Radiofrequency ablation of atrial flutter.
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Adult↗
Biomedical subjects
W G Stevenson
Publications and source records attributed to W G Stevenson.
Ablation of ventricular tachycardia with a saline-cooled radiofrequency catheter: anatomic and histologic characteristics of the lesions in humans.
INTRODUCTION: In animal models, active cooling of the electrode during radiofrequency (RF) ablation allows creation of larger lesions, presumably by increasing the power that can be delivered without coagulum formation. These RF lesions have not been characterized in human myocardium in regions of infarction and scarring. METHODS AND RESULTS: Cooled-tip RF catheter ablation of ventricular tachycardias (VTs) was performed in two patients who had severe congestive heart failure and subsequently underwent cardiac transplantation. The first patient had four different monomorphic VTs. RF applications along the inferoseptal margin of a scarred region abolished all inducible VTs. The second patient had sarcoidosis involving the myocardium and four different inducible VTs. RF current applied at an inferobasal VT exit and at the right and left septa failed to abolish the VTs. The explanted hearts were examined at the time of cardiac transplantation 18 and 21 days later, respectively. Lesions extended to depths up to 7 mm, reaching clusters of myocardial cells deep to regions of fibrosis. Microscopically, the ablation sites contained coagulation necrosis with hemorrhage, surrounded by a rim of granulation tissue. CONCLUSION: Saline-irrigated RF catheter ablation produces relatively large lesions capable of penetrating deep into scarred myocardium.
Adult↗
Proarrhythmia.
Proarrhythmia is defined as the provocation of a new arrhythmia or the aggravation of a pre-existing one during therapy with a drug at doses or plasma concentrations below those considered to be toxic. Suggested criteria for proarrhythmia include (1) the new appearance of a sustained ventricular tachyarrhythmia; (2) change from a nonsustained to a sustained tachyarrhythmia; (3) acceleration of tachycardia rate; or (4) the new appearance of a clinically significant bradyarrhythmia or conduction defect. Proarrhythmia can be the direct result of a drug's electrophysiologic effects on conduction velocity, refractoriness, and automaticity. However, it may also be the result of metabolic abnormalities, changes in autonomic state, or drug/drug interactions that amplify or alter the drug's electrophysiologic effects. Some forms of ventricular proarrhythmia, such as torsade de pointes, are difficult to forecast and occur in patients with structurally normal hearts as well as in those with serious heart disease. Other forms of ventricular proarrhythmia, such as monomorphic ventricular tachycardia, occur predominantly in patients with structural heart disease or pre-existing ventricular arrhythmia. Atrial flutter with 1 : 1 conduction and bradyarrhythmias can be manifestations of proarrhythmia, particularly during drug therapy for atrial fibrillation. In patients with pacemakers or implantable cardiac defibrillators, antiarrhythmic drugs can change pacing thresholds and can alter the ability of a device to recognize or terminate a sustained ventricular tachyarrhythmia.
Anti-Arrhythmia Agents↗
Recipient-to-donor atrioatrial conduction after orthotopic heart transplantation: surface electrocardiographic features and estimated prevalence.
Recipient-to-donor atrioatrial conduction across a suture line has been rarely reported after orthotopic heart transplantation. The relation of such conduction to symptomatic arrhythmias and its prevalence are not known. Recipient-to-donor atrioatrial conduction was demonstrated in a 28-year-old woman with paroxysmal supraventricular tachycardia 7 years after orthotopic heart transplantation. Atrial tachycardia in the recipient atria conducted 2:1 to the donor atria and was eliminated by radiofrequency catheter ablation of a left-sided atrioatrial electrical connection. The electrocardiogram at rest and during exercise, recorded before ablation of the recipient-to-donor connection, showed frequent atrial premature complexes, with variable coupling to the preceding sinus beats, and a change in P-wave morphology during exercise, which reverted to normal during the recovery period. These findings were eliminated by ablation of the recipient-to-donor connection. To determine the prevalence of recipient-to-donor atrioatrial conduction late after transplantation, we evaluated the exercise electrocardiograms of 50 subjects > 5 years after heart transplantation for these features of recipient-to-donor conduction. At least 1 feature was present in 5 subjects, and both were present in 1 subject. Electrical conduction can occur across surgical suture lines in the atria. Recipient-to-donor atrioatrial conduction may occur in < or = 10% of patients late after heart transplantation. It is a potential cause of arrhythmias that can be effectively treated with radiofrequency catheter ablation.
Adult↗
Radiofrequency catheter ablation of ventricular tachycardia after myocardial infarction.
BACKGROUND: Patients with ventricular tachycardia (VT) after myocardial infarction often have multiple morphologies of inducible VT, which complicates mapping and is viewed by some as a relative contraindication to ablation. Attempting to identify and target a single "clinical" VT is often limited by inability to obtain 12-lead ECGs of VTs that are terminated emergently or by defibrillators. This study assesses the feasibility of ablation in patients selected without regard to the presence of multiple VTs by targeting all VTs that allow mapping. METHODS AND RESULTS: Radiofrequency catheter ablation targeting all inducible monomorphic VTs that allowed mapping was performed in 52 patients with prior myocardial infarction. Antiarrhythmic drug therapy had failed in 41 (79%) patients including amiodarone in 36 (69%) patients. An average of 3.6+/-2 morphologies of VT were induced per patient. More than 1 ablation session was required in 16 (31%) patients. Complications occurred in 5 (10%) patients, including 1 (2%) death caused by acute myocardial infarction. During follow-up 59% of patients continued to receive amiodarone; 23 (45%) had implantable defibrillators. During a mean follow-up of 18+/-15 months (range 0 to 51 months) 1 patient died suddenly, 2 died from uncontrollable VT, and 5 died from heart failure. Three-year survival rate was 70+/-10%, and rate for risk of VT recurrence was 33+/-7%. CONCLUSIONS: Radiofrequency catheter ablation controls VT that is sufficiently stable to allow mapping in 67% of patients despite failure of antiarrhythmic drug therapy and multiple inducible VTs. However, ablation was largely adjunctive to amiodarone and defibrillators in this referral population.
Adult↗
Anatomic and electrophysiologic relation between the coronary sinus and mitral annulus: implications for ablation of left-sided accessory pathways.
To determine whether precise left-sided accessory pathway localization is possible from the coronary sinus, electrocardiogram (ECG) characteristics from the coronary sinus pair demonstrating earliest activation via the accessory pathway were compared to simultaneous mitral annular ablation catheter ECGs at successful ablation sites in 48 patients. To define the coronary sinus-mitral annular relation, the coronary sinus to mitral annulus distance (D) was measured at sequential distances from the coronary sinus os in 10 cadaver hearts. Mitral annular ECGs demonstrated earliest activation via the accessory pathway more frequently than the earliest coronary sinus pair (p < 0.001), more frequent continuous electrical activity (p < 0.001), and more frequent accessory pathway potentials (p < 0.01). D was >10 mm at 20, 40, and 60 mm, respectively, from the coronary sinus os. Coronary sinus ECGs do not precisely localize left-sided accessory pathways, which may be due in part to an average anatomic separation of more than 10 mm between the coronary sinus and accessory pathways bridging the mitral annulus.
Adult↗
Entrainment mapping and radiofrequency catheter ablation of ventricular tachycardia in right ventricular dysplasia.
OBJECTIVES: The purpose of this study was to determine if entrainment mapping techniques and predictors of successful ablation sites previously tested in coronary artery disease can be applied to ventricular tachycardia (VT) in arrhythmogenic right ventricular dysplasia (ARVD). BACKGROUND: VT in ARVD has not been well characterized. Reentry circuits in areas of abnormal myocardium are the likely cause, but these circuits have not been well defined. METHODS: Mapping of 19 VTs in 5 patients with ARVD was performed. At 58 sites pacing entrained VT and radiofrequency current (RF) was applied to assess acute termination of VT. RESULTS: Sites classified as exits, central/proximal, inner loop, outer loop, remote bystander and adjacent bystander were identified by entrainment criteria. The reentrant circuit sites were clustered predominantly around the tricuspid annulus and in the right ventricular outflow tract (RVOT). RF ablation acutely terminated VT at 13 sites or 22% of the applications. Of the 19 VTs, eight were rendered noninducible and three were modified to a longer cycle length. In 2 patients ablation at a single site abolished two VTs. CONCLUSION: VT in ARVD shows many of the characteristics of VT due to myocardial infarction. Entrainment mapping techniques can be used to characterize reentry circuits in ARVD. The use of entrainment mapping to guide ablation is feasible.
Adult↗
Identification and ablation of macroreentrant ventricular tachycardia with the CARTO electroanatomical mapping system.
Monomorphic ventricular tachycardias associated with regions of scar are most commonly due to reentry. Catheter based techniques have recently been described for mapping of reentry circuits. Fluoroscopic methods have obvious limitations when attempting to map large ventricular reentry circuit and localize target-sites of radiofrequency ablation. Three-dimensional right ventricular endocardial mapping was performed in a 38-year-old patient with ventricular tachycardia 28 years after surgical correction of tetralogy of Fallot by using the CARTO electroanatomical system. The map of electrogram voltage showed low amplitude electrograms over the anterior wall of the right ventricle extending into the right ventricular outflow tract, consistent with the location of the ventriculotomy scar. Recording of local activation time was combined with entrainment mapping to define the macroreentrant circuit during ventricular tachycardia. Since the activation propagated through a broad path around the right ventriculotomy scar, ablation was performed by creating a line of block, which was facilitated by tagging of the lesion sites on the endocardial activation map. Large ventricular reentry circuits can be identified and interrupted by creation of a line of block to interrupt a broad path. A practical approach to mapping combining analysis of electrogram voltage, activation sequence, and entrainment is presented.
Adult↗
Arrhythmia of the month: shortening of ventriculoatrial conduction time during radiofrequency catheter ablation of a concealed accessory pathway.
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Atrioventricular Node↗
Use of telemetered permanent pacemaker intracardiac electrograms to diagnose ventricular tachycardia.
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Anti-Arrhythmia Agents↗
Ablation therapy for cardiac arrhythmias.
Ablation has become an important and, in some cases, the first-line therapy for a number of tachyarrhythmias. The feasibility of treating arrhythmias with ablation was initially demonstrated with surgical ablation techniques. Recently, catheter ablation techniques have replaced the surgical approach in nearly all cases. Catheter ablation is highly effective for the Wolff-Parkinson-White syndrome, atrioventricular nodal reentry, and atrial ectopic tachycardia. It is effective for atrial flutter, although approximately one quarter of patients treated with catheter ablation continue to require therapy for concomitant atrial fibrillation. The surgical maze procedure has proved to be feasible for preventing atrial fibrillation. The risks and long-term efficacy of catheter ablation maze procedures for atrial fibrillation need to be defined. The efficacy of ablation for ventricular tachycardia varies with the type of tachycardia. Catheter ablation is very effective for the rare idiopathic ventricular tachycardias that occur in structurally normal hearts and for bundle-branch reentry ventricular tachycardia, which occurs most frequently in patients with dilated cardiomyopathy. When performed at an experienced center, surgical ablation is an excellent option for selected patients with ventricular tachycardia due to prior myocardial infarction who have a discrete aneurysm but otherwise well-preserved ventricular function. Catheter ablation shows promise for this arrhythmia, but it can be offered only to those patients who have relatively slow tachycardias that allow catheter mapping. Substantial advances in mapping and ablation technology will continue to occur, allowing nonpharmacologic control of cardiac arrhythmias to be achieved in an ever greater number of patients.
Arrhythmias, Cardiac↗
Catheter ablation as an adjunct to ICD therapy.
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Catheter Ablation↗
Risk of initiating antiarrhythmic drug therapy for atrial fibrillation in patients admitted to a university hospital.
BACKGROUND: The risks of antiarrhythmic therapy are increasingly recognized, but the risks associated with the initiation of antiarrhythmic therapy in patients hospitalized for atrial fibrillation are poorly defined. OBJECTIVE: To determine the incidence, time course, and predictors of adverse cardiac events that require intervention during initiation of antiarrhythmic drug therapy for atrial fibrillation. DESIGN: Retrospective chart review. SETTING: University hospital. PARTICIPANTS: 417 consecutive patients who underwent a total of 597 drug trials during a total of 550 hospitalizations for atrial fibrillation. INTERVENTION: Initiation of therapy with antiarrhythmic drugs: procainamide (189 trials), quinidine (179 trials), disopyramide (20 trials), propafenone (110 trials), flecainide (2 trials), sotalol (72 trials), and amiodarone (25 trials). Electrical conversion was performed during 247 trials. MEASUREMENTS: Incidence of adverse events and daily hazard rate were measured. Logistic regression was done to identify risk factors. RESULTS: During the 597 drug trials, 80 (13.4%) cardiac adverse events occurred in 73 patients. The risk was greatest during the first 24 hours of therapy. Bradyarrhythmias were the most common adverse event, occurring in 47 trials (7.9%); prolongation of the QT interval warranting discontinuation of drug therapy (9 trials; 1.5%) and ventricular arrhythmias (8 trials; 1.3%) were less frequent. In multivariate analysis, previous myocardial infarction was associated with increased risk (odds ratio, 1.90 [95% CI, 1.05 to 3.43]) and the association between older age and increased risk (odds ratio, 1.29 per decade [CI, 0.97 to 1.72]) was of borderline statistical significance. CONCLUSIONS: A significant risk for cardiac adverse events exists during initiation of antiarrhythmic therapy in patients hospitalized for atrial fibrillation. Observation with electrocardiographic monitoring seems advisable for 24 to 48 hours during initiation of antiarrhythmic therapy, particularly for elderly patients and patients who have previously had myocardial infarction.
Adult↗
Exploring postinfarction reentrant ventricular tachycardia with entrainment mapping.
Ventricular tachycardia late after myocardial infarction is usually due to reentry in the infarct region. These reentry circuits can be large, complex and difficult to define, impeding study in the electrophysiology laboratory and making catheter ablation difficult. Pacing through the electrodes of the mapping catheter provides a new approach to mapping. When pacing stimuli capture the effects on the tachycardia depend on the location of the pacing site relative to the reentry circuit. The effects observed allow identification of various portions of the reentry circuit, without the need for locating the entire circuit. Isthmuses where relatively small lesions produced by radiofrequency catheter ablation can interrupt reentry can often be identified. A classification that divides reentry circuits into one or more functional components helps to conceptualize the reentry circuit and predicts the likelihood that heating with radiofrequency current will terminate tachycardia. These methods are helping to define human reentry circuits.
Cardiac Pacing, Artificial↗
Catheter ablation of ventricular tachycardia after myocardial infarction: relation of endocardial sinus rhythm late potentials to the reentry circuit.
OBJECTIVES: We sought to determine whether endocardial late potentials during sinus rhythm are associated with reentry circuit sites during ventricular tachycardia (VT). BACKGROUND: During sinus rhythm, slow conduction through an old infarct region may depolarize tissue after the end of the QRS complex. Such slow conduction regions can cause reentry. METHODS: Endocardial catheter mapping and radiofrequency ablation were performed in 24 patients with VT late after myocardial infarction. We selected for analysis a total of 103 sites where the electrogram was recorded during sinus rhythm and, without moving the catheter, VT was initiated and radiofrequency current applied in an attempt to terminate VT. RESULTS: Late potentials were present at 34 sites (33%). During pace mapping, the stimulus-QRS complex was longer at late potential sites, consistent with slow conduction, than at sites without late potentials (p < 0.0001). Late potentials were present at 15 (71%) of 21 sites classified as central or proximal in the reentry circuit based on entrainment, but also occurred frequently at bystander sites (13 [33%] of 39) and were often absent at the reentry circuit exit (3 [23%] of 13). Late potentials were present at 20 (54%) of 37 sites where ablation terminated VT, compared with 14 (21%) of 66 sites where ablation did not terminate VT (p = 0.004). Ablation decreased the amplitude of the late potentials present at sites where ablation terminated VT. CONCLUSIONS: Although sites with sinus rhythm late potentials often participate in VT reentry circuits, many reentry circuit sites do not have late potentials. Late potentials can also arise from bystander regions. Late potentials may help identify abnormal regions in sinus rhythm but cannot replace mapping during induced VT to guide ablation.
Action Potentials↗
Pharmacologic and nonpharmacologic treatment of ventricular arrhythmias in heart failure.
Ventricular arrhythmias are common in patients with heart failure. The risk and benefits of antiarrhythmic therapies continue to be defined. Class I antiarrhythmic drugs should be avoided due to proarrhythmic and negative inotropic effects that may be responsible for increased mortality in some trials. For patients resuscitated from sustained ventricular tachycardia or ventricular fibrillation, amiodarone or an implantable cardioverter-defibrillator should be considered. Implantable cardioverter-defibrillators markedly reduce sudden death in ventricular tachycardia and ventricular fibrillation survivors, but in advanced heart failure, this may not markedly extend survival. Catheter or surgical ablation can be considered for selected patients with bundle branch reentry ventricular tachycardia or difficult to control monomorphic ventricular tachycardia. For patients who have not had sustained ventricular tachycardia or ventricular fibrillation antiarrhythmic therapy should generally be avoided, but may benefit some high risk patients. Amiodarone may be beneficial in patients with advanced heart failure and rapid resting heart rates. Implantable cardioverter-defibrillators may improve survival in selected patients with depressed ventricular function after myocardial infarction, who also have nonsustained and inducible ventricular tachycardia.
Amiodarone↗
Preferential locations for critical reentry circuit sites causing ventricular tachycardia after inferior wall myocardial infarction.
INTRODUCTION: For relatively slow monomorphic ventricular tachycardia (VT) after myocardial infarction, entrainment can be used to identify reentry circuit "isthmus sites" (exit sites and sites proximal to the exit) where radiofrequency (RF) catheter ablation has the greatest likelihood of interrupting reentry. Similarities in coronary and ventricular anatomy may cause such sites to form in preferential locations. The objective of this study is to determine if there are preferential locations for reentry circuit isthmus regions in chronic inferior wall infarctions causing VT. METHODS AND RESULTS: Catheter mapping and RF catheter ablation was performed in 21 patients with an old inferior wall myocardial infarction and VT. The inferior wall was divided into 9 anatomic regions: 3 apical, 3 mid, and 3 basal segments. Of 46 different VTs, an endocardial isthmus site was identified in one or more zones in 28 (61%), with 10 VTs having isthmus sites in two or more adjacent regions. Isthmus zones were found in a basal region of the left ventricle in 24 (86%) of 28 VTs, in a mid segment in 9 (32%) VTs, and in an apical segment in 1 (4%) (P = 0.002). Of 30 RF current applications that terminated VT, 21 (70%) were at basal isthmus sites. CONCLUSION: The high prevalence of endocardial isthmus zones near the base of the left ventricle suggests that the mitral annulus often plays a role in defining the margins of reentry circuits that cause relatively slow VTs after inferior wall myocardial infarction.
Aged↗
Effect of recording site on postpacing interval measurement during catheter mapping and entrainment of postinfarction ventricular tachycardia.
INTRODUCTION: During entrainment of reentrant ventricular tachycardia (VT), the difference between the postpacing interval (PPI) and the VT cycle length (VTCL) measured at the pacing site is an indication of the conduction time from the pacing site to the reentry circuit. The difference is usually < or = 30 msec at successful ablation sites. However, electrical noise during pacing sometimes obscures the electrograms recorded directly from the pacing site. The objective of this study is to determine if the PPI-VTCL difference measured at the mapping catheter electrodes proximal to the stimulating electrode accurately predicts the PPI-VTCL difference at the stimulating electrode. METHODS AND RESULTS: Endocardial catheter mapping was performed in 26 patients with infarct-related VT. At 191 sites during 56 VTs, unipolar pacing from the distal electrode entrained VT and electrograms recorded from the mapping catheter were discernable following pacing in both the bipolar recordings from the distal electrode pair (BI 1-2) and the electrode pair 6 mm proximal to the distal electrode (BI 3-4). The PPI-VTCL difference at BI 1-2 correlated well with that measured at BI 3-4 (r = 0.88, P = 0.001). A PPI-VTCL difference at BI 3-4 < or = 30 msec predicted a PPI-VTCL difference at BI 1-2 < or = 30 msec with a sensitivity of 95%, specificity of 87 %, and predictive accuracy of 91%. CONCLUSIONS: Measurement of the PPI from electrodes proximal to the stimulating electrode is a reasonable alternative when the PPI cannot be assessed from the pacing electrode.
Aged↗