps of 31 patients with scar‐related ventricular tachycardia were reviewed. Five hundred twenty‐three pairs of endo‐ and epicardial points were selected according to predefined criteria. The endocardial points adjacent to epicardial scar (bipolar voltage <1.5 mV) had smaller unipolar voltage than those distant from epicardial scar (P<0.001). In multivariable analysis, unipolar voltage was the only endocardial electrogram predictor of epicardial scar (P<0.001, OR 0.94, 95% CI 0.93 to 0.97). An endocardial unipolar amplitude <4.4 mV in the right ventricular (RV) (sensitivity 93%, specificity 76%) and <5.1 mV in the left ventricular (LV) (sensitivity 91%, specificity 75%) was the optimal cutoff predicting epicardial scar. Applying these thresholds to electroanatomical maps, revealed a good match between endocardial unipolar abnormality and epicardial scar for 67% of LV and 75% of RV maps, respectively, but notably poor matches occurred in 8 (29%) maps (7 with nonischemic cardiomyopathy). Site‐by‐site correlations were better for ischemic than nonischemic cardiomyopathy.ConclusionsThis study supports the contention that unipolar electrograms are capable of indicating overlying epicardial scar during endocardial mapping, but illustrates limitations that appear to differ with nonischemic as compared to ischemic cardiomyopathy. The presence of epicardial arrhythmia substrate cannot be excluded by analysis of unipolar endocardial maps in some patients.

Abstract 036: The Role Of Spinal Modulation On The Ventricular Electrophysiology In A Porcine Model

Background: Enhanced cardiac sympathetic tone has been associated with ventricular arrhythmias and sudden cardiac death. The spinal cord is an important integrative region of afferent and efferent pathways that participate in cardiovascular regulation. The purpose of this study is to investigate the role of spinal processing of cardiac afferent information on ventricular electrophysiology during cardiac sympathoexcitation. Methods: Female Yorkshire pigs (n=5) underwent surgical exposure of the heart and left stellate ganglion (LSG) through thoractomy as well as the dorsal and ventral roots of the spinal cord through laminectomy. A 56-electrode sock was placed over the ventricles to record epicardial electrograms. Animals underwent LSG stimulation in intact, after dorsal root transaction (DRTx), and followed by ventral root transaction (DVRTx). Activation recovery intervals (ARIs) were measured at each electrode before and during LSG stimulation. Results: With intact roots LSG stimulation resulted in significant global ARI shortening by 12.9% (p&lt;0.05). After DRTx, mean global ARI shortened by 7.2%. LSG stimulation after DRTx and DVRTx resulted in greater ARI shortening compared to LSG stimulation with intact roots (21.5 and 18.4 vs 12.9%, p&lt;0.05, see figure 1 below). ARI shortened more during LSG stimulation after DRTx than that after DVRTx (21.5 vs. 18.4%, p&lt;0.05). Conclusion: Spinal afferent pathways play an inhibitory role in sympathoexcitation of ventricle induced by LSG stimulation. This finding provides insight into the mechanism underlying the beneficial effects of thoracic epidural anesthesia in reducing ventricular arrhythmias.

Functional differences between junctional and extrajunctional adrenergic receptor activation in mammalian ventricle

Increased cardiac sympathetic activation worsens dispersion of repolarization and is proarrhythmic. The functional differences between intrinsic nerve stimulation and adrenergic receptor activation remain incompletely understood. This study was undertaken to determine the functional differences between efferent cardiac sympathetic nerve stimulation and direct adrenergic receptor activation in porcine ventricles. Female Yorkshire pigs (n = 13) underwent surgical exposure of the heart and stellate ganglia. A 56-electrode sock was placed over the ventricles to record epicardial electrograms. Animals underwent bilateral sympathetic stimulation (BSS) (n = 8) or norepinephrine (NE) administration (n = 5). Activation recovery intervals (ARIs) were measured at each electrode before and during BSS or NE. The degree of ARI shortening during BSS or NE administration was used as a measure of functional nerve or adrenergic receptor density. During BSS, ARI shortening was nonuniform across the epicardium (F value 9.62, P = 0.003), with ARI shortening greatest in the mid-basal lateral right ventricle and least in the midposterior left ventricle (LV) (mean normalized values: 0.9 ± 0.08 vs. 0.56 ± 0.08; P = 0.03). NE administration resulted in greater ARI shortening in the LV apex than basal segments [0.91 ± 0.04 vs. 0.63 ± 0.05 (averaged basal segments); P = 0.003]. Dispersion of ARIs increased in 50% and 60% of the subjects undergoing BSS and NE, respectively, but decreased in the others. There is nonuniform response to cardiac sympathetic activation of both porcine ventricles, which is not fully explained by adrenergic receptor density. Different pools of adrenergic receptors may mediate the cardiac electrophysiological effects of efferent sympathetic nerve activity and circulating catecholamines.

Inverse Solution Mapping of Epicardial Potentials

Background— Catheter ablation of ventricular tachycardia (VT) is still one of the most challenging procedures in cardiac electrophysiology, limited, in part, by unmappable arrhythmias that are nonsustained or poorly tolerated. Calculation of the inverse solution from body surface potential mapping (sometimes known as ECG imaging) has shown tremendous promise and can rapidly map these arrhythmias, but we lack quantitative assessment of its accuracy in humans. We compared inverse solution mapping with computed tomography–registered electroanatomic epicardial contact catheter mapping to study the resolution of this technique, the influence of myocardial scar, and the ability to map VT. Methods and Results— For 4 patients undergoing epicardial catheter mapping and ablation of VT, 120-lead body surface potential mappings were obtained during implantable defibrillator pacing, catheter pacing from 79 epicardial sites, and induced VT. Inverse epicardial electrograms computed using individualized torso/epicardial surface geometries extracted from computed tomography images were compared with registered electroanatomic contact maps. The distance between estimated and actual epicardial pacing sites was 13±9 mm over normal myocardium with no stimulus-QRS delay but increased significantly over scar ( P =0.013) or was close to scar ( P =0.014). Contact maps during right ventricular pacing correlated closely to inverse solution isochrones. Maps of inverse epicardial potentials during 6 different induced VTs indicated areas of earliest activation, which correlated closely with clinically identified VT exit sites for 2 epicardial VTs. Conclusions— Inverse solution maps can identify sites of epicardial pacing with good accuracy, which diminishes over myocardial scar or over slowly conducting tissue. This approach can also identify epicardial VT exit sites and ventricular activation sequences.

The Electrophysiological Cardiac Ventricular Substrate in Patients After Myocardial Infarction: Noninvasive Characterization With Electrocardiographic Imaging

The aim of this study was to noninvasively image the electrophysiological (EP) substrate of human ventricles after myocardial infarction and define its characteristics. Ventricular infarct border zone is characterized by abnormal cellular electrophysiology and altered structural architecture and is a key contributor to arrhythmogenesis. The ability to noninvasively image its electrical characteristics could contribute to understanding of mechanisms and to risk-stratification for ventricular arrhythmia. Electrocardiographic imaging, a noninvasive functional EP imaging modality, was performed during sinus rhythm (SR) in 24 subjects with infarct-related myocardial scar. The abnormal EP substrate on the epicardial aspect of the scar was identified, and its location, size, and morphology were compared with the anatomic scar imaged by other noninvasive modalities. Electrocardiographic imaging constructs epicardial electrograms that have characteristics of reduced amplitude (low voltage) and fractionation. Electrocardiographic imaging colocalizes the epicardial electrical scar to the anatomic scar with a high degree of accuracy (sensitivity 89%, specificity 85%). In nearly all subjects, SR activation patterns were affected by the presence of myocardial scar. Late potentials could be identified and were almost always within ventricular scar. Electrocardiographic imaging accurately identifies areas of anatomic scar and complements standard anatomic imaging by providing scar-related EP characteristics of low voltages, altered SR activation, electrogram fragmentation, and presence of late potentials.

Impact of Scar, Viable Myocardium, and Epicardial Fat on Substrate Identification of Ventricular Tachycardia in a Case with Nonischemic Cardiomyopathy

A 56-year-old man with nonischemic cardiomyopathy underwent orthotopic cardiac transplantation after endocardial and epicardial radiofrequency catheter ablation for pleomorphic ventricular tachycardia. The myocardial substrate and epicardial fat were comprehensively analyzed with three-dimensional electroanatomic maps, late gadolinium enhanced ex-vivo cardiac magnetic resonance, and histological examination. The association of scar, viable myocardium, and epicardial fat with endocardial and epicardial electrogram voltage and duration was quantitatively defined. This case provides a unique opportunity to explore the reliability of electrical surrogates of scar in nonischemic cardiomyopathy.

Drug-Induced Torsade de Pointes Arrhythmias in the Chronic AV Block Dog Are Perpetuated by Focal Activity

The electrically remodeled canine heart after chronic AV block (CAVB) has a high susceptibility for drug-induced torsade de pointes (TdP) arrhythmias. Although focal mechanisms have been considered for initiation, there is still controversy about whether reentry is the dominant mechanism for perpetuation of TdP. In this animal model with known nonuniform prolongation of repolarization, the mechanism of perpetuation of TdP arrhythmia was explored. Seventeen TdP-sensitive CAVB and 10 sinus rhythm (SR) dogs were studied. In 6 animals, 66 needle electrodes were evenly distributed transmurally to record 240 unipolar local electrograms simultaneously. Activation times and activation recovery intervals were determined before and during ibutilide-induced TdP. In 12 CAVB and 9 SR dogs, left ventricular (LV) and right ventricular (RV) epicardial electrograms were recorded with a 208-point multiterminal grid electrode allowing conduction velocity (CV) and ventricular effective refractory period (VERP) measurements. Biopsy specimens were processed for connexin43 (Cx43) expression and collagen content. Ventricular myocytes were isolated to determine sodium current (I(Na)) density and cell dimensions. Computer simulations were used to assess the effects of changes therein. In CAVB, VERP and ARI were increased, whereas CV was unaltered in LV. Transversal but not longitudinal CV was increased in RV. I(Na) was reduced by 37% in LV but unaltered in RV. LV and RV cell size were increased, but collagen and Cx43 content remained unchanged. Simulations showed increase in CV of RV as a consequence of increased cell size at normal I(Na). Ibutilide increased ARI, ERP, and maximal transmural dispersion of ERP (45 ± 25 to 120 ± 65 ms; P < 0.05). Twenty-eight of 47 episodes of self-terminating TdP (43 ± 72 beats) were analyzed. The majority (> 90%) of beats were focal; reentry was observed only occasionally. Focal activity is the dominant mechanism involved in perpetuation of ibutilide-induced TdP in CAVB dogs based on detailed 3D mapping. This conclusion is in line with unaltered conduction and documented increase in VERP.

Relationship of the J Waves on 12-Lead Electrocardiogram and the Left Ventricular Epicardium

The purpose of this study was to evaluate the relationship of the J waves on 12-lead electrocardiogram (ECG) and the left ventricular epicardium. Methods and Results: Forty-seven patients with paroxysmal atrial fibrillation were studied. To analyze the epicardial electrograms in the basal inferior and inferolateral LV wall, unipolar electrograms (with 0.05- to 100-Hz filters) of the CS electrodes positioned from the ostium to the 2 o’clock position of CS were examined. The J waves in the inferior and/or lateral leads on 12-lead ECG were observed in 14 patients (early repolarization (ER) group) but not in 33 patients (non-ER group). In all of the 14 ER group patients, J wave on the CS unipolar electrograms was observed. In the other 33 non-ER group patients, J wave on the CS unipolar electrograms was also observed in 21 of them (100% versus 63.6%, P<0.01). In a 40 year-old, non-ER male patient with VT, we constructed an additional three-dimensional electroanatomic map of unipolar electrograms on the whole surface of the LV epicardium. The prominent J waves were observed at the basal inferior LV wall, which matched the location of the J waves detected on the CS electrodes. Conclusions: J wave on the epicardium is observed at the basal inferior LV wall, whether or not the J wave is on 12-lead ECG.

The use of epicardial electrogram as a simple guide to select the optimal site of left ventricular pacing in cardiac resynchronization therapy.

Cardiac resynchronization therapy (CRT) has been demonstrated to improve symptoms and survival in patients with left ventricular (LV) systolic dysfunction and dyssynchrony. To achieve this goal, the LV lead should be positioned in a region of delayed contraction. We hypothesized that pacing at the site of late electrical activation was also associated with long-term response to CRT. We conducted a retrospective study on 72 CRT patients. For each patient, we determined the electrical delay (ED) from the onset of QRS to the epicardial EGM and the ratio of ED to QRS duration (ED/QRS duration). After a followup of 30 ± 20 months, 47 patients responded to CRT. Responders had a significantly longer ED and greater ratio of ED/QRS duration than nonresponders. An ED/QRS duration ≥0.38 predicted a response to CRT with 89% specificity and 53% sensitivity.

A Case of J-Wave Syndrome, That Was Suggested to Be Related to the Autonomic Tone

We describe a case of a ventricular fibrillation (VF) storm related to a prominent and widely distributed J-wave. A 34-year-old man, without any family history of sudden cardiac death or structural heart disease, suffered from a VF storm unresponsive to repeated defibrillation attempts and drugs including amiodarone. After the VF disappeared, his electrocardiogram (ECG) exhibited prominent J-waves and ST-segment elevation in almost all the leads. The J-point elevation slowly decreased without any recurrence of VF within a few days, and finally the J-waves remained only in the inferolateral leads. In the electrophysiological study, we tried to record an epicardial electrogram from the coronary sinus on the lateral wall, but no definite delayed potentials were observed. After implanting an implantable cardioverter-defibrillator, we performed pharmacologic stress tests (pilsicainide, protanol, mexan and atropine). The J-waves increased only during bradycardia after administering mexan. In the Holter ECG, transient ST-segment elevation was repetitively observed only while asleep. With the J-wave syndrome, it has been suggested that autonomictone plays a major role in the J-wave variability. In this case, prominent J-waves and ST-segment elevation were observed during bradycardia and sleep. This is a very rare case of J-wave syndrome with transient J-wave changes suggesting some relationship to the autonomic tone.

Antifibrillatory effect of ranolazine during severe coronary stenosis in the intact porcine model

Clinical evidence suggests that the antianginal agent ranolazine has antiarrhythmic properties, but its effects on vulnerability to ventricular fibrillation (VF) and T-wave alternans (TWA) during coronary artery stenosis have not been measured. We investigated whether the antiarrhythmic effect of ranolazine during acute coronary stenosis could be quantified by measuring VF threshold and TWA magnitude. Electrode catheters placed in the left ventricular apex were used to determine VF threshold during ventricular pacing at 130 beats/min, and TWA was quantified from epicardial electrograms using modified moving average method (N = 18). Left anterior descending coronary flow was reduced with a balloon occluder by 75% for 10 minutes. The I(Kr) blocker E-4031 was used to distinguish effects of late I(Na) and I(Kr) inhibition by ranolazine. Before stenosis, ranolazine and E-4031 increased VF threshold from 32 ± 4 mA to 46 ± 4 mA (mean ± SEM), P = .02, and from 33 ± 5 mA to 40 ± 9 mA, P = .02, respectively. During stenosis, ranolazine increased VF threshold from 19 ± 2 mA to 33 ± 3 mA (P = .02), whereas E-4031 decreased VF threshold from 21 ± 3 mA to 15 ± 3 mA (P = .02). The ischemia-induced increase in TWA was suppressed by ranolazine but not by E-4031, consistent with effects of these agents on VF threshold. Ranolazine exerts significant antifibrillatory effects during coronary stenosis through direct effects on cardiac electrical properties independent of coronary flow. Ranolazine's antifibrillatory action during myocardial ischemia does not appear to be mediated by blockade of I(Kr) but rather by inhibition of late I(Na). TWA changes paralleled vulnerability to VF as indicated by VF threshold testing.

Electrical remodelling precedes heart failure in an endothelin-1-induced model of cardiomyopathy

Binary transgenic (BT) mice with doxycycline (DOX)-suppressible cardiac-specific overexpression of endothelin-1 (ET-1) exhibit progressive heart failure (HF), QRS prolongation, and death following DOX withdrawal. However, the molecular basis and reversibility of the electrophysiological abnormalities in this model were not known. Here, we assess the mechanisms underlying ET-1-mediated electrical remodelling, and its role in HF. BT vs. non-BT littermate controls were withdrawn from DOX and serially studied with ultrasound biomicroscopy, octapolar catheters, multielectrode epicardial mapping, histopathology, western blot, immunohistochemistry, and qRT-PCR. Abnormalities in ventricular activation and -dV/dt were detected as early as 4 weeks after transgene activation, when the structure and function of the heart remained unaffected. By 8 weeks of ET-1 overexpression, biventricular systolic and diastolic dysfunction, myocardial fibrosis, and cardiomyocyte hypertrophy were observed. Intracardiac and epicardial electrograms revealed prolonged conduction and ventricular activation, reduced -dV/dt, and abnormal atrioventricular nodal function. Within 4 weeks of ET-1 induction, connexin 40 (Cx40) protein and Cx43 mRNA, protein, and phosphorylation levels were reduced by 36, 64, 93, and 69%, respectively; Na(v)1.5 mRNA and protein levels were reduced by 30 and 50%, respectively, as was Na(+) channel conductance. Importantly, the associated electrophysiological abnormalities at this time point were reversible upon suppression of ET-1 overexpression and completely prevented the development of structural and functional remodelling. ET-1-mediated electrical remodelling correlates with reduced Cx40, Cx43, and Na(v)1.5 expression and decreased Na(+) channel conductance and precedes HF. The sequence and reversibility of this phenotype suggest that a primary abnormality in electrical remodelling may contribute to the pathogenesis of HF.

Protective effect of Xinning tablet on acute myocardial ischemia in anesthesia dogs

Abstract This work aimed to observe the protective effect of Xinning tablets on experimental myocardial ischemia. The canine model of acute myocardial infarction was established by ligating the anterior descending coronary artery of dogs. The ultrasound Doppler method was adopted to determine myocardial blood flow. Heart membrane electrical diagram coup and nitro blue tetrazolium (N-BT) staining were used to calculate the extent of myocardial ischemia and myocardial infarct size. Radioimmunoassay was used to determine plasma ET, TXB 2 and 6-Keto-PGF 1α levels. 30-180 min after administration of Xinning tablets at 1.2 and 0.6 g/kg, the dog myocardial ischemia icon measured from the epicardial electrogram was significantly reduced; the infarct area was decreased according to NBT staining. 30-120 min after the administration, cardiac blood flow was significantly increased in the myocardial ischemia area, the levels of plasma ET and TXB 2 were greatly inhibited, and the 6-Keto-PGF1α content to TXB 2 /6-Keto-PGF1α ratio was increased. Taken together, Xinning tablets have significant protective effect on dog acute myocardial ischemia and myocardial infarction, the mechanism of which may be related to ET inhibition, TXA 2 release and increased myocardial blood flow, consequently improving the impaired heart function.

Serial changes in epicardial electrograms during and after a coronary artery occlusion

Suddenly occurring ventricular tachyarrhythmias are a complication during off-pump coronary artery bypass (OPCAB) surgery, potentially leading to the need for conversion to on-pump surgery. We examined serial changes in the spatial dispersion of the electrical activity and refractoriness at the myocardial ischemia border zones during and after coronary occlusion. Unipolar epicardial electrograms were continuously recorded from the anterior left ventricle at the border zones during and after a 10-min occlusion of the left anterior descending (LAD) coronary artery in 22 patients undergoing OPCAB. The local electrogram amplitude and local refractoriness were evaluated by the unipolar peak-to-peak amplitude (UPPA) and activation recovery interval (ARI), respectively. The spatial dispersion of the electrical activity and refractoriness were examined using the coefficient of variation of these parameters. No sustained ventricular tachyarrhythmias occurred in any patients. The UPPA dispersion significantly increased up to 5 min after the LAD occlusion and then returned to a nonsignificant level and again increased after reperfusion. The ARI dispersion gradually increased after the LAD occlusion, reached a significantly increased level 3 min after the occlusion, and stayed at a significantly increased level for at least 5 min after the reperfusion. There were unique serial changes in the spatial dispersion of the electrical activity and refractoriness at the myocardial ischemia border zones during and after coronary occlusions. Continuous monitoring of these parameters may be useful for predicting the critical electrophysiological conditions prone to the occurrence of ventricular tachyarrhythmias in patients undergoing OPCAB.

Image-based electrode array tracking for epicardial electrophysiological mapping in minimally invasive arrhythmia surgery

Electrophysiological mapping is effective in realizing a precise minimally invasive arrhythmia surgery. Recently, an epicardial electrophysiological mapping system for minimally invasive arrhythmia surgery was reported. The system requires a small electrode array, a tracking system and a global mapping algorithm. The optical tracking system employed in the research requires line of sight and complicated configuration. This paper proposes a new tracking method for locating an electrode array. We developed a small electrode array and optical markers. Center points of respective optical markers and the electrode array are tracked via an endoscopic stream and calculated in image space. The orientation of the electrode array is calculated using the dot product between the vector joining two center points of two upper optical markers and the vector joining two end points of the longest edge of the electrode array. Mean tracking errors of position and orientation of the electrode array were 0.51 mm and 0.64°, respectively. And the processing time was constant at 46 ms per frame. Our method could successfully track the electrode array on the epicardium during in vivo experiment and a global epicardial electrophysiological map was reconstructed from separately measured epicardial electrograms by the small electrode array. An image-based tracking method for locating an electrode array was proposed. Tracking accuracy, processing time and applicability to surgical environment of our method proved to be acceptable. Consequently, our method enables the electrode array tracking system to be simplified with no separate tracking system.

Letter to the editor: “Depolarization and repolarization alternans in an anesthetized canine ischemia model”

Letters to the EditorLetter to the editor: “Depolarization and repolarization alternans in an anesthetized canine ischemia model”John E. MadiasJohn E. MadiasMount Sinai School of Medicine, New York University, and Division of Cardiology, Elmhurst Hospital Center, New York, New YorkPublished Online:01 Feb 2010https://doi.org/10.1152/ajpheart.01097.2009MoreSectionsPDF (26 KB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInEmailWeChat to the editor: The article by Gordon et al. (1) provides plenty of food for thought, particularly in terms of its possible extrapolation to the clinical situation. The authors used cardiac electrical alternans (EA) of depolarization and repolarization measured in unipolar epicardial electrograms in an anesthetized canine ischemia model to predict ischemia-induced spontaneous ventricular fibrillation (VF). Data consisted of unipolar epicardial electrograms acquired 4 s before and 5 min after the inception of ischemia. The prevalence, and not the amplitude, of EA of both the QRS and ST/T EA after ischemia was predictive of VF. I would appreciate receiving a comment from the authors on the following. First, since EA was also seen before ischemia, is it not a contradiction that the presence, and not the amplitude, of EA is predictive of VF? Second, could the methodology used be implemented in standard ECGs or Holter monitorings? Third, in Fig. 3, S waves appear to be present in the electrograms before ischemia, which disappeared after ischemia, (a well-known accompaniment of ischemia in animal experimentation and clinical experience); was this a consistent finding? Fourth, was there any correlation between the amplitude of the QRS, or ST/T, and the amplitude of EA noted in the 8 × 14 electrode matrix the authors employed, and if yes, does this calls for an adjustment of the latter by the former? An index has been proposed for such an adjustment (2), which possibly may be in the same vein as the authors' assertion that the presence of EA may be predictive of VF, and not the amplitude, which could be a reflection of the corresponding amplitudes of QRS and ST/T.DISCLOSURESNo conflicts of interest are declared by the author.REFERENCES1. Gordon D, Kadish AH, Koolish D, Taneja T, Ulphani J, Goldberger JJ, Ng J. High-resolution electrical mapping of depolarization and repolarization alternans in an ischemic dog model. Am J Physiol Heart Circ Physiol . (November 13, 2009). doi: 10.1152/ajpheart.00914.2009.Google Scholar2. Madias JE. A proposal for a T-wave alternans index. J Electrocardiol 40: 479–481, 2007.Crossref | PubMed | ISI | Google ScholarAUTHOR NOTESAddress for reprint requests and other correspondence: J. E. Madias, Div. of Cardiology, Elmhurst Hospital Ctr., 79-01 Broadway, Elmhurst, NY 11373 (e-mail:[email protected]). Download PDF Previous Back to Top Next FiguresReferencesRelatedInformationCited ByReply to “Letter to the editor: ‘Depolarization and repolarization alternans in an anesthetized canine ischemia model’”David Gordon, Alan H. Kadish, Jeffrey J. Goldberger, and Jason Ng1 February 2010 | American Journal of Physiology-Heart and Circulatory Physiology, Vol. 298, No. 2 More from this issue > Volume 298Issue 2February 2010Pages H728-H728 Copyright & PermissionsCopyright © 2010 the American Physiological Societyhttps://doi.org/10.1152/ajpheart.01097.2009PubMed20090011History Published online 1 February 2010 Published in print 1 February 2010 Metrics