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Guilherme Fenelon

Publications and source records attributed to Guilherme Fenelon.

10 recordsLinked to original sources

Epicardial radiofrequency ablation of ventricular myocardium: factors affecting lesion formation and damage to adjacent structures.

UNLABELLED: We evaluated the factors affecting epicardial radiofrequency (RF) lesion formation in normal ventricular myocardium. In 16 dogs, a minithoracotomy was made and a sheath was placed in the pericardial space. Standard ablation lesions (4-mm tip catheter; 70 ( composite function) C/60 seconds) were created in each ventricle under fluoroscopy guidance (n = 7) or hand-held with direct visualization of the catheter to assure optimal electrode-tissue contact (n = 6). In the latter, thermally-shielded (TS) electrodes (50% tip surface along its 4 mm length) were used in 3/6 dogs. Catheter tip (4 mm) irrigation (13 mL/minutes; 40 ( composite function) C/60 seconds) was employed with conventional techniques in 3 additional dogs. RESULTS: With optimal electrode-tissue contact (11 lesions), power (3.4 +/- 2.3 W vs. 16 +/- 13 W; p < 0.001) and pacing thresholds (0.2 +/- 0.0 mA vs. 3.6 +/- 5.7 mA; p = 0.004) were lower than standard RF (25 lesions). However, lesion dimensions were similar and transmural lesions did not occur (depth 2.8 +/- 1.1 mm vs. 3.0 +/- 1.5 mm). Catheter irrigation allowed high power outputs (43 +/- 6.1 W; p < 0.001) generating transmural lesions, 5/9 (55%), depth 6.4 +/- 2.1 mm. At constant power (2 W), catheter-tip temperature (52 +/- 5.2( composite function) C vs. 57 +/- 6.6( composite function) C; p = NS) and lesion (10 in each group) dimensions were similar for conventional and TS electrodes, but damage to parietal pericardium and lungs occurred with conventional electrodes only (70% vs. 0% p = 0.02). CONCLUSION: Standard epicardial RF ablation does not produce deep lesions and exhibits a significant energy loss probably due to poor electrode-tissue contact. Catheter irrigation allows delivery of high power outputs to the epicardium consistently creating deeper lesions than standard ablation. TS electrodes may reduce damage to neighboring structures during epicardial RF ablation.

Analysis of Variance↗

Acute and chronic effects of extensive radiofrequency lesions in the canine caval veins: implications for ablation of atrial arrhythmias.

BACKGROUND: Although radiofrequency (RF) ablation within the caval veins has been increasingly used to treat a variety of atrial tachyarrhythmias, the consequences of RF ablation in the caval veins are unknown. We explored the acute and chronic angiographic and pathological effects of extensive RF ablation in the caval veins. METHODS: Under fluoroscopy guidance, conventional (4 mm tip, 60 degrees C, 60 seconds) RF applications (n = 6-7) were delivered in each vena cava (from +/-2 cm into the vein to the veno-atrial junction) of 15 dogs (10 +/- 3 kg). Animals were killed 1 hour and 5 weeks after ablation for histological analysis. Angiography was performed before ablation (acute dogs only) and at sacrifice to assess the degree of vascular stenosis. RESULTS: In acute dogs (n = 5), luminal narrowing was noted in 10/10 (100%) targeted veins (mild in two; moderate in three and severe in five, including two total occlusions). In the six chronic animals that completed the protocol (four died during follow-up), stenosis was also observed in 12/12 (100%) ablated veins (mild in six; moderate in four and severe in two). Of these, one superior vena cava was suboccluded with development of extensive collateral circulation. Histologically, acute lesions displayed typical transmural coagulative necrosis, whereas chronic lesions revealed intimal proliferation, necrotic muscle replaced with collagen, endovascular contraction, and disruption and thickening of the internal elastic lamina. CONCLUSION: In this model, extensive RF ablation in the caval veins may result in significant vascular stenosis. These findings may have implications for catheter ablation of arrhythmias originating within the caval veins.

Acute Disease↗

Combined therapy with steroids and antioxidants prevents ultrastructural damage surrounding chronic radiofrequency lesions.

We evaluated the effects of combined therapy with anti-inflammatory and antioxidant drugs on the healing of radiofrequency (RF) lesions (70 degrees C, 60 s) produced in the right atrium and each ventricle of 21 adult dogs. Three groups were studied: acute (n= 7, sacrificed 1 hour after RF); control (n = 7, sacrificed 54 +/- 29 days after RF); and dogs (n = 7, sacrificed 32 +/- 5 days after RF) receiving combined therapy with allopurinol (400 mg p.o. 24 and 2 hours before RF); verapamil (200 microg/kg i.v. 15 min before and after RF); hydrocortisone (10 mg/kg i.v. after RF) and prednisone (20 mg p.o. for 29 days). Atrial (n = 37) and ventricular (n = 70) lesion dimensions were determined and 21 right ventricular apex lesions (1 per dog) were selected for light and electron microscopy analysis. Histological and ultrastructural (US) characteristics in three zones extending from the visible lesion border, A (0-3 mm); B (3-6 mm); and C (6-9 mm), were assessed. In chronic groups, atrial and ventricular lesion dimensions were similar, but delayed scar formation was noted in treated animals. Acutely and at follow-up, significant US abnormalities occurred in zones A and B and chronic lesions exhibited type I collagen proliferation. In Zone A, the extent of US injury and collagen proliferation was significantly less in treated dogs. Further, Zone B was normal in 5/7 (71%) treated dogs and in 0/7 (0%) controls. Zone C was essentially normal in all groups. Combined therapy with steroids, verapamil, and allopurinol is effective in limiting US damage surrounding chronic RF lesions.

Allopurinol↗

Characterization of the in vivo cardiac electrophysiologic effects of high-dose cocaine in closed-chest, anesthetized dogs with normal hearts.

OBJECTIVE: To characterize the cardiac electrophysiologic effects of cocaine. METHODS: In 8 dogs (9-13 kg), electrophysiologic parameters and programmed stimulation were undertaken using transvenous catheters at baseline, and after cocaine intravenous infusion (12 mg/kg bolus followed by 0.22 mg/kg/min for 25 minutes). RESULTS: Cocaine plasma levels (n=5) rose to 6.73 +/- 0.56 mg/mL. Cocaine did not affect sinus cycle length and arterial pressure. Cocaine prolonged P wave duration (54 +/- 6 vs 73 +/- 4 ms, P<0.001), PR interval (115 +/- 17 vs 164 +/- 15 ms, P<0.001), QRS duration (62 +/- 10 vs 88 +/- 14 ms, P<0.001), and QTc interval (344 +/- 28 vs 403 +/- 62 ms, P=0.03) but not JT interval (193 +/- 35 vs 226 +/- 53 ms, NS). Cocaine prolonged PA (9 +/- 6 vs 23 +/- 8 ms, P<0.001), AH (73 +/- 16 vs 92 +/- 15 ms; P=0.03), and HV (35 +/- 5 vs 45 +/- 3 ms; P<0.001) intervals and Wenckebach point (247 +/- 26 vs 280 +/- 28 ms, P=0.04). An increase occurred in atrial (138 +/- 8 vs 184 +/- 20 ms; P<0.001) and ventricular (160 +/- 15 vs 187 +/- 25 ms; P=0.03) refractoriness at a cycle length of 300 ms. Atrial arrhythmias were not induced in any dog. Ventricular fibrillation (VF) was induced in 2/8 dogs at baseline and 4/8 dogs after cocaine. CONCLUSION: High doses of cocaine exert significant class I effects and seem to enhance inducibility of VF but not of atrial arrhythmias.

Anesthesia↗

Steroids prevent late extension of radiofrequency lesions in the thigh muscle of infant rats: implications for pediatric ablation.

INTRODUCTION: Marked late enlargement of radiofrequency (RF) lesions may occur in immature myocardium, suggesting that late proarrhythmic effects may occur in infants and small children undergoing RF ablation. Because late lesion extension may be involved in this phenomenon, we evaluated the impact of corticosteroids on the healing of RF lesions created in the thigh muscle of 29 infant Wistar rats (30 days; 55 g). METHODS: Lesion dimensions and histological characteristics were assessed acutely (n = 11), and at 30 days in controls (n = 11, 183 g) and rats (n = 7, 173 g) receiving hydrocortisone after ablation and betametasone for 29 days. Acute (n = 16) and chronic (30 days; n = 5) lesions were also evaluated in adult Wistar rats (300 g). RESULTS: Acutely, lesions in adults and infants were well demarcated from the surrounding tissue. In adults, chronic lesions did not increase in size and were well demarcated histologically. Controls and treated infant rats did not differ with respect to the gross appearance of chronic lesions. Late lesions doubled in size (20 mm in diameter) and were poorly demarcated from the surrounding tissue, exhibiting multiple collagen strands extending from the lesion into normal muscular tissue. In the treatment group, healing was markedly delayed and the extent of collagen proliferation was significantly less than controls. CONCLUSION: RF lesions created in the thigh muscle of infant rats reveal late enlargement and invasion of normal muscle by intense collagen proliferation. Steroids seem to limit late extension of RF lesions. These findings may have implications for RF ablation procedures in pediatric populations.

Animals↗

Clinical usefulness of electrophysiologic testing in patients with ventricular tachycardia and chronic chagasic cardiomyopathy treated with amiodarone or sotalol.

INTRODUCTION: This study assessed the role of electrophysiologic testing to identify therapeutic strategies for the treatment of patients with sustained ventricular tachycardia (VT) and chronic chagasic cardiomyopathy treated with amiodarone or sotalol. METHODS AND RESULTS: One hundred fifteen patients [69 men (60%); mean age 52 +/- 10 years] with chagasic cardiomyopathy presenting with symptomatic VT were studied after loading with Class III antiarrhythmic drugs; 78 had a history of sustained VT, and 37 with symptomatic nonsustained VT had sustained VT induced at baseline electrophysiologic study. All but 12 patients also underwent baseline electrophysiologic study. Mean left ventricular ejection fraction was 0.49 +/- 0.14. Based on results of electrophysiologic study after loading with Class III drugs, patients were divided into three groups: group 1 (n = 23) had no sustained VT induced; group 2 (n = 45) had only tolerated sustained VT induced; and group 3 (n = 47) had hemodynamically unstable sustained VT induced. After a mean follow-up of 52 +/- 32 months, total mortality rate was 39.1%; it was significantly higher in group 3 than in groups 2 and 1 [69%, 22.2%, and 26%, respectively, P < 0.0001, hazard ratio (HR) 10.4, 95% confidence interval (CI) 3.8, 21.8]. There was no significant difference in total mortality rate between groups 1 and 2 (P = 0.40, HR 1.5, 95% CI 0.75, 4.58). Cardiac mortality and sudden cardiac death rates also were higher in group 3 patients. CONCLUSION: In patients with chagasic cardiomyopathy and sustained VT, electrophysiologic testing can predict long-term efficacy of Class III antiarrhythmic drugs. This may help in the selection of patients for implantable cardioverter defibrillator therapy.

Adult↗

Characterization of sustained atrial tachycardia in dogs with rapid ventricular pacing-induced heart failure.

INTRODUCTION: Atrial arrhythmias often complicate congestive heart failure (CHF). We characterized inducible atrial tachyarrhythmias and electrophysiologic alterations in dogs with CHF and atrial enlargement produced by rapid ventricular pacing. METHODS AND RESULTS: Endocardial pacing leads were implanted in the right ventricle, right atrium, and coronary sinus in 18 dogs. The right ventricular lead was connected to an implanted pacemaker capable of rapid ventricular pacing. The atrial leads were used to perform electrophysiologic studies in conscious animals at baseline in all dogs, during CHF induced by rapid ventricular pacing at 235 beats/min in 15 dogs, and during recovery from CHF in 6 dogs. After 20 +/- 7 days of rapid ventricular pacing, inducibility of sustained atrial tachycardia (cycle length 120 +/- 12 msec) was enhanced in dogs with CHF. Atrial tachycardia required a critical decrease in atrial burst pacing cycle length (< or = 130 msec) for induction and often could be terminated by overdrive pacing. Calcium antagonists (verapamil, flunarizine, ryanodine) terminated atrial tachycardia and suppressed inducibility. Effective refractory periods at 400- and 300-msec cycle lengths in the right atrium and coronary sinus were prolonged in dogs with CHF. Atrial cells from dogs with CHF had prolonged action potential durations and reduced resting potentials and delayed afterdepolarizations (DADs). Mitochondria from atrial tissue from dogs with CHF were enlarged and had internal cristae disorganization. CONCLUSIONS: CHF promotes inducibility of sustained atrial tachycardia. Based on the mode of tachycardia induction, responses to pacing and calcium antagonists, and presence of DADs, atrial tachycardia in this CHF model has a mechanism most consistent with DAD-induced triggered activity resulting from intracellular calcium overload.

Action Potentials↗

Focal origin of atrial tachycardia in dogs with rapid ventricular pacing-induced heart failure.

UNLABELLED: Mapping and Ablation of Atrial Tachycardia in Heart Failure. INTRODUCTION: Dogs with rapid ventricular pacing-induced congestive heart failure (CHF) have inducible atrial tachycardia (AT), with a mechanism consistent with delayed afterdepolarization-mediated triggered activity. We assessed the hypothesis that AT has a focal origin. METHODS AND RESULTS: Twenty-one CHF dogs undergoing 3 to 4 weeks of ventricular pacing at 235 beats/min were studied. Biatrial epicardial mapping of 20 sustained AT episodes (cycle length [CL], 175 +/- 53 msec) in 5 dogs revealed an area of earliest activation in the right atrial (RA) free wall (13 episodes), RA appendage (4 episodes), or between the pulmonary veins (3 episodes). Total epicardial activation time during AT (73 +/- 19 msec) was similar to that during sinus rhythm (72 +/- 13 msec) and on average was <50% of the AT CL. Higher-density mapping of the RA free wall during 30 sustained AT episodes (163 +/- 55 msec) in 9 dogs identified a site of earliest activation along the sulcus terminalis most frequently as a stable, focal activation pattern from a single site. Endocardial mapping of 49 sustained AT episodes (156 +/- 27 msec) in 10 dogs revealed multiple sites of AT origin arising along the crista terminalis and pulmonary veins. Right and left ATs were terminated with discrete radiofrequency ablation, but other ATs remained inducible. A rapid, left AT generating an ECG pattern of atrial fibrillation was ablated inside the pulmonary vein. CONCLUSION: AT induced in this CHF model after 3 to 4 weeks of rapid ventricular pacing has an activation pattern consistent with a focal origin. Sites of earliest activation are distributed predominately along the crista terminalis and within or near the pulmonary veins.

Animals↗

Left ventricular dysfunction is associated with prolonged average ventricular fibrillation cycle length in patients with implantable cardioverter defibrillators.

OBJECTIVES: In cellular studies, ventricular refractoriness (ERP) is prolonged in heart failure (CHF), but clinical evidence is lacking. The average ventricular fibrillation cycle length (VFCL) has been shown to correlate with local ERP. We hypothesized that the VFCL increases with left ventricular (LV) dysfunction. Therefore, we evaluated intracardiac VFCL recorded by implantable defibrillators (ICD) in patients with and without LV dysfunction. METHODS: We analyzed intracardiac VFCL recorded by sensing leads of Ventak MINI (Guidant) ICD in 49 patients (35 men; age 54 +/- 13 years; 25 (51%) with coronary artery disease; mean LV ejection fraction (EF) 41 +/- 17%, range 76-10) from the European Ventak MINI Investigator Group. No patients were receiving antiarrhythmic drugs, including beta-blockers. Mean and median VFCL were obtained at predischarge testing during first charge time (4.5 +/- 2.7 s, range 1.4-11). RESULTS: Mean median VFCL was 186 +/- 21ms (range 150-230 ms). Patients with LVEF >/= 50% (n = 14) had shorter median VFCL than patients with LVEF < 50% (n = 35), (171 +/- 14 vs. 191 +/- 20 ms; p = 0.002). Median VFCL correlated with LVEF (r = -0.41; p = 0.003) and age (r = 0.28, p = 0.04), but was not significantly associated with charge time and defibrillation threshold at implant. Similar results occurred with mean VFCL. In multiple linear regression and correlation models, only LVEF% was a significant predictor (p < 0.05 for all models) of median VFCL. CONCLUSIONS: LV dysfunction prolongs averaged VFCL in patients at risk for malignant ventricular arrhythmias who have implantable cardioverter defibrillators. This phenomenon might be related to alterations in the ventricular refractory period.

Analysis of Variance↗

Examination of the in vivo cardiac electrophysiological effects of nesiritide (human brain natriuretic peptide) in conscious dogs.

BACKGROUND: Human brain natriuretic peptide (hBNP) is a new therapeutic agent, nesiritide, indicated in patients with decompensated congestive heart failure, a group at significant risk of developing cardiac arrhythmias. Whether hBNP has cardiac electrophysiologic effects has not been reported. METHODS AND RESULTS: In 9 healthy, chronically instrumented, conscious dogs, hemodynamic and electrophysiologic parameters were assessed at baseline and during recombinant hBNP (nesiritide) infusion at 0.03 and 0.09 microg/kg/min after 1 hour at each dose. Infusion of hBNP produced dose-related increases (P <.001) in hBNP and cyclic GMP plasma levels and reductions (P <.05) in mean arterial pressure. Mean central venous pressure and sinus cycle length did not change significantly. Infusion of hBNP produced no significant changes in any of the electrophysiologic parameters including no change in surface ECG variables (P wave duration, PR interval, QRS duration, and QTc interval), corrected sinus node recovery time, atrioventricular nodal Wenckebach cycle length, and atrial and ventricular effective refractory periods measured at a 400 ms cycle length. Spontaneous or induced arrhythmias were not observed during hBNP infusion. CONCLUSIONS: In conscious, healthy dogs, short-term infusion of recombinant hBNP has no significant effects on atrial or ventricular electrophysiologic parameters.

Animals↗