Left Ventricular Endocardial Sites Research Articles

Left ventricular electrical delay predicts volumetric response to leadless Cardiac Resynchronization Therapy

BackgroundLeadless left ventricular (LV) endocardial pacing is an emerging cardiac resynchronization therapy (CRT) technology. Predictors of response to leadless CRT are poorly understood. Implanting the LV endocardial pacing electrode in sites with increased electrical latency (Q-LV) may improve response rates. ObjectiveTo examine the association between Q-LV and echocardiographic remodelling response to leadless CRT delivered with the WiSE-CRT system. MethodsA post-hoc analysis (n=122) of the SOLVE-CRT trial examined the relationship between LV pacing site Q-LV with rate of LV end-systolic volume (LVESV) reduction >15% at 6 months. Multivariable regression analysis, adjusting for age, sex, prior CRT non-response, cardiomyopathy aetiology, QRS morphology and QRS duration was performed, followed by ROC analysis and analysis of variance by Q-LV quartile. A subgroup analysis of the ischaemic cardiomyopathy cohort was undertaken. ResultsComplete Q-LV data was available in 122/153 (80%) of patients in the active arms SOLVE-CRT. Overall, the 6-month LVESV response rate was 46%. Logistic regression identified Q-LV as an independent response predictor with borderline significance (adjusted odds ratio 1.015, p=0.05). Analysis by Q-LV quartile demonstrated a significant improvement in response rate in quartile 4 (longest Q-LV, 64%) compared to quartile 1 (shortest Q-LV, 28%), p<0.01. This association was primarily driven by strong Q-LV-response correlation in patients with ischaemic cardiomyopathy, demonstrated by subgroup logistic regression (adjusted odds ratio 1.034, p=0.004). ConclusionIncreased Q-LV was associated with improved reverse remodelling following leadless CRT. Targeting LV endocardial sites of high Q-LV may deliver additional benefit compared to empirical LV electrode implantation.

Real-Time Localization of VentricularTachycardia Origin From the 12-Lead Electrocardiogram.

The aim of this study was to develop rapid computational methods for identifying the site of origin of ventricular activation from the 12-lead electrocardiogram. Catheter ablation of ventricular tachycardia in patients with structural heart disease frequently relies on a substrate-based approach, which may use pace mapping guided by body-surface electrocardiography to identify culprit exit sites. Patients undergoing ablation of scar-related VT (n= 38) had 12-lead electrocardiograms recorded during pacing at left ventricular endocardial sites (n= 1,012) identified on 3-dimensional electroanatomic maps and registered to a generic left ventricular endocardial surface divided into 16 segments and tessellated into 238 triangles; electrocardiographic data were reduced for each lead to 1 variable, consisting of QRS time integral. Two methods for estimating the origin of activation were developed: 1) a discrete method, estimating segment of activation origin using template matching; and 2) a continuous method, using population-based multiple linear regression to estimate triangle of activation origin. A variant of the latter method was derived, using patient-specific multiple linear regression. The optimal QRS time integral included the first 120 ms of the QRS interval. The mean localization error of population-based regressions was 12 ± 8 mm. Patient-specific regressions can achieve localization accuracy better than 5mm when at least 10 training-set pacing sites are used; this accuracy further increases with each added pacing site. Computational intraprocedure methods can automatically identify the segment and site of left ventricular activation using novel algorithms, with accuracy within<10 mm.

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Acute Hemodynamic Effect of Left Ventricular Endocardial Pacing in Cardiac Resynchronization Therapy

Background— During cardiac resynchronization therapy (CRT) device implantation, the pacing lead is usually positioned in the coronary sinus (CS) to stimulate the left ventricular (LV) epicardium. Transvenous LV endocardial pacing via transseptal puncture has been proposed as an alternative method. In the present study, we evaluated the acute hemodynamic effects of CRT through LV endocardial pacing in heart failure patients by analyzing LV pressure–volume relationships. Methods and Results— LV pressure and volume data were determined via conductance catheter during CRT device implantation in 10 patients. In addition to the standard epicardial CS pacing, the following endocardial LV sites were systematically assessed: the site transmural to the CS lead, the LV apex, the septal midwall, the basal lateral free wall, and the midlateral free wall. Four atrioventricular delays were tested. There was a significant improvement of systolic function with CRT in all LV pacing configurations, whereas no differences in systolic or diastolic function were detected between LV epicardial and endocardial transmural sites. The optimal pacing site varied among patients but was rarely related to relatively longer activation delays, as assessed by analyzing endocardial electric activation maps. Nonetheless, positioning the pacing lead at the optimal endocardial LV site in each patient significantly improved LV performance in comparison with conventional CS site stimulation (stroke volume, 83 [79–112] mL versus 73 [62–89] mL; P =0.034). Conclusions— Pacing at the optimal individual LV endocardial site yields enhanced LV performance in comparison with conventional CS site stimulation. Endocardial LV pacing might constitute an alternative approach to CRT, when CS pacing is not viable.

Cyclical modulation of human ventricular repolarization by respiration.

Background: Respiratory modulation of autonomic input to the sinus node results in cyclical modulation of heart rate, known as respiratory sinus arrhythmia (RSA). We hypothesized that the respiratory cycle may also exert cyclical modulation on ventricular repolarization, which may be separately measurable using local endocardial recordings. Methods and Results: The study included 16 subjects with normal ventricles undergoing routine clinical electrophysiological procedures for supraventricular arrhythmias. Unipolar electrograms were recorded from 10 right and 10 left ventricular endocardial sites. Breathing was voluntarily regulated at 5 fixed frequencies (6, 9, 12, 15, and 30 breaths per min) and heart rate was clamped by RV pacing. Activation-recovery intervals (ARI: a surrogate for APD) exhibited significant (p < 0.025) cyclical variation at the respiratory frequency in all subjects; ARI shortened with inspiration and lengthened with expiration. Peak-to-peak ARI variation ranged from 0–26 ms; the spatial pattern varied with subject. Arterial blood pressure also oscillated at the respiratory frequency (p < 0.025) and lagged behind respiration by between 1.5 s and 0.65 s from slowest to fastest breathing rates respectively. Systolic oscillation amplitude was significantly greater than diastolic (14 ± 5 vs. 8 ± 4 mm Hg ± SD, p < 0.001). Conclusions: Observations in humans with healthy ventricles using multiple left and right ventricular endocardial recordings showed that ARI action potential duration (APD) varied cyclically with respiration.

Optimal Left Ventricular Endocardial Pacing Sites for Cardiac Resynchronization Therapy in Patients With Ischemic Cardiomyopathy

We sought to investigate the impact of left ventricular (LV) pacing site on mechanical response to cardiac resynchronization therapy (CRT) in patients with ischemic cardiomyopathy (ICM). CRT reduces morbidity and mortality in patients with dyssynchronous LV failure; however, variability in response, particularly in ICM patients, poses ongoing challenges. Endocardial biventricular (BiV) stimulation may provide more flexibility in LV site selection and yield more natural transmural activation patterns. Whether this applies to ICM and whether optimal LV endocardial pacing locations vary among ICM patients remain unknown. Peak rate of LV pressure increase (dP/dt(max)) was measured at baseline, during VDD pacing at the right ventricular apex, and during BiV pacing from the right ventricular apex and 51 +/- 14 different LV endocardial sites in patients with ICM (n = 11). Seven patients already had an epicardial LV lead (CRT) in place, allowing comparison of epicardial BiV stimulation with that using an endocardial site directly transmural to the CRT-coronary sinus lead tip. Electroanatomic 3-dimensional maps with color-coded dP/dt(max) response defined optimal pacing regions delivering >or=85% of maximal increase in dP/dt(max). Endocardial BiV pacing improved dP/dt(max) over right ventricular apex pacing in all patients (mean increase 241 +/- 38 mm Hg/s; p < 0.0001). In patients with pre-existing CRT leads, LV endocardial versus epicardial pacing at transmural sites yielded equivalent dP/dt(max) values. However, dP/dt(max) at the best endocardial site exceeded that achieved with the pre-implanted CRT device (mean increase 111 +/- 25 mm Hg/s; p = 0.004). An average of approximately 2 optimal endocardial sites were identified for each patient, located at the extreme basal lateral wall (8 of 11 patients) and other regions (9 of 11). Standard mid-LV free wall pacing yielded suboptimal LV function in 73% of patients. Optimal pacing sites were typically located in LV territories remote (9.3 +/- 3.6 cm) from the infarct zone. CRT delivered at best LV endocardial sites is more effective than via pre-implanted coronary sinus lead pacing. The location of optimal LV endocardial pacing varies among patients with ICM, and individual tailoring may improve CRT efficacy in such patients.

Ablation of Idiopathic Ventricular Tachycardia in Two Separate Regions of the Outflow Tract: Prevalence and Electrocardiographic Characteristics

Few studies have clarified the prevalence and characteristics of idiopathic outflow tachycardia (OT-VT) with an altered QRS morphology after radiofrequency catheter ablation (RFCA), requiring additional RFCA applications at a different portion of the outflow tract (OT) to abolish the OT-VT. Among 344 patients (97 VTs and 247 premature ventricular contractions), 12 (3.5%; VTs-7, PVCs-5; 6 women) had dynamic QRS morphology changes following the RFCA, requiring additional RFCA applications at a different portion to abolish the OT-VT. In 8 of 12 patients (67%), this phenomenon occurred following RFCA at right (RVOT; n = 7) or left ventricular (LVOT; n = 1) endocardial sites of the OT: The second OT-VT was consistently associated with an increase in the R-wave amplitude in the inferior leads, and in five it was finally abolished by RFCA at the left sinus of Valsalva (LSV). Conversely, in four patients (33%), the second OT-VT appeared after RFCA at the LSV: two required additional RFCA applications at the LVOT to abolish the second OT-VT, and one at the RVOT, and all were associated with a decrease in the R-wave amplitude in the inferior leads. This kind of dynamic QRS morphology change was often observed when RFCA was applied to either the first or second OT-VT at a right or left ventricular endocardial site, with the other site being the LSV. A detailed continuous observation of the QRS morphology, especially of the R-wave in the inferior leads, is important for identifying changes in the QRS morphology during RFCA.

Prevalence and characteristics of idiopathic outflow tract tachycardia with QRS alteration following catheter ablation requiring additional radiofrequency ablation at a different point in the outflow tract.

Subtle variations in QRS morphology occurs during idiopathic outflow tract ventricular tachycardia (OTVT), but no studies have clarified the prevalence and characteristics of the OTVT with altered QRS morphology following radiofrequency catheter ablation (RFA), which then require an additional RF application at a different portion of the outflow tract to abolish OTVT. Of 202 patients with a monomorphic VT or premature ventricular contraction (PVC) originating from the outflow tract, 6 (3%) showed changes in QRS morphology in the OTVT following RFA, requiring an additional RF application to the outflow tract at a different portion. In all six patients, RFA was applied for the first or second OTVT to a right or left ventricular endocardial site, with the other site being the left sinus of Valsalva. In each patient, OTVT before or after the changes in QRS morphology had characteristic ECG findings originating from a particular portion of the outflow tract. Changes in QRS morphology consistently included an increase or decrease in R wave amplitude in all inferior leads. Detailed continuous observation of QRS morphology in OTVT, especially R wave amplitude in inferior leads, is important for identifying changes of QRS morphology during catheter ablation. Mapping and ablation at a different portion of the outflow tract is then needed for cure.

Voltage and activation mapping. how the recording technique affects the outcome of catheter ablation procedures in patients with congenital heart disease

The aim of this study was to develop rapid computational methods for identifying the site of origin of ventricular activation from the 12-lead electrocardiogram.Catheter ablation of ventricular tachycardia in patients with structural heart disease frequently relies on a substrate-based approach, which may use pace mapping guided by body-surface electrocardiography to identify culprit exit sites.Patients undergoing ablation of scar-related VT (n = 38) had 12-lead electrocardiograms recorded during pacing at left ventricular endocardial sites (n = 1,012) identified on 3-dimensional electroanatomic maps and registered to a generic left ventricular endocardial surface divided into 16 segments and tessellated into 238 triangles; electrocardiographic data were reduced for each lead to 1 variable, consisting of QRS time integral. Two methods for estimating the origin of activation were developed: 1) a discrete method, estimating segment of activation origin using template matching; and 2) a continuous method, using population-based multiple linear regression to estimate triangle of activation origin. A variant of the latter method was derived, using patient-specific multiple linear regression.The optimal QRS time integral included the first 120 ms of the QRS interval. The mean localization error of population-based regressions was 12 ± 8 mm. Patient-specific regressions can achieve localization accuracy better than 5 mm when at least 10 training-set pacing sites are used; this accuracy further increases with each added pacing site.Computational intraprocedure methods can automatically identify the segment and site of left ventricular activation using novel algorithms, with accuracy within <10 mm.

Optimal frequency of radiofrequency catheter ablation in vitro and in vivo for treating ventricular tachycardias--a study using various frequencies.

The purpose of this study was to determine the optimal frequency for radiofrequency catheter ablation of ventricular tachycardias. A radiofrequency current was delivered from a 6F bipolar electrode catheter with a tip electrode width of 4 mm. Ablation was performed for a pulse duration of 10 sec at 20 watts (50 V and 0.4 A) at seven different frequencies between 10 and 500 kHz. We used 35 canine isolated left ventricular endocardial sites in vitro and 14 anesthetized dogs in vivo. The lesions which were ablated at frequencies of 200 and 300 kHz were significantly larger than those at other frequencies, with a mean surface areas of 78.5 and 76.3 mm2, and mean depths of 4.0 and 4.1 mm, respectively (p < 0.05). The appearance of ventricular arrhythmias during ablation increased as the frequency decreased. One dog, to which a frequency of 100 kHz was applied, developed spontaneous ventricular fibrillation and died. All of the dogs which received a current with a frequency under 50 kHz exhibited muscle cramping during ablation. Ventricular stimuli applied after ablation did not induce ventricular tachycardia. These results suggest that the optimal frequency for ablating a large lesion is between 200 and 300 kHz. To avoid inducing malignant ventricular arrhythmia during ablation, the frequency must exceed 200 kHz. Furthermore, a frequency below 100 kHz should not be used in radiofrequency catheter ablation because of the risk of arrhythmias and muscle cramping.

Radiofrequency Catheter Ablation: The Effect of Electrode Size on Lesion Volume In Vivo

Radiofrequency current is a promising alternative to high voltage direct current defibrillator discharges for catheter ablation of arrhythmias. However, lesions produced with radiofrequency current are relatively small and use of high power is limited by the impedance rise that occurs with desiccation of tissue and coagulum formation. The effect of electrode size on radiofrequency ablation was assessed by comparing results of radiofrequency application using a standard 6 French electrode catheter (distal electrode 2 mm in length) to those using catheters modified with longer distal electrodes (3, 4, 6, 8, and 10 mm in length). Radiofrequency ablation was performed at 47 left ventricular endocardial sites in 20 anesthetized dogs. A constant power of 13.3 +/- 1.3 watts at 550 kHz was applied between the distal catheter electrode and a skin electrode until a total of 500 joules had been delivered or a rise in impedance occurred. Increasing electrode length from 2 to 4 mm more than doubled lesion volume from a mean of 143 to 326 mm3 (P = 0.025). Increasing electrode length beyond 4 mm produced progressively smaller lesions (157 mm3, 155 mm3, and 67 mm3 for 6-, 8-, and 10-mm electrode lengths, respectively). Impedance rise was significantly less likely with larger electrodes and took longer to occur. Increasing the size of electrodes used for radiofrequency ablation allows application of higher power without an impedance rise. Optimizing electrode size (3 or 4 mm in this study) results in larger lesions and may improve the effectiveness of radiofrequency ablation of arrhythmias.

Comparison of blood-based and asanguineous cardioplegic solutions administered at 4° C: An ultrastructural morphometric study in the dog

Although several studies have shown better myocardial preservation with blood-based than asanguineous cardioplegic solutions at myocardial temperatures above 15 degrees C, one might suspect that blood would become unsafe at lower temperatures because of increased oxygen-hemoglobin affinity and viscosity. We compared myocardial preservation in dogs subjected to 6 hours of aortic crossclamping and treated with modified Roe's asanguineous cardioplegic solution at 4 degrees C (group CA), blood cardioplegic solution at 4 degrees C (CB), or blood cardioplegic solution at 27 degrees C (WB, four dogs per group). Myocardial preservation was assessed by triphenyltetrazolium staining of whole hearts, and by analysis of ultrastructure and morphometric analysis of mitochondria in myocardial biopsies from three sites in each heart (left ventricle subepicardium and subendocardium and right ventricle). Tetrazolium staining showed no difference in preservation among the three treatment groups (no necrosis in any heart). For two of the three biopsy sites (left ventricular subepicardium and right ventricle), ultrastructural and morphometric analyses demonstrated signs of more severe subcellular injury in group CA than in CB (p = 0.013 to 0.004), whereas equivalent preservation with all treatments was observed in the left ventricular endocardial site. Functional recovery also appeared to be equivalent between treatments, to the extent that all dogs were successfully weaned from bypass after 20 minutes of reperfusion. We conclude that the safety and effectiveness of blood cardioplegia is not compromised by infusion at 4 degrees C compared with 27 degrees C and that myocardial preservation is not improved by using asanguineous cardioplegia instead of blood cardioplegia at 4 degrees C.

Drug-induced torsades de pointes: Role of early afterdepolarizations and dispersion of repolarization

Drug-induced torsades de pointes [l] is a polymorphic ventricular tachycardia, sometimes showing a characteristic twisting QRS morphology, that is consistently associated with prominent late diastolic U waves, a prolonged QTU interval, and bradycardiac pauses [2-4]. The basic electrophysiologic mechanism(s) of the arrhythmia is not known. The two mechanisms that have been suggested are increased dispersion of repolarization [5] and early afterdepolarization [6,7]. We have recently shown right ventricular monophasic action potential (MAP) recordings in a patient with quinidine-induced torsades de pointes and suggested that the arrhythmia may be due to bradycardia-dependent early afterdepolarizations giving rise to triggered activity [a]. The current report describes a patient with procainamide-related torsades de pointes in whom simultaneous recordings of MAP from right and left ventricular endocardial sites necessitate a re-evaluation of our conclusions. The findings suggest that both early afterdepolarization and dispersion of repolarization may be involved in the genesis of the arrhythmia. An increased understanding of the mechanism of drug-induced torsades de pointes can help improve the overall management of cardiac arrhythmias.

Electrocardiographic localization of the site of origin of ventricular tachycardia in patients with prior myocardial infarction

The utility of the 12 lead electrocardiogram (ECG) in identifying the site of origin of sustained ventricular tachycardia in patients with previous myocardial infarction was studied. A new mapping grid, based on biplanar fluoroscopic imaging of the heart, was utilized for the definition of left ventricular endocardial sites. On the basis of QRS configurations resulting from left ventricular endocardial pacing at disparate sites in 22 patients (Group I), ECG features that were specific for particular sites were identified and used to construct an algorithm. Apical and basal sites were differentiated by the QRS configuration in leads V4 and aVR, anterior and inferior sites by that in leads III III and V6 and septal and lateral sites were differentiated using leads I, aVL and V1.The algorithm was used to predict the site of earliest endocardial activation during 44 episodes of sustained ventricular tachycardia in a second group of 42 patients (Group II) in a blinded fashion. Anterior sites were correctly predicted in 83% of cases, inferior sites in 84%, septal sites in 90% and lateral sites in 82% of cases. Apical and basal sites were each correctly predicted in 70% of cases, whereas intermediate sites were less well predicted (29 to 55%) on the basis of QRS configuration. Precise localization of the site of origin of ventricular tachycardia (in all three planes) was achieved in 17 cases (39%), and in 16 cases (36%) the site of origin was immediately adjacent to the predicted site.Prediction of the site of origin of ventricular tachycardia from the 12 lead ECG may serve as a useful, time-saving adjunct to, but not a substitute for, activation sequence mapping during ventricular tachycardia.

Effects of lidocaine and procainamide on normal and abnormal intraventricular electrograms during sinus rhythm.

The effect of lidocaine (n = 6) and procainamide (n = 12) on electrogram characteristics from electrically normal right ventricular and electrically abnormal left ventricular endocardial sites was determined in 18 patients with prior myocardial infarction. Bipolar electrograms were recorded during sinus rhythm with No. 6F catheters positioned at a left ventricular abnormal site (electrograms fulfilling two of the following criteria: amplitude less than 3 mV, duration greater than 70 msec, or an amplitude to duration ratio less than .046) and normal sites at the right ventricular apex (RVA) and right ventricular outflow tract (RVOT). All electrograms were recorded from the same location before and after intravenous lidocaine or procainamide administered to obtain mean serum concentrations of 4.2 +/- 0.6 and 9.42 +/- 2 micrograms/ml respectively. Lidocaine and procainamide had no significant effect on sinus cycle length or electrogram amplitude. After lidocaine, no significant change in QRS width (112 +/- 23 vs 114 +/- 24 msec), left ventricular electrogram duration (76 +/- 21 vs 78 +/- 15 msec), or right ventricular electrogram duration (RVA 33 +/- 9 vs 33 +/- 10 msec, RVOT 31 +/- 9 vs 33 +/- 11 msec) was noted during sinus rhythm. At a paced cycle length of 600 msec, there was also no change in the paced QRS duration (197 vs 198 msec), the RVA electrogram duration (30 vs 32 msec), the RVOT electrogram duration (49 vs 52 msec), or the left ventricular electrogram duration (102 vs 108 msec).(ABSTRACT TRUNCATED AT 250 WORDS)

Monophasic action potential mapping in human subjects with normal electrocardiograms: direct evidence for the genesis of the T wave.

T wave concordance in the normal human electrocardiogram (ECG) generally is explained by assuming opposite directions of ventricular depolarization and repolarization; however, direct experimental evidence for this hypothesis is lacking. We used a contact electrode catheter to record monophasic action potentials (MAPs) from 54 left ventricular endocardial sites during cardiac catheterization (seven patients) and a new contact electrode probe to record MAPs from 23 epicardial sites during cardiac surgery (three patients). All patients had normal left ventricular function and ECGs with concordant T waves. MAP recordings during constant sinus rhythm or right atrial pacing were analyzed for activation time (AT) = earliest QRS deflection to MAP upstroke, action potential duration (APD) = MAP upstroke to 90% repolarization, and repolarization time (RT) = AT plus APD. AT and APD varied by 32 and 64 msec, respectively, over the left ventricular endocardium and by 55 and 73 msec, respectively, over the left ventricular epicardium. On a regional basis, the diaphragmatic and apicoseptal endocardium had the shortest AT and the longest APD, and the anteroapical and posterolateral endocardium had the longest AT and the shortest APD (p less than .05 to less than .0001). RT was less heterogeneous than APD, and no significant transventricular gradients of RT were found. In percent of the simultaneously recorded QT interval, epicardial RT ranged from 70.8 to 87.4 (mean 80.7 +/- 3.9) and endocardial RT ranged from 80 to 97.8 (mean 87.1 +/- 4.4) (p less than .001).(ABSTRACT TRUNCATED AT 250 WORDS)

Endocardial mapping in humans in sinus rhythm with normal left ventricles: activation patterns and characteristics of electrograms.

Endocardial catheter mapping was performed in 15 patients in sinus rhythm who had no evidence of structural heart disease and normal left ventricles. Mapping was performed with the use of 10 mm interelectrode distance from various left ventricular endocardial sites. In 10 patients a quantitative analysis of electrographic amplitude, duration, and amplitude/duration ratio was performed. The normal left ventricular bipolar electrograms had an amplitude of greater than 3 mV, a duration of less than 70 msec, and an amplitude/duration ratio of greater than 0.045. Local activation times were also assessed in the 15 patients. This analysis revealed two endocardial breakthrough sites, one on the midinferior septum and a second on the anterior wall near the insertion of the anterior papillary muscle. We therefore have defined normal quantitative characteristics of left ventricular bipolar electrograms and the normal left ventricular activation sequence in the intact normal human left ventricle.

Long-term recording of monophasic action potentials from human endocardium

In 36 patients undergoing routine cardiac catheterization, a new “contact electrode” catheter technique was used to record monophasic action potentials (MAPs) from right atrial and right and left ventricular endocardial sites without the application of suction. Although of smaller amplitude, typically ranging from 15 to 40 mV, and of different reversal ratio (33 ± 3%), MAP recordings closely resembled transmembrane action potentials in configuration and duration. Continuous MAP recordings of stable amplitude and, during regular pacing, of constant duration (± 1% at 90% repolarization) could be made from the same endocardial site for test periods of 1 hour (n = 4), permitting direct evaluation of the effect of cycle length alterations on local myocardial repolarization. A linear relation was found between MAP duration and basic cycle length varying from 350 to 700 ms. These rate-dependent changes in MAP duration were caused by a change in the slow phase of repolarization (phase 2), whereas the slope of rapid repolarization (phase 3) was unaltered. Single premature MAPs or MAPs after a pause showed changes in both phases. No MAPs could be recorded in areas of infarcted, aneurysmal myocardium, indicating that local viable myocardium is a prerequisite for the generation of the monophasic signal. Thus, in human subjects this catheter permits safe, long-term recording of MAPs which, although of smaller amplitude than transmembrane action potentials, bear appropriate and predictable phase relations. Such recordings may be useful in evaluating changes in local myocardial electrical activity induced by pacing or resulting from myocardial disease, or both.

Ventricular activation during ventricular endocardial pacing: I. Electrocardiographic patterns related to the site of pacing

The QRS configuration produced by pacing at multiple left ventricular endocardial sites was evaluated in eight patients with (group 1) and six patients without (group 2) left ventricular wall motion abnormalities. Pacing was performed at a total of 122 sites, 4 to 13 sites in each patient. The QRS configuration resulting from apical pacing locations was compared with that at basal, septal to lateral and inferior to superior locations. Significant differences in QRS configuration during pacing from apical and basal locations were observed in electrocardiographic leads I, V 1, V 2 and V 6 (probability [p] < 0.01). Specifically, a QS pattern in leads I, V 2 and V 6 was more characteristic of an apical pacing location ( p < 0.001), and a monophasic R wave in leads V 1 and V 2 was more characteristic of a basal pacing location ( p < 0.01). Significant differences in leads V 1 and V 2 were observed when septal and lateral pacing sites were compared ( p < 0.001). A monophasic R wave in leads V 1 and V 2 was more characteristic of a lateral pacing location ( p < 0.01); a QS complex in lead V 2 was more characteristic of a septal pacing location ( p < 0.001). Pacing at superior sites usually produced an inferior axis and vice versa ( p < 0.001). The electrocardiographic patterns produced by pacing at similar sites in patients in group 1 were less consistent than those in patients in group 2. The QRS complex during ventricular pacing was wider in patients in group 1 (159 ± 30 ms) than in patients in group 2 (132 ± 18 ms) ( p < 0.001). It is concluded that the QRS configuration recorded with 12 lead electrocardiography during endocardial pacing can help locate the region of the pacing site in patients with and without organic heart disease, although precise localization is not possible.

Sustained ventricular tachycardia in recent canine myocardial infarction.

To study recurrent ventricular tachycardia in the late phase or myocardial infarction (MI), transmural anteroapical infarcts were created by ligation of the left anterior descending (LAD) coronary artery in 25 dogs. Twenty dogs survived LAD ligation and underwent an open-chest electrophysiologic study an average of 20 days after MI. Programmed electrical stimulation was carried out using the extrastimulus technique and short bursts of rapid ventricular pacing via bipolar electrodes positioned at multiple left ventricular endocardial sites. Sixteen dogs had electrically induced ventricular tachycardia, and in 11, sustained ventricular tachycardia was reproducibly initiated and terminated by programmed ventricular stimulation. Short bursts of rapid left ventricular pacing from areas in periinfarct zone was the most effective technique for initiating ventricular tachycardia. The electrophysiologic phenomena in this model of sustained ventricular tachycardia in 3-week-old MI included electrically induced changes in rate and morphology and biventricular capture without termination during tachycardia.