Precordial Lead Research Articles

Spatiotemporal characterization of atrial activation in persistent human atrial fibrillation: Multisite electrogram analysis and surface electrocardiographic correlations—A pilot study

The mechanisms of persistent human atrial fibrillation (AF) are not well understood. The purpose of this study was to examine whether left atrial (LA) drivers are present in persistent AF by performing a comprehensive evaluation of atrial activation frequency and organization using multisite atrial recordings and correlating the findings with atrial waveform frequency and organization on surface ECG. Nine patients undergoing catheter ablation for persistent AF were studied. Electrograms were recorded from at least 10 sites in each atrium, tagged to an electroanatomic map, and subjected to spectral analysis. Dominant frequency (DF) and regularity index were calculated at each site. Surface ECG recordings were analyzed to obtain precordial lead DFs and AF vector stability index. Mean, maximum, and minimum DF and mean regularity index were higher in LA than right atrium (RA). DF was correlated with regularity index (R = 0.59, P <.0001) and negatively correlated with distance from maximal DF site (R = -0.80, P <.0001). Precordial lead DFs were highly correlated with atrial DFs. Vector stability index was 0.39 +/- 0.12 (P <.01 vs predicted if AF vector direction was random). LA-RA DF gradient and vector stability index were negatively correlated (R = -0.83, P <.05). The existence of LA-RA frequency gradients in most patients in this study along with the regularity of LA activation and centrifugal dissipation of activation frequency suggest that LA drivers are often present in persistent AF. Analysis of AF vectors from surface ECG demonstrates spatial stability and correlates with intracardiac recordings. These findings may have implications for catheter ablation of persistent AF.

Optimal Surface Electrocardiogram Lead for Identification of the Mechanism of Supraventricular Tachycardia in Children

Although supraventricular tachycardia (SVT) can be identified from any lead of the bedside monitor, the mechanism of tachycardia is not always obvious. We analyzed the 12-lead electrocardiogram (ECG) in SVT of pediatric patients with different mechanisms of SVT to determine if there is a consistent optimal lead for rhythm identification. Twelve-lead ECGs during SVT were available for retrospective analysis in 54 patients. The tachycardia mechanism was determined either by intracardiac or transesophageal recording, or after cardioversion analysis of atrial flutter or fibrillation. Blinded analysis of each separate lead of the 12-lead ECG was done to determine the best lead to diagnose the mechanism of tachycardia. For statistical analysis, chi(2) or Fisher exact test was used. From analysis of the surface ECG, the mechanism of SVT could be identified in 49 (91%) of 54 patients. Lead V1 was the most useful lead to determine the tachycardia mechanism. V1 identified the mechanism in 39 (80%) of 49 patients compared with 29 (59%) of 49 in lead III (P < 0.05), 22 (51%) of 49 in lead II (P < 0.01), and 12 (24%) of 49 in V6 (P < 0.001). Lead V1 identified accessory pathway-mediated tachycardia in 15 (68%) of 22 patients, atrial flutter in 12 (87%) of 14 patients, atrial fibrillation in 7 (70%) of 10, and atrioventricular nodal reentrant tachycardia in 5 (62%) of 8 patients. The mechanism of tachycardia was more readily diagnosed using a combination of V1 and lead III (47/49 patients, 96%) compared with V1 alone (P < 0.05). A right precordial lead (V1) is the best single lead to diagnose the mechanism of SVT. Furthermore, a combination of V1 and lead III increases the number of patients in whom the mechanism could be identified. Therefore, we recommend that V1 should be combined with an inferior limb lead during cardiac monitoring for optimal identification of the mechanism of SVT in children.

Isolated right ventricular infarction — An uncommon cause of acute anterior ST segment elevation

We describe a case of isolated right ventricular myocardial infarction as the cause of anterior precordial lead ST segment elevation. This case illustrates that anterior ST segment elevation may occur with occlusion of the right coronary artery. It is important to recognize this scenario as the treatment of right ventricular myocardial infarction differs from that of left ventricular myocardial infarction.

Cardiac repolarization abnormalities and potential evidence for loss of cardiac sodium currents on electrocardiograms of patients with Chagas heart disease

Some individuals with Chagas disease develop right precordial lead ST segment elevation in response to an ajmaline challenge test, and the prevalence of right bundle branch block (RBBB) is also high in Chagas disease. Because these same electrocardiographic abnormalities occur in the Brugada syndrome, which involves genetically defective cardiac sodium channels, acquired damage to cardiac sodium channels may also occur in Chagas disease. We studied several conventional and advanced resting 12-lead/derived Frank-lead ECG parameters in 34 patients with Chagas -related heart disease (mean age 39 14 years) and in 34 age-/gender-matched healthy controls. All ECG recordings were of 5-10 min duration, obtained in the supine position using high fidelity hardware/software (CardioSoft, Houston, TX). Even after excluding those Chagas patients who had resting BBBs, tachycardia and/or pathologic arrhythmia (n=8), significant differences remained in multiple conventional and advanced ECG parameters between the Chagas and control groups (n=26/group), especially in their respective QT interval variability indices, maximal spatial QRS-T angles and low frequency HRV powers (p=0.0006, p=0.0015 and p=0.0314 respectively). In relation to the issue of potential damage to cardiac sodium channels, the Chagas patients had: 1) greater than or equal to twice the incidence of resting ST segment elevation in leads V1-V3 (n=10/26 vs. n=5/26) and of both leftward (n=5/26 versus n=0/26) and rightward (n=7/26 versus n=3/26) QRS axis deviation than controls; 2) significantly increased filtered (40-250 Hz) QRS interval durations (92.1 8.5 versus 85.3 plus or minus 9.0 ms, p=0.022) versus controls; and 3) significantly decreased QT and especially JT interval durations versus controls (QT interval: 387.5 plus or minus 26.4 versus 408.9 plus or minus 34.6 ms, p=0.013; JT interval: 290.5 plus or minus 26.3 versus 314.8 plus or minus 31.3 ms; p=0.0029). Heart rates and Bazett-corrected QTc/JTc intervals were not significantly different between groups. Patients with Chagas heart disease have increased cardiac repolarization abnormalities, especially by advanced ECG. Moreover, as a group, they have decreased uncorrected JT and QT interval durations and increased filtered QRS interval durations (versus age/gender-matched controls), all suggesting a potential loss of cardiac sodium channel function that might be mediated, in part, by cardiac autonomic damage. Overall findings support Brugada et al's recent hypothesis that the pathway leading to sudden death may often be similar in Chagas' disease and Brugada syndrome i.e., damage to the sodium channel (infectious/immunologic/autonomic in Chagas' genetic in Brugada) with consequent loss of sodium currents may facilitate a phase II-reentry based arrhythmic substrate for ventricular fibrillation in both conditions. In general, JT interval-related results have been underreported in the Chagas literature.

Comparison of conduction delay in the right ventricular outflow tract between Brugada syndrome and right ventricular cardiomyopathy: investigation of signal average ECG in the precordial leads

In both Brugada syndrome (BS) and arrhythmogenic right ventricular cardiomyopathy (ARVC), electrical abnormalities in the right ventricular outflow tract (RVOT) are important for arrhythmogenesis. The aim of this study was to compare conduction delay in the right ventricular in BS with that in ARVC using the signal-averaged electrocardiogram. Twenty patients with BS (18 men and 2 women; 55 +/- 12 years old; 9 symptomatic and 11 asymptomatic) and eight patients with ARVC (six men and two women; 53 +/- 16 years old) were included. We assessed the presence of late potentials (LPs) and the filtered QRS duration (fQRSd) in V(2) and V(5) using a high-pass filter of 40 Hz (fQRSd:40) and 100 Hz (fQRSd:100). In ARVC, there was no significant difference in fQRSd:40 between V2 and V5 (158 +/- 19 vs. 145 +/- 17 ms, respectively): however, in BS, fQRSd:40 in V2 was significantly longer than fQRSd:40 in V5 (147 +/- 15 vs. 125 +/- 10 ms, P < 0.001). In ARVC, there was no significant difference between fQRSd:40 and fQRSd:100 in V(2) and V(5) (158 +/- 19 vs. 142 +/- 23 ms and 145 +/- 17 vs. 132 +/- 9 ms, respectively). In contrast, in BS, fQRSd:100 was significantly shorter than fQRSd:40 in V2 (110 +/- 8 ms vs. 147 +/- 15, P < 0.001). The relative decrease in fQRSd:100 compared with fQRSd:40 in V2 was significantly greater in BS than in ARVC. The dominant prolongation of the fQRSd in the right precordial lead in BS was different from the characteristics of ARVC, which may be caused by the conduction delay due to fibro-fatty replacement in RV.

ST segment depression: the possible role of global repolarization dynamics

BackgroundAt least some clinical data suggests that, regardless of which major coronary artery is narrowed, the early ST segment body surface pattern is characterized by a minimum near precordial lead V5 and a broad area of left precordial negative potentials. Some clinical data also suggests that late ST segment potentials can localize an ischemic heart region.ObjectiveA computer model of a heart/torso system was implemented to study the relationship between transmembrane potentials throughout the heart and clinically observed body surface potential patterns during the early and late ST segments in ischemic patients.MethodsTransmembrane potentials were selected to produce body surface potentials that matched the clinical data.ResultsThe early ST segment pattern was matched by assigning: (i) an epicardial transmembrane potential gradient that is consistent with the normal activation/repolarization sequence, according to which the left lateral epicardium activates relatively late; (ii) an endocardial transmembrane potential distribution with the lowest transmembrane potentials in the ischemic region; and (iii) overall lower transmembrane potentials to the endocardium compared to the epicardium. Late ST segment potentials, which localized the area of the ischemic region, were generated by reducing the epicardial transmembrane potential gradient and increasing the endocardial transmembrane potential gradient.ConclusionThe non-localizing nature of early ST segment depression could be due to global epicardial and endocardial transmembrane potential gradients related to the activation/repolarization sequence, whereas the possibly localizing nature of late ST segment depression could be due to the relative removal of the epicardial gradient, and an increase of the transmembrane potential gradient across the endocardium.

Transient precordial ST elevation by a spasm of the conus artery during right coronary angiography

During coronary angiography of right coronary artery (RCA), a catheter wedged into a conus artery, and a remarkable coved-type ST elevation was seen in precordial lead through V1–3. LCA angiography did not show any abnormal findings, but we recognized a slow contrast flow in a conus artery by RCA angiography. The patient was free from chest pain, and a ST elevation was improved. The slow flow of a conus artery was recovered within five minutes. Precordial ST elevation may be caused by a catheter-induced spasm of a conus artery.

Contrast-Enhanced Cardiovascular Magnetic Resonance Imaging of Right Ventricular Infarction

We assessed the role of late enhancement cardiovascular magnetic resonance imaging (LE-CMR) for the diagnosis of right ventricular infarction (RVI). Right ventricular infarction occurs in about one-half of patients with inferior myocardial infarction (MI). It is associated with an unfavorable prognosis, but established methods often lack the diagnostic accuracy to detect it. Late enhancement cardiovascular magnetic resonance imaging accurately detects left ventricular MI. Thirty-seven patients with acute inferior MI were included. To test for RVI, they prospectively underwent a physical examination, an electrocardiogram (ECG) for ST-segment elevation in the V4r right precordial lead, and an echocardiogram. After coronary reperfusion, LE-CMR was performed for assessing presence and extent of late enhancement in the right ventricular (RV) wall. The LE-CMR data were compared with the other results; interobserver variability was assessed. The LE-CMR was repeated after 13 months. Late enhancement cardiovascular magnetic resonance imaging detected RVI in 21 of 37 (57%) patients with acute inferior MI. Interobserver variability was very good (kappa 0.83); physical exam was positive for RVI in 7 of 37 (19%) patients, V4r ECG in 13 of 37 (35%) patients, and echocardiogram in 6 of 37 (16%) patients. The LE-CMR findings for RVI showed only mild agreement with findings for RVI on physical exam (kappa 0.30), V(4)r ECG (kappa 0.38), and echocardiography (kappa 0.32). Irreversible injury of the RV persisted at 13 months (kappa 0.85). In patients with acute inferior MI, RVI is more frequently detected by LE-CMR than by current standard diagnostic techniques. Further CMR studies might allow for analyzing its clinical and prognostic relevance.

An Electrocardiographic Algorithm for Determining the Location of Pacemaker Electrode in Patients With Right Bundle Branch Block Configuration During Permanent Ventricular Pacing

The expected morphology of right ventricular pacing is a left bundle branch block (LBBB) pattern. However, right bundle branch block (RBBB) can also be seen during permanent right ventricular pacing. The aim of this study was to develop an electrocardiographic algorithm to differentiate this benign condition from septal and free wall perforation with subsequent left ventricular pacing. Three hundred consecutive patients who had permanent ventricular or dual-chamber pacemaker implantation between 1999 and 2000 were screened and 25 patients (8.3%) who exhibited RBBB configuration were included in the study. Echocardiograms and chest radiographs were evaluated in order to identify the pacing lead location in this group. The authors formed a study group with their own 25 patients and 22 cases of RBBB with permanent pacemaker from previous publications (total 47 patients). Frontal axis, QRS morphology in lead V(1), and the precordial transition point, which is defined as the precordial lead where R wave amplitude is equal to S wave amplitude, were examined. Placement of precordial leads V(1) and V(2) 1 interspace lower than the standard location (Klein maneuver) eliminated the RBBB pattern in 12 patients. RBBB pattern with "true right ventricular pacing" was detected in 24 of the 25 patients, and in 11 of the 22 patients reported in the literature (total 35 patients). Right ventricular pacing was correctly identified in 34 of 35 patients with use of criteria including left superior axis deviation, RS or qR morphology in lead V(1), and precordial transition at lead V(3) with a high sensitivity and specificity. A simple surface electrocardiogram can accurately predict the lead location in patients having RBBB morphology with right ventricular pacing.

P6-110: Coronary venous ablation of epicardial ventricular premature contractions with distinctive QRS morphology

The patient was a 50-year-old man with a history of palpitations caused by ventricular premature contractions (VPCs). The number of VPCs was 38464/day. Twelve-lead ECG during VPCs showed rS in I and aVL, RS in V5 and V6, notched wide R wave in II, III, aVF, and wide R wave in V1-4. QRS duration was 192 ms, and peak deflection index (PDI), which was determined as the time from QRS onset to earliest peak deflection in any precordial lead divided by the total QRS duration, was 0.54. Pace mapping at an endocardial site close to the origin showed QRS duration of 170 ms to be shorter and PDI of 0.5 to be lower than those of the clinical VPCs.

Letters Regarding Article by Coronel et al, “Right Ventricular Fibrosis and Conduction Delay in a Patient With Clinical Signs of Brugada Syndrome: A Combined Electrophysiological, Genetic, Histopathologic, and Computational Study”

To the Editor: We read with interest the report by Coronel et al1 of a case of Brugada syndrome with structural abnormalities of the heart. We would like to comment on the ECG presentation of the patient, which, in our opinion, raises an important interpretation issue. According to the criteria proposed by a group of experts that included 2 authors of the aforementioned report,2 the ECG of the patient reported in the article by Coronel et al1 does not appear to be diagnostic for Brugada syndrome. In fact, the Second Consensus Conference2 states that only “type 1 is diagnostic of Brugada syndrome and is characterized by a coved ST-segment elevation ≥2 mm, followed by a negative T wave, observed in >1 right precordial lead.” In the tracings of the patient presented by Coronel and colleagues,1 the ST-segment elevation is present only in lead V1, does not show a coved morphology in >1 lead, and has no negative T wave. As the authors discuss in the article,1 the presence of a mutation in the SCN5A gene is …

Clinical Features of Emergency Electrocardiography in Patients With Acute Myocardial Infarction Caused by Left Main Trunk Obstruction

To diagnose left main trunk (LMT) infarction by 12-lead standard electrocardiogram (ECG) is an important emergency technique, but the features in LMT infarctions have not been clarified. The study enrolled 140 subjects who were divided into 4 groups according to the location of the culprit artery: 35 with LMT, 35 with left anterior descending artery (LAD), 35 with right coronary artery and 35 with left circumflex artery. Various parameters obtained from the ECGs were analyzed. Average QTc interval (0.51 +/- 0.06 s) in LMT group was markedly longer than that in the 3 other groups. Average QRS axis (-10 +/- 77 degrees) in LMT infarction showed a remarkable left deviation. ST-segment elevation in lead aVR occurred in 28 patients (80.0%) in the LMT group. The ECG features of the LMT group could be classified into 2 main groups: right bundle branch block (RBBB) with a marked left axis deviation (RBBB + LADEV type) and ST-segment elevation in leads V2-5, I and aVL without abnormal axis deviation (LAD type). Either ST-segment elevation in lead aVR and marked prolongation of both the QRS width and QTc interval with a prominent abnormal axis deviation or ST-segment elevation in the broad anterior precordial lead with a normal QRS axis strongly suggests LMT infarction.

Endotracheal administration of adrenaline in cardiopulmonary resuscitation of anaesthetized dogs

In this study, we wanted to determine the effectiveness of endotracheal (ET) adrenaline administration on an anesthetized model of dog in hypoxia and cardiac arrest. We wanted to simulate the most frequent clinical state where urgent administration of drugs is necessary, but it's difficult to provide an intravenous (IV) route. Healthy dogs (n=37) were used for this study. They were anesthetized, endotracheally intubated and ventilated mechanically. A precordial lead II ECG was recorded throughout the experiment. The animals were provided with arterial and central venous lines. During the experiment we measured arterial blood pressure (SP, DP, MAP) by an invasive technique, central venous pressure by H2O manometer, hearth rate, acid-base value, glycemia and electrolytes. Control group: after IV adrenaline administration, concentrations in the arterial blood were continually measured. I exp. group: Under equal conditions, we used ET route for adrenaline administration whereby measuring their concentration and following their haemodynamic effects. In exp. group II adrenalin in a dose of 1.5 mg was administered endotracheally using the same tehnique as in group I. In the second part of the experiment, ET administration of adrenaline under conditions of cardiac arrest was studied. Hypoxia and cardiac arrest were induced by disconnecting from the breading machine. The influence of ET adrenalin administration on lung tissue were established by histophatological analysis and acid-base values. The maximum concentration of adrenalin in the blood after the ET route are almost equal to the concentrations of the drugs after IV administration, but ET doses of adrenaline must be higher than IV doses. Adrenalin was retained in the blood for a longer period after ET administration than after IV route. As the optimal solvent for adrenalin we recommend 0.9% NaCL, and we recommend using a long cateter via the endotracehal tube deep in to the tracheobronchial system as the optimal technique for ET administration. Hypoxia and cardiac arrest do not derange absorption of drugs after ET administration. By measuring the concentration of adrenalin in arterial blood following their haemodynamic effects in different experimental conditions and by evaluating the successfulness

Cibenzoline induced Brugada ECG pattern

We report a case of a 61-year-old female patient who presented with palpitations. The baseline electrocardiogram showed incomplete right bundle branch block with saddle back pattern of the ST segment in one precordial lead, but without any significant ST elevation. She was treated with oral cibenzoline. The subsequent ECG showed a coved Brugada ECG (type I) pattern, which resolved following the discontinuation of cibenzoline. An ajmaline test reproduced the coved type Brugada ECG pattern. Our case is the first report of oral cibenzoline therapy unmasking the diagnostic coved Brugada ECG pattern in a patient with a baseline normal ECG. Cibenzoline, a class I sodium channel blocker antiarrhythmic drug, should probably be avoided in the treatment of patients with Brugada syndrome.

Electrocardiographic Left Atrial Abnormalities and Risk of Ischemic Stroke

We evaluated the association between electrocardiographic left atrial abnormality (ECG-LAA) and ischemic stroke, especially whether ECG-LAA provides additional prognostic information to that provided by echocardiography. A population-based, case-control study included 146 patients with first ischemic stroke and 195 age-, gender-, and race/ethnicity-matched community control subjects. ECG-LAA was defined as either P-wave duration >120 ms or P-terminal force in precordial lead V1 (PTFV1) >40 ms.mm. PTFV1 >40 ms.mm was associated with ischemic stroke after adjustment for other stroke risk factors (odds ratio [OR], 2.32; 95% CI, 1.29 to 4.18). The association remained significant after adding echocardiographic left atrial diameter to the model (OR, 2.31; 95% CI, 1.28 to 4.17). PTFV1 was independently associated with stroke in patients in the upper half of echocardiographically determined left ventricular mass (adjusted OR, 4.5; 95% CI, 2.20 to 9.15) but not in those in the lower half (OR, 0.58; 95% CI, 0.20 to 1.65; P=0.0008). ECG-LAA can supplement 2D echocardiography in assessing the risk of ischemic stroke, especially in subjects with increased left ventricular mass.

Prolonged recovery time in the left precordial leads reflects increased left ventricular mass in the hypertensive patients

Hypertensive left ventricular hypertrophy (LVH) is considered to be a risk for arrhythmogenicity, but the quantification of the changes in T-wave morphology, as the reflection of repolarization abnormality, has not been fully established. The purpose of this study was to quantify the T-wave changes in the hypertensive patients and to investigate the relationship with the increased left ventricular mass. Standard 12-lead electrocardiogram and echocardiogram were recorded in 90 hypertensive patients. Activation time (AT), activation recovery interval (ARI), and recovery time (RT) were measured in the precordial lead and QT interval in the 12 leads. To compare the left precordial T-wave changes among patients, measurements of ARI and RT in the right precordial negative T wave were excluded. Each parameter excluding AT was corrected with Bazett formula, and then the dispersion was calculated. Left ventricular mass index was determined echocardiographically to select non-LVH group (n = 31) and LVH group (n = 59). In both groups, AT, ARI, and RT in the left precordial leads were larger compared with those in the right precordial leads. Dispersion of AT was not different between the 2 groups. However, the dispersion of ARI and RT in LVH group was significantly greater than that in non-LVH group. There were correlations between left ventricular mass index and the dispersion of RT ( r = 0.66, P < .001), ARI ( r = 0.61, P < .001), and 12-lead QT ( r = 0.42, P < .001). In patients with LVH, significant prolongation of RT in the left precordial leads was observed, suggesting that this RT change resulted from the nonuniformity of epicardial action potential duration.

Electrocardiographic Predictors of Cardiovascular Outcome in Women: The National Heart, Lung, and Blood Institute-Sponsored Women’s Ischemia Syndrome Evaluation (WISE) Study

We sought to analyze the value of infrequently measured parameters of the 12-lead electrocardiogram (ECG) in predicting cardiovascular events in women with suspected myocardial ischemia who were referred for cardiac catheterization. Routinely analyzed ECG parameters have low predictive value for cardiovascular events in women with preserved left ventricular function and suspected myocardial ischemia. The predictive value of ECG parameters for cardiovascular disease has not been fully determined. Women enrolled in the National Heart, Lung, and Blood Institute-sponsored Women's Ischemia Syndrome Evaluation (WISE) study who had complete digital 12-lead ECG and quantitative angiography data were studied. Clinical and ECG predictors of cardiovascular disease events, defined as death, congestive heart failure, and non-fatal myocardial infarction, were determined. Of 143 women with ECG and angiographic data (mean age 59 +/- 13 years, left ventricular ejection fraction 64.1 +/- 8.6%), 13% had events during a mean follow-up period of 3.3 +/- 1.6 years. Independent predictors of event occurrences included a wider QRS-T angle (i.e., the spatial electrical angle between the QRS complex and the T-wave; p = 0.0005), wider QRS complex (p = 0.004), longer QTrr (i.e., age- and gender-adjusted QT interval; p = 0.0004), a more depressed ST-segment in precordial lead V5 (p = 0.0002), and a higher coronary artery disease severity score (p = 0.02). Several 12-lead ECG parameters, such as the QRS-T angle and the QRS and QTrr duration, are predictive of future cardiovascular events in women with suspected myocardial ischemia.

Viability pattern, mapping and ablation in patients with right ventricular cardiomyopathy and ventricular tachycardia

Objective: Ventricular tachycardia (VT) may originate from the epicardium (EPI). We hypothesized that QRS morphology and activation times might make ECG criteria that are not patient and site specific, unreliable in distinguishing EPI vs endocardial (ENDO) origin, but that site specific EPI vs ENDO QRS activation and QRS morphology differences should exist. We further hypothesized that QRS intervals would be markedly increased at EPI sites and the QRS morphology in lead I would change from r/s to QS or QR when transitioning from ENDO to EPI sites. Methods: Electroanatomic shells of ENDO and EPI were constructed in sinus rhythm. Pacing with 4 mm tip electrode was performed from 16 distinct non-septal ENDO Josephson sites and their counterpart EPI locations (cycle length: 400-600 ms; diastolic threshold) in 3 patients (pts) undergoing ablation for idiopathic VT. 12-lead ECG was recorded and analyzed for QRS morphology in lead I, widest QRS duration (QRSd) in any lead, and time to latest QRS nadir (QRS-N) in precordial leads. Results: Site to site and pt to pt overlap precluded utility of absolute QRS intervals in identifying EPI origin. Site specific (EPI vs corresponding ENDO) comparisons revealed: 1) increased QRSd 20ms for 13/16 (81%); 2) increased time to QRS-N 20ms for 11/16 (69%) and 3) initial negative forces in lead I (QS or QR) were seen in 9/16 (56%) EPI and no ENDO sites. One or more of above three criteria were seen in 15/16 (94%) EPI vs ENDO sites. In all 3 patients clinical VT was of EPI origin and consistently demonstrated above criteria compared to ENDO PMs. Identical EPI PMs were seen for all 3 VT morphologies and 2 of the VT were successfully ablated. One VT had SOO adjacent to coronary vessel and was not targeted. Conclusions: PM of EPI sites revealed wider QRS complexes with later time to QRS-N and more frequent / marked initial negative forces in lead I compared with corresponding ENDO locations. These findings are site specific. By comparing ENDO PM of comparable morphology to clinical VT, identification of an epicardial SOO is possible. A QRSd increase by 20ms, time to QRS-N in precordial lead increase 20ms and/or a QS or qr in lead I compared to ENDO PM strongly suggest an epicardial origin.

General anesthesia for patients with Brugada syndrome. A report of six cases

To review six cases of Brugada syndrome presenting for insertion of a cardioverter-defibrillator under general anesthesia. All patients had a history of syncope, ST segment elevation in the right precordial lead of the electrocardiogram (ECG) which became prominent after a pilsicainide challenge test. Routine monitors, right precordial lead of the ECG and an external defibrillator were installed prior to anesthesia. We administered propofol/midazolam for induction, and propofol/sevoflurane combined with fentanyl for maintenance of anesthesia. Atropine and ephedrine were administered to decrease vagal tone. No ECG change or arrhythmia was observed perioperatively. After the successful implantation of the defibrillator, all patients were discharged without any adverse event. By avoiding agents or conditions that may exacerbate Brugada syndrome during anesthesia, we were able to manage the patients uneventfully for implantation of a cardioverter-defibrillator.

Spinal Anesthesia of a Patient with Brugada Syndrome: A case report

Brugada syndrome is an arrhythmic syndrome characterized by right bundle branch block, ST segment elevation in the precordial lead (), and sudden death caused by ventricular fibrillation, but with no evidence of an underlying structural heart disease. We report one case of spinal anesthesia for an appendectomy in a 44-year-old male patient diagnosed as having Brugada syndrome by characteristic ECG findings without untoward cardiovascular events.