Implementation of ultraportable echocardiography in an adolescent sudden cardiac arrest screening program.

BACKGROUND: Over a 12-month period, adolescent heart-screening programs were performed for identifying at-risk adolescents for sudden cardiac death (SCD) in our community. Novel to our study, all adolescents received an abbreviated, ultraportable echocardiography (UPE). In this report, we describe the use of UPE in this screening program. METHODS AND RESULTS: Four hundred thirty-two adolescents underwent cardiac screening with medical history questionnaire, physical examination, 12-lead electrocardiogram (ECG), and an abbreviated transthoracic echocardiographic examination. There were 11 abnormalities identified with uncertain/varying clinical risk significance. In this population, 75 adolescents had a murmur or high ECG voltage, of which only three had subsequent structural abnormalities on echocardiography that may pose risk. Conversely, UPE discovered four adolescents who had a cardiovascular structural abnormality that was not signaled by the 12-lead ECG, medical history questionnaire, and/or physical examination. CONCLUSIONS: The utilization of ultraportable, handheld echocardiography is feasible in large-scale adolescent cardiovascular screening programs. UPE appears to be useful for finding additional structural abnormalities and for risk-stratifying abnormalities of uncertain potential of adolescents' sudden death.

Mapping and ablation of frequent post-infarction premature ventricular complexes.

INTRODUCTION: Premature ventricular complexes (PVCs) occur frequently in patients with heart disease. The sites of origin of PVCs in patients with prior myocardial infarction and the response to catheter ablation have not been systematically assessed. METHODS AND RESULTS: In 28 consecutive patients (24 men, age 60 ± 10, ejection fraction [EF] 0.37 ± 0.14) with remote myocardial infarction referred for catheter ablation of symptomatic refractory PVCs, the PVCs were mapped by activation mapping or pace mapping using an irrigated-tip catheter in conjunction with an electroanatomic mapping system. The site of origin (SOO) was classified as being within low-voltage (scar) tissue (amplitude ≤1.5 mV) or tissue with preserved voltage (>1.5 mV). The SOO was confined to endocardial scar tissue in 24/28 patients (86%). The SOO was outside of scar in 3 patients and could not be identified in 1 patient. At the SOO, local endocardial activation preceded the PVC by 46 ± 19 ms, and the electrogram amplitude during sinus rhythm was 0.48 ± 0.34 mV. The PVCs were effectively ablated in 25/28 patients (89%), resulting in a decrease in PVC burden on a 24-hour Holter monitor from 15.6 ± 12.3% to 2.4 ± 4.2% (P < 0.001). The SOO most often was confined to scar tissue located in the left ventricular septum and the papillary muscles. CONCLUSION: Similar to post-infarction ventricular tachycardia, PVCs after remote myocardial infarction most often originate within scar tissue. Catheter ablation of these PVCs has a high-success rate.

Mapping and ablation of epicardial idiopathic ventricular arrhythmias from within the coronary venous system.

BACKGROUND: The prevalence of epicardial idiopathic ventricular arrhythmias that can be ablated from within the coronary venous system (CVS) has not been described. METHODS AND RESULTS: In a consecutive group of 189 patients with idiopathic ventricular arrhythmias referred for ablation, the site of origin (SOO) of ventricular tachycardia and/or premature ventricular contractions was determined by activation mapping and pace mapping. Mapping was performed within the CVS if endocardial mapping did not reveal an SOO. Venography of the CVS and coronary angiography were performed before ablation in the CVS. In 27 of 189 patients (14%+/-5%; 95% confidence interval), the SOO of the ventricular arrhythmia was identified from within the coronary venous system, either in the great cardiac vein (n=26) or the middle cardiac vein (n=1). The mean activation time at the SOO was -29+/-8 ms. Twenty of 27 patients (74%) underwent successful ablation within the CVS. Epicardial ventricular arrhythmias displayed a broader R wave in V(1) compared with arrhythmias in the control group (85 ms [interquartile range, 40] versus 65 ms [interquartile range, 95]; P<0.01). Two patients had recurrent premature ventricular contractions within 2 weeks after ablation, and no recurrences occurred in the remaining patients during a median follow-up of 13 months (range, 25). In the 7 patients with unsuccessful ablation, failure was because the ablation catheter could not be advanced to the SOO within the great cardiac vein (n=4), inadequate power delivery at the SOO (n=1), proximity to the phrenic nerve (n=1), or proximity of the SOO to a major coronary artery (n=1). Transcutaneous epicardial ablation was effective in 1 of 2 patients in whom it was attempted. CONCLUSIONS: Almost 15% of idiopathic ventricular arrhythmias have an epicardial origin. ECG characteristics help to differentiate epicardial arrhythmias from endocardial ventricular arrhythmias. The SOO of epicardial arrhythmias can be ablated from within the CVS in approximately 70% of patients.

Isolated potentials and pace-mapping as guides for ablation of ventricular tachycardia in various types of nonischemic cardiomyopathy.

BACKGROUND: In patients with prior infarction, isolated potentials (IPs) during sinus rhythm reflect fixed scar and often indicate sites critical for ventricular tachycardia (VT). The purpose of this study was to determine the value of IPs in conjunction with pace-mapping to guide VT ablation in patients with various types of nonischemic cardiomyopathy. METHODS: Mapping and ablation of VT were performed in 35 consecutive patients (26 men, age 55 ± 13 years, ejection fraction 0.31 ± 0.14) with VT and various etiologies of nonischemic cardiomyopathy. Pace-mapping was performed at sites with low voltage. Radiofrequency energy was delivered at sites with concealed entrainment or matching pace-maps. RESULTS: One hundred ninety-five VTs (mean cycle length 363 ± 88 ms) were induced. Sites with prespecified ablation criteria displaying IPs during sinus rhythm were recorded in 21 of 35 patients (60%, IP-positive). In these patients, a total of 216 sites meeting prespecified ablation criteria were identified and 146 of 216 sites (68%) displayed IPs. Fifteen of 21 IP-positive patients (71%) no longer had inducible VT after ablation. In 14 of 35 patients, no sites with IPs where prespecified ablation criteria were met were identified (IP-negative) despite combined endocardial and epicardial mapping in 7 of 14 patients. Only 1 of 14 IP-negative patients (7%) no longer had inducible VT at the end of the ablation procedure. During a mean follow-up of 18 ± 13 months, 14 of 21 IP-positive patients (67%) remained arrhythmia-free, compared to 1 of 14 IP-negative patients (7%; P < 0.01). Half of the IP-negative patients had major adverse events due to recurrent arrhythmias, compared to none in IP-positive patients. CONCLUSION: IPs in conjunction with pace-mapping are helpful for identifying critical isthmus areas for ablation of VT in patients with various types of nonischemic cardiomyopathy. Patients with nonischemic cardiomyopathy in whom the arrhythmogenic substrate is characterized by IPs have a more favorable outcome than patients in whom IPs are absent.

Ventricular arrhythmias originating from papillary muscles in the right ventricle.

BACKGROUND: Premature ventricular complexes (PVCs) and ventricular tachycardia (VT) with origin in the left ventricular papillary muscle have recently been described. There are no prior studies describing the characteristics of the ventricular arrhythmias (VAs) arising from the right ventricular papillary muscles (RV PAPs). METHODS: Among 169 consecutive patients who underwent a catheter ablation of a VA, eight patients with RV PAPs were identified (seven men, mean PVC burden 17.0% +/- 20%). A control group consisted of 10 consecutive patients with arrhythmias originating from the right ventricle (10 women, mean PVC burden 13.9% +/- 12.8%). All patients underwent cardiac magnetic resonance imaging (MRI). Intracardiac echocardiography was used to identify the site of origin of the RV PAP arrhythmias. The site of origin of a total of 15 distinct PAP arrhythmias was mapped to the following papillary muscles: posterior (n = 3), anterior (n = 4), or septal (n = 8). RESULTS: Postablation echocardiograms did not reveal new tricuspid regurgitation. During a mean follow-up of 8 +/- 9 months, there were no adverse outcomes. The PVC burden was reduced from 17% +/- 20% preablation to 0.6% +/- 0.8% postablation in the RV PAP group and from 13.9% +/- 12.8% to 0.3% +/- 0.4% in the control group. The QRS complex was broader in the RV PAP group compared with in the control group (163 +/- 21 ms vs. 141 +/- 22 ms; P = .02). RV PAP arrhythmias originating from the posterior or anterior RV PAPs more often had a superior axis with late R-wave transition (>V4) compared with septal RV RAP arrhythmias, which more often had an inferior axis with an earlier R-wave transition in the precordial leads (

Relationship between burden of premature ventricular complexes and left ventricular function.

BACKGROUND: Frequent idiopathic premature ventricular complexes (PVCs) can result in a reversible form of left ventricular dysfunction. The factors resulting in impaired left ventricular function are unclear. Whether a critical burden of PVCs can result in cardiomyopathy has not been determined. OBJECTIVE: The objective of this study was to determine a cutoff PVC burden that can result in PVC-induced cardiomyopathy. METHODS: In a consecutive group of 174 patients referred for ablation of frequent idiopathic PVCs, the PVC burden was determined by 24-hour Holter monitoring, and transthoracic echocardiograms were used to assess left ventricular function. Receiver-operator characteristic curves were constructed based on the PVC burden and on the presence or absence of reversible left ventricular dysfunction to determine a cutoff PVC burden that is associated with left ventricular dysfunction. RESULTS: A reduced left ventricular ejection fraction (mean 0.37 +/- 0.10) was present in 57 of 174 patients (33%). Patients with a decreased ejection fraction had a mean PVC burden of 33% +/- 13% as compared with those with normal left ventricular function 13% +/- 12% (P <.0001). A PVC burden of >24% best separated the patient population with impaired as compared with preserved left ventricular function (sensitivity 79%, specificity 78%, area under curve 0.89) The lowest PVC burden resulting in a reversible cardiomyopathy was 10%. In multivariate analysis, PVC burden (hazard ratio 1.12, 95% confidence interval 1.08 to 1.16; P <.01) was independently associated with PVC-induced cardiomyopathy. CONCLUSION: A PVC burden of >24% was independently associated with PVC-induced cardiomyopathy.

A critical decrease in dominant frequency and clinical outcome after catheter ablation of persistent atrial fibrillation.

BACKGROUND: Termination of persistent atrial fibrillation (AF) by radiofrequency ablation (RFA) is associated with a high probability of freedom from AF but requires extensive ablation and long procedure times. OBJECTIVE: The purpose of this study was to determine whether a critical decrease in the dominant frequency (DF) of AF is a sufficient endpoint for RFA of persistent AF. METHODS: Antral pulmonary vein isolation (APVI) followed by RFA of complex fractionated atrial electrograms (CFAEs) in the atria and coronary sinus was performed in 100 consecutive patients with persistent AF. The DF of AF in lead V1 and in the coronary sinus was determined by fast Fourier transform (FFT) analysis at baseline and before termination of AF to identify a critical decrease in DF predictive of sinus rhythm after RFA. RESULTS: A > or =11% decrease in DF had the highest accuracy in predicting freedom from atrial arrhythmias, with a sensitivity of 0.71 and a specificity of 0.82 (P <.001). At a mean follow-up of 14 +/- 3 months after one ablation procedure, sinus rhythm was maintained off antiarrhythmic drugs in 8/35 (23%) and 20/26 (77%) of patients with a <11% and > or =11% decrease in DF, respectively (P <.001). Sinus rhythm was maintained in 24/39 patients (62%) in whom RFA terminated AF. The duration of RFA and total procedure time were longer in patients with AF termination (95 +/- 23 and 358 +/- 87 minutes) than in patients with a <11% decrease in the DF (77 +/- 16 and 293 +/- 70 minutes) or > or =11% decrease in DF (80 +/- 17 and 289 +/- 73 minutes), respectively (P <.01). Among the variables of age, gender, left atrial diameter, duration of AF, left ventricular ejection fraction, duration of RFA, a > or =11% decrease in DF, and termination of AF, a > or =11% decrease in DF (odds ratio = 9.89, 95% confidence interval [CI] 2.84-34.47) and termination during RFA (OR = 4.38, 95% CI 1.50-12.80) were the only independent predictors of freedom from recurrent atrial arrhythmias. CONCLUSION: In a retrospective analysis of consecutive patients with persistent AF, a decrease in the DF of AF by 11% in response to APVI and ablation of CFAEs was associated with a probability of maintaining sinus rhythm that was similar to that when RFA terminates AF.

Inadvertent electrical isolation of the left atrial appendage during catheter ablation of persistent atrial fibrillation.

BACKGROUND: Left atrial appendage (LAA) isolation is rare and may be associated with impaired transport function and thromboembolism. OBJECTIVE: The purpose of this study was to determine the mechanisms of inadvertent isolation of the LAA during atrial fibrillation (AF) ablation. METHODS: This study consisted of 11 patients (ejection fraction 0.43 +/- 0.18, left atrial diameter 51 +/- 8 mm) with persistent AF who had LAA conduction block during a procedure for AF (n = 8) or atrial tachycardia (AT) (n = 3). RESULTS: LAA conduction block occurred during ablation at the Bachmann bundle region in 6 patients, mitral isthmus in 3, LAA base in 2, and coronary sinus in 1. The mean distance from the ablation site to the LAA base was 5.0 +/- 1.9 cm. LAA isolation was transient in all 6 patients in whom LAA conduction was monitored and was permanent in the 4 patients in whom conduction was not monitored during energy delivery. The remaining patient was noted to have LAA isolation during a redo procedure before any ablation. Nine of (82%) the 11 patients have remained arrhythmia-free without antiarrhythmic drugs at mean follow-up of 6 +/- 7 months, and all have continued taking warfarin. CONCLUSION: Electrical isolation of the LAA may occur during ablation of persistent AF and AT even when the ablation site is remote from the LAA. This likely is due to disruption of the Bachmann bundle and its leftward extension, which courses along the anterior left atrium and bifurcates to surround the LAA. Monitoring of LAA conduction during ablation of persistent AF or AT is important in avoiding permanent LAA isolation.

Utility of tachycardia cycle length variability in discriminating atrial tachycardia from ventricular tachycardia.

BACKGROUND: Inappropriate implantable cardioverter-defibrillator (ICD) therapy of atrial tachycardia (AT) with 1:1 atrioventricular (AV) conduction is common because it is difficult to discriminate from ventricular tachycardia (VT) with 1:1 retrograde conduction. Tachycardia cycle length (CL) variability and the relationship between atrial and ventricular CLs may be useful in discriminating AT from VT with 1:1 retrograde conduction. OBJECTIVE: The purpose of this study was to evaluate the usefulness of the relationship between the atrial and ventricular CLs in differentiating AT with 1:1 conduction from VT with 1:1 retrograde conduction. METHODS: We studied 71 patients who had a tachycardia with a 1:1 AV relationship and significant CL variability. Thirty-nine patients had AT (21 inducible and 18 simulated), and 32 patients had VT (11 inducible and 21 simulated). The relationship between atrial and ventricular CLs was examined. RESULTS: A change in atrial CL predicted the change in subsequent ventricular CL in 37 (95%) of 39 patients with AT and in none of the patients with VT. A change in preceding ventricular CL predicted the change in atrial CL in 31 (97%) of 32 patients with VT and in only one (3%) of 39 patients with AT. The sensitivity, specificity, and positive and negative predictive values of a change in atrial CL predicting the change in ventricular CL for AT with significant CL variability were 95%, 100%, 100%, and 94%, respectively. The corresponding values for the change in preceding ventricular CL predicting the change in atrial CL for AT with significant CL variability were 97%. CONCLUSION: The relationship between atrial and ventricular CL is useful in differentiating AT from VT with retrograde conduction. A change in atrial CL that predicts the change in subsequent ventricular CL rules in AT and excludes VT.

Radiofrequency ablation guided by mechanical termination of idiopathic ventricular arrhythmias originating in the right ventricular outflow tract.

BACKGROUND: Termination of ventricular tachycardia (VT) by mechanical pressure has been described for fascicular and postinfarction VT. Mechanical interruption of idiopathic ventricular arrhythmias (VT/premature ventricular complexes [PVCs]) arising in the right ventricular outflow tract (RVOT) has not been described in systematic fashion. METHODS: Eighteen consecutive patients (13 females, age 49 +/- 13 years, ejection fraction 0.55 +/- 0.12) underwent mapping and ablation of RVOT VT or PVCs. In 7 patients, 9 distinct VTs (mean cycle length 440 +/- 127 ms), and in 11 patients, 11 distinct PVCs originating in the RVOT were targeted. Mechanical termination was considered present if a reproducibly inducible VT was no longer inducible or if frequent PVCs suddenly ceased with the mapping catheter at a particular location. Endocardial activation time, electrogram characteristics, and pace-mapping morphology were assessed at this location. Radiofrequency energy was delivered if mechanical termination was observed. RESULTS: All targeted arrhythmias were successfully ablated. In 7 of 18 patients (39%), catheter manipulation terminated the arrhythmia with the mapping catheter located at a particular site. Local endocardial activation time was earlier at sites of mechanical termination (-31 +/- 7 ms) compared with effective sites without termination (-25 +/- 3 ms, P = 0.04). The 10-ms isochronal area was smaller in patients with mechanical interruption (0.35 +/- 0.2 cm(2)) than in patients without mechanical termination (1.33 +/- 0.9 cm(2), P = 0.01). At all sites susceptible to mechanical trauma, the pace map displayed a match with the targeted VT/PVC. All sites where mechanical termination of VT or PVCs occurred were effective ablation sites. CONCLUSIONS: Mechanical suppression at the site of origin of idiopathic RVOT arrhythmias frequently occurs during the mapping procedure and is a reliable indicator of effective ablation sites. Mechanical termination of RVOT arrhythmias may be indicative of a more localized arrhythmogenic substrate.

Clinical value of noninducibility by high-dose isoproterenol versus rapid atrial pacing after catheter ablation of paroxysmal atrial fibrillation.

BACKGROUND: AF can be induced by RAP or ISO in >85% of patients with PAF. METHODS: ISO was administered in escalating doses of 5, 10, 15, and 20 microg/min in 112 patients (age = 56 +/- 13 years) with PAF before radiofrequency catheter ablation. AF was inducible in 97 of 112 patients (87%) at a mean dose of 15 +/- 5 microg/min. RAP induced AF in the remaining 14 of 15 patients. Antral pulmonary vein (PV) isolation (APVI) was followed by ablation of complex fractionated atrial electrograms (CFAEs) as necessary to terminate AF and render AF noninducible in response to ISO. RESULTS: AF terminated during APVI in 72 of 111 patients (65%) and after APVI plus ablation of CFAEs in 11 of 111 patients (10%). In the remaining 28 patients (25%), sinus rhythm was restored by transthoracic cardioversion. RAP was performed in the last 61 consecutive patients who were rendered noninducible by ISO. RAP initiated AF in 20 of 61 patients (33%) and atrial flutter in 6 patients (10%). No additional ablation was performed if AF was induced with RAP; however, atrial flutter was targeted. At 12 +/- 5 months, 63/75 patients (84%) who were noninducible by ISO and 2 of 8 (25%) who still were reinducible by ISO were free from recurrent AF after a single ablation procedure without antiarrhythmic drugs (P = 0.001). AF recurred in 20 of 36 patients (56%) who required cardioversion for persistent AF after ablation (P < 0.001). Among the 61 patients who also underwent RAP, 12 of 20 (60%) who were, and 31 of 41 (76%) who were not inducible by RAP were free from recurrent AF (P = 0.21). The accuracy of noninducibility as a predictor of clinical outcome was 83% with ISO and 64% by RAP (P = 0.03). CONCLUSIONS: The response to isoproterenol after catheter ablation of PAF more accurately predicts clinical outcome than the response to RAP.

Prevalence of fever in patients undergoing left atrial ablation of atrial fibrillation guided by barium esophagraphy.

BACKGROUND: Real-time esophageal imaging is critical in avoiding esophageal injury. However, the safety of esophageal imaging with barium has not been specifically explored. METHODS: Three hundred seventy consecutive patients underwent left atrial (LA) ablation of atrial fibrillation (AF) under conscious sedation. One hundred eighty-five patients (50%) underwent the ablation procedure with, and 185 patients (50%) underwent the procedure without administration of barium. Fever, as a surrogate for aspiration, was defined as a maximal temperature >or=100 degrees F within the first 24 hours following the ablation procedure. RESULTS: Thirty of the 370 patients (8%) developed fever within 24 hours after LA ablation. The prevalence of fever was 9% (17/185) among patients who received barium and 7% (13/185) among those who did not receive barium (P = 0.6). Evaluation revealed the following causes of fever in 14 of the 30 patients (47%) with no difference in prevalence between the 2 groups: pericarditis, venous thromboembolism, hematoma, and infiltrate on chest radiography. Multivariate analysis failed to reveal any factors associated with development of fever. None of the patients experienced serious complications such as respiratory failure or atrioesophageal fistula. CONCLUSIONS: Fever may occur in approximately 10% of patients undergoing LA ablation of AF. Administration of barium is not associated with fever or other complications such as aspiration pneumonia. Real-time imaging of the esophagus with barium administration in conjunction with conscious sedation appears to be safe.

Delayed-enhanced magnetic resonance imaging in nonischemic cardiomyopathy: utility for identifying the ventricular arrhythmia substrate.

OBJECTIVES: The purpose of this study was to assess the value of delayed-enhanced magnetic resonance imaging (DE-MRI) to guide ablation of ventricular arrhythmias in patients with nonischemic cardiomyopathy (NIC). BACKGROUND: In patients with NIC, ventricular arrhythmias often are associated with scar tissue. DE-MRI can be used to precisely define scar tissue. METHODS: DE-MRI was performed in 29 consecutive patients (mean age 50 +/- 15 years) with NIC (mean ejection fraction 37 +/- 9%) referred for catheter ablation of ventricular tachycardia (VT) or premature ventricular complexes (PVCs). Scar was extracted from DE-MRIs and was then integrated into the electroanatomic map. Mapping data were correlated with respect to the localization of scar tissue. RESULTS: Scar was identified by DE-MRI in 14 of 29 patients. Nine of these patients had VT and 5 had PVCs. In 5 of the patients there was predominantly endocardial scar, and mapping and ablation of arrhythmias was effectively performed from the endocardium in all 5 patients. In 2 patients scar was either intramural or epicardial with extension to the endocardium. In both patients with partial endocardial scar extension, the ablation was effective in eliminating some but not all arrhythmias. In 2 patients most of the scar tissue was confined to the epicardium; mapping identified and eliminated an epicardial origin in both patients. No effect on arrhythmias could be achieved in the other 5 patients with predominantly intramural scar. CONCLUSIONS: DE-MRI in patients without prior infarctions can help to identify the arrhythmogenic substrate; furthermore, it helps to plan an appropriate mapping and ablation strategy.

Mechanical displacement of the esophagus in patients undergoing left atrial ablation of atrial fibrillation.

BACKGROUND: Left atrial (LA) ablation of atrial fibrillation (AF) may rarely be complicated by an atrio-esophageal fistula. OBJECTIVE: The purpose of this study was to determine the feasibility of mechanical displacement of the esophagus in patients undergoing LA ablation. METHODS: Twelve patients underwent mechanical displacement of the esophagus performed by an endoscopist during an LA ablation procedure under conscious sedation. RESULTS: The intrinsic course of the esophagus was near the left pulmonary veins (PVs) in 6 patients, the right PVs in 5 patients, and the mid-LA in 1 patient. In 10 (83%) of the 12 patients, the esophagus could be displaced with the endoscope. The maximal displacement toward the left-sided and right-sided PVs was 2.4 and 2.1 cm, respectively. In 2 (22%) of the 9 patients in whom a prior procedure was unsuccessful because of an unfavorable esophageal course, the esophagus remained at the same location to which it was displaced after removal of the endoscope, facilitating energy delivery at the target site. In the remaining 7 patients, the esophagus returned to its original location after the endoscope was removed. There were no complications related to the endoscopic procedure. CONCLUSION: The esophagus can be mechanically displaced with an endoscope during an LA ablation procedure under conscious sedation. However, in most patients, the esophagus assumes its original course after removal of the endoscope. In some patients in whom PV isolation is problematic because of an unfavorable esophageal course, endoscopic displacement may facilitate safe energy delivery over the posterior LA.

Ventricular arrhythmias originating from a papillary muscle in patients without prior infarction: a comparison with fascicular arrhythmias.

BACKGROUND: The papillary muscles (PAP) have been implicated in arrhythmogenesis, largely based on theoretical considerations and experimental studies. Few clinical studies have described papillary muscle arrhythmias. OBJECTIVE: This study sought to describe ventricular arrhythmias arising from the left ventricular PAPs in a consecutive series of patients without prior myocardial infarction and to compare these arrhythmias with fascicular arrhythmias. METHODS: Nine of 122 consecutive patients (7%) presenting with symptomatic premature ventricular complexes (PVCs) or nonsustained ventricular tachycardia (VT) were found to have a site of origin in the anterolateral or posteromedial left ventricular PAP. Their mean age was 57 +/- 9 years, and the mean ejection fraction was 0.49 +/- 13. Four of 9 patients had idiopathic cardiomyopathy. The PAP involvement was established by intracardiac echocardiography. Eight of the 122 patients (6.5%) had idiopathic VT originating in the left anterior or posterior fascicle, and these patients served as a control group. RESULTS: Compared with patients with fascicular arrhythmias, the QRS width was significantly greater in patients with PAP arrhythmias (150 +/- 15 ms vs. 127 +/- 11 ms; P = .001). Presystolic Purkinje potentials were identified at all effective ablation sites for fascicular arrhythmias, but in arrhythmias originating from PAPs, more distal Purkinje potentials often were recorded from the Purkinje-myocardial interface located at the PAP. All arrhythmias originating from the PAPs and the fascicles were effectively ablated. Echocardiography before and after radiofrequency ablation did not show new or worsened mitral insufficiency. CONCLUSION: The PAPs can give rise to ventricular arrhythmias in normal and structurally abnormal hearts without prior infarcts. Intracardiac echocardiography seems helpful in recognizing and guiding radiofrequency ablation of PAP arrhythmias.

Mechanisms of ventricular arrhythmias in heart failure.

Congestive heart failure continues to be a leading cause of mortality and morbidity worldwide. In approximately 50% of these patients, the mode of death is sudden. Ventricular tachycardia and fibrillation represent the majority of arrhythmias; the mechanisms responsible are heterogeneous and complex. Myocardial scar, a potent environment for reentry, is likely to contribute to many of the ventricular arrhythmias in ischemic heart failure. Altered calcium handling and changes in potassium currents may contribute to the increase in early and delayed afterdepolarizations seen in the failing heart. In addition, compensatory mechanisms may become deleterious and potentially arrhythmogenic via a variety of mechanisms. This article provides a general overview of the mechanisms thought to be responsible for ventricular arrhythmias in chronic heart failure.