Late potentials are unaffected by radiofrequency catheter ablation in patients with ventricular tachycardia.

Reentrant ventricular tachycardia is dependent on an area of myofibers, embedded in scar tissue, which exhibit slow conduction. Late potentials recorded by signal-averaged electrocardiography appear to correspond to these zones of slow conduction and frequently are present in patients with VT. We hypothesized that elimination of inducible VT by catheter-mediated ablation of critical areas of slow conduction would alter late potentials. Four patients underwent catheter ablation in which radiofrequency current was delivered to zones of slow conduction exhibiting isolated mid-diastolic potentials that could not be dissociated from the tachycardia. The four patients had developed VT (cycle length 382 +/- 50 msec; mean +/- SEM) 13-180 months after inferior myocardial infarction. Late potentials were present in each patient before catheter ablation was attempted. Although VT was not inducible in any patient immediately after ablation, late potentials were still present in all four patients and there was no significant difference in the QRS duration (136.5 +/- 4.0 msec postablation; 135.7 +/- 4.5 msec preablation), root mean square voltage in the terminal 40 msec of the QRS (10.0 +/- 1.0 microV postablation; 5.9 +/- 0.4 microV preablation), or in the duration of the low amplitude signal (69.2 +/- 2.0 msec postablation; 62.7 +/- 3.4 msec preablation). At follow-up electrophysiology study performed 14 +/- 7 days after ablation, one of the four patients had inducible VT. In conclusion, late potentials persist even after successful radiofrequency catheter ablation and do not appear to be useful for predicting results of follow-up electrophysiology study.

Treatment of supraventricular tachycardia due to atrioventricular nodal reentry by radiofrequency catheter ablation of slow-pathway conduction.

BACKGROUND: Atrioventricular nodal reentrant tachycardia (AVNRT), the most common form of supraventricular tachycardia, results from conduction through a reentrant circuit comprising fast and slow atrioventricular nodal pathways. Antiarrhythmic-drug therapy is not consistently successful in controlling this rhythm disturbance. Catheter ablation of the fast pathway with radiofrequency current eliminates AVNRT, but it can produce heart block. We hypothesized that catheter ablation of the site of insertion of the slow pathway into the atrium would eliminate AVNRT while leaving normal (fast-pathway) atrioventricular nodal conduction intact. METHODS AND RESULTS: Eighty patients with symptomatic AVNRT were studied. Retrograde slow-pathway conduction (in which the earliest retrograde atrial potential was recorded at the posterior septum, close to the coronary sinus) was present in 33 patients. The retrograde atrial potential was preceded by a potential consistent with activation of the atrial end of the slow pathway (ASP). In 46 of the 47 patients without retrograde slow-pathway conduction, a potential with the same characteristics as the ASP potential was recorded during sinus rhythm. Radiofrequency current delivered through a catheter to the ASP site (in the posteroseptal right atrium or coronary sinus) abolished or modified slow-pathway conduction in 78 patients, eliminating AVNRT without affecting normal atrioventricular nodal conduction. In the single patient without ASP, the application of radiofrequency current to the proximal coronary sinus ablated the fast pathway and AVNRT: Atrioventricular block occurred in one patient (1.3 percent) with left bundle-branch block, after inadvertent ablation of the right bundle branch. AVNRT has not recurred in any patient during a mean (+/- SD) follow-up of 15.5 +/- 11.3 months. Electrophysiologic study 4.3 +/- 3.3 months after ablation in 32 patients demonstrated normal atrioventricular nodal conduction without AVNRT: CONCLUSIONS: Catheter ablation of the atrial end of the slow pathway using radiofrequency current, guided by ASP potentials, can eliminate AVNRT with very little risk of atrioventricular block.

Transesophageal echocardiographic evaluation for mural thrombus following radiofrequency catheter ablation of accessory pathways.

BACKGROUND: Catheter ablation of accessory pathways (APs) provides a definitive therapy for patients with Wolff-Parkinson-White Syndrome. The reported incidence of thrombus formation on ablation-induced injuries with direct current shock varies from 0%-20% in animal studies. The purpose of this study was to determine the prevalence of mural thrombus following catheter ablation with radiofrequency current of accessory pathways in humans. METHODS AND RESULTS: Radiofrequency current (30-35 watts) was applied through a catheter electrode placed against the mitral or tricuspid annulus guided by catheter recordings of AP potentials. Transthoracic (TTE) and transesophageal echocardiography (TEE) were performed in 95 of 111 patients, at 18 +/- 6 hours following catheter ablation. After ablation, no thrombus was identified at or near the ablation site in any patient. Two out of 95 patients had a mural thrombus at a remote site that was detected by TEE but not by TTE. No new wall motion abnormality was detected in any patient. No significant regurgitant valvular lesion was found in any patient. CONCLUSION: Intracardiac thrombus was not identified at the site of catheter ablation, possibly owing to the small lesions produced by radiofrequency energy and high blood flow normally present in those areas. However, patients may be at small risk for mural thrombus at a remote site from prolonged placement of catheters.

Factors associated with recurrence of accessory pathway conduction after radiofrequency catheter ablation.

Catheter ablation of 215 accessory pathways (APs) using radiofrequency current (RF) was attempted in 204 consecutive patients. Two hundred twelve of the 215 (99%) APs were successfully ablated. After a minimum of follow-up period of 1 month (mean 8.5 +/- 5.4 months), AP conduction had returned in 17 patients (8%). Recurrence of AP conduction was manifest by atrioventricular (AV) reentrant tachycardia in six patients, palpitations suggestive of AV reentrant tachycardia in five patients, ventricular preexcitation on electrocardiogram in five patients, and inducible AV reentrant tachycardia during a follow-up electrophysiological study in one asymptomatic patient. AP conduction returned as early as 12 hours and as late as 4.7 months, but was evident within 2 months of ablation in 15 of 17 (88%) patients. AP conduction recurred in 12%-14% of anteroseptal, right free-wall, and posteroseptal APs, but only 5% of left free-wall APs (P less than 0.01). Retrograde only conducting APs (concealed APs) had recurrence of AP conduction more frequently (16%) than APs that exhibited antegrade conduction (5.5%; P less than 0.01). Failure to record AP potentials from the ablation electrode, reflecting poor AP localization, was a strong predictor for recurrence of AP conduction. AP conduction returned in 19% of 48 APs when AP potentials were not recorded, compared to 5% of 164 APs where AP potentials were recorded from the ablation electrode (P less than 0.01). The time to block of AP conduction from the onset of RF current application was longer in APs with recurrence of conduction (4.9 +/- 6.1 sec vs 2.9 +/- 3.4 sec; P less than 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)

Catheter ablation of accessory atrioventricular pathways (Wolff-Parkinson-White syndrome) by radiofrequency current.

BACKGROUND: Surgical or catheter ablation of accessory pathways by means of high-energy shocks serves as definitive therapy for patients with Wolff-Parkinson-White syndrome but has substantial associated morbidity and mortality. Radiofrequency current, an alternative energy source for ablation, produces smaller lesions without adverse effects remote from the site where current is delivered. We conducted this study to develop catheter techniques for delivering radiofrequency current to reduce morbidity and mortality associated with accessory-pathway ablation. METHODS: Radiofrequency current (mean power, 30.9 +/- 5.3 W) was applied through a catheter electrode positioned against the mitral or tricuspid annulus or a branch of the coronary sinus; when possible, delivery was guided by catheter recordings of accessory-pathway activation. Ablation was attempted in 166 patients with 177 accessory pathways (106 pathways in the left free wall, 13 in the anteroseptal region, 43 in the posteroseptal region, and 15 in the right free wall). RESULTS: Accessory-pathway conduction was eliminated in 164 of 166 patients (99 percent) by a median of three applications of radiofrequency current. During a mean follow-up (+/- SD) of 8.0 +/- 5.4 months, preexcitation or atrioventricular reentrant tachycardia returned in 15 patients (9 percent). All underwent a second, successful ablation. Electrophysiologic study 3.1 +/- 1.9 months after ablation in 75 patients verified the absence of accessory-pathway conduction in all. Complications of radiofrequency-current application occurred in three patients (1.8 percent): atrioventricular block (one patient), pericarditis (one), and cardiac tamponade (one) after radiofrequency current was applied in a small branch of the coronary sinus. CONCLUSIONS: Radiofrequency current is highly effective in ablating accessory pathways, with low morbidity and no mortality.

Premature ventricular complex morphology. A marker for left ventricular structure and function.

The shape of a premature ventricular complex (PVC) might reflect the presence or absence of myocardial disease. To test this, 100 patients with a PVC on a 12-lead electrocardiogram at cardiac catheterization or nuclear angiography were classified according to PVC morphology. Group 1 (n = 50) had PVC QRS complexes with either smooth and uninterrupted contour or with narrow (less than 40 msec) notching. Group 2 (n = 50) demonstrated PVC with broad (greater than or equal to 40 msec) notching or shelves. Clinical, electrocardiographic and angiographic variables were assessed to define group differences. All patients had one or more etiological forms of heart disease none of which distinguished either group. Groups 1 and 2 differed with respect to a history of congestive heart failure (12% vs. 66%, p = 0.0004), dilated cardiomyopathy (2% vs. 38%, p = 0.0005), and the presence of mitral regurgitation (13% vs. 58%, p = 0.001), respectively. In group 1, 45 of 50 (90%) patients with a PVC had no notching. Patients in group 2 had greater PVC QRS duration as compared with patients in group 1 (181 +/- 6 vs. 134 +/- 3 msec, p = 0.0001). End-diastolic volume index (EDVI) (78 +/- 3 vs. 139 +/- 11 ml/m2, p = 0.0000) and ejection fraction (EF) (0.59 +/- 0.02 vs. 0.34 +/- 0.03, p = 0.0000) significantly discriminated between group 1 and 2, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Efficacy of intravascular volume resuscitation in dogs with acute cardiac tamponade.

Whether cardiac tamponade causes myocardial ischemia and whether volume resuscitation can improve coronary perfusion pressure and myocardial blood flow were studied by hemodynamic responses to three blood infusions of 15 ml/kg in dogs with left ventricular hypovolemia produced by cardiac tamponade (N = 10) or hemorrhage (N = 10). Coronary perfusion pressure decreased to 37 +/- 2 mm Hg with tamponade and 39 +/- 1 mm Hg with hemorrhage, causing significant blood flow decreases in both ventricles. Myocardial oxygen extraction increased significantly in both groups without affecting lactate extraction. Volume resuscitation after hemorrhage progressively restored hemodynamic variables to baseline values. Volume resuscitation after tamponade did not increase stroke volume, whereas it increased coronary sinus pressure to 19.2 +/- 1.0 mm Hg (p less than 0.05). Coronary perfusion pressure increased to 53 +/- 5 mm Hg following the first infusion (p less than 0.05), but exhibited no further improvement. Tamponade did not produce myocardial ischemia. Coronary perfusion pressure and blood flow were not restored to baseline values with volume resuscitation since coronary sinus pressure rose incrementally with each volume infusion.