RADIOFREQUENCY ABLATION OF FIBRILLATION: What clinicians should know.
DR CARLOS LABADETElectrophysiology Sector
Dr. Cosme Argerich Hospital
WHAT ARRHYTHMIAS ARE CURED?
• Wolff-Parkinson-White syndrome
• Supraventricular paroxysmal tachycardia
• Atrial flutter
• Atrioventricular node
• Atrial tachycardias
SUCCESS 90 - 100 %
ADVANCEMENTS IN ABLATION
• ATRIAL FIBRILLATION
• VENTRICULAR TACHYCARDIAS
• VENTRICULAR EXTRASYSTOLE
• ATYPICAL ATRIAL FLUTTERS
Sucess…~ 70%
ATRIAL FIBRILLATIONProblems
• Increase in mortality!• Embolism and stroke• Hospitalization • CHF: lack of atrial systole Cardiomyopathy by tachycardia• Left atrial (LA) dilatation by AF• Chronic anticoagulation • Chronic symptoms of AF (palpitations, fatigue,
etc.)
Increase of LA
LV systolic dysfunction
LV diastolic dysfunction
HTN
Toxic
Genetic
Tachycardia begets more tachycardia
Age
Obesity
Metabolic syndrome
Diabetes
Sleep apneaRespiratory
disorders
Inflammation
Degenerative
diseases
Atrial fibrosis
ATRIAL FIBRILLATION
HOW TO AVOID THIS WITH AN “ANTIARRHYTHMIC” DRUG??
Endocrinological disorders
Pericardial fat
AF: WHAT IS THE MECHANISM
• AF is started by focused triggers, 95% in the pulmonary veins (PV)
• AF is perpetuated by multiple microreentries or “rotors”
• Dominant rotors locate in the PV-LA junction
• Vagal impulse can trigger and maintain AF. There are vagal ganglionic areas in the PV-LA junction.
LA
LSVP
Anatomia e Histologia de venas pulmonares Anatomy and histology of pulmonary veins
Myocardial bands
MECHANISM OF AF AND OBJECTIVES OF ABLATION
PULMONARY VEIN ABLATION – Potential mechanisms
• PV and foci isolation
• Removal of focused triggers
• Modification of substrate
• Autonomic denervation (vagal plexi)
STROKE /YEAR: SINUS RHYTHM 0.4% AF 2%
Nademanee JACC 08,50:843
EF>40 SR
EF<40 AF
EF>40 AF
EF<40 SR
(AFFIRM type) >65 y.o.+ HTN-Diab-CHF-ACV-LVEF<40%
JACC 2009;53:1798
• 162 centers with 45,115 procedures in 32,569 pts.(1995-2006) Mortality at 30 days = 0.98/1,000 pts.
SPANISH REGISTRY OF ABLATION SPANISH REGISTRY OF ABLATION 20072007
1,624 accessory pathways: mortality = 1,624 accessory pathways: mortality = 1/10001/1000
2,065 nodal reentry: mortality = 2,065 nodal reentry: mortality = 0.5/10000.5/1000
Post-AF ablation – immediate control
• Remain with anticoagulation for 1-3 months• During first 72 hs pericarditis may appear
(fever, precordial pain, effusion, evaluate by echo)
• PAF commonly appears as an effect of rF• Discharge at 24-48 h• Maintain antiarrhythmic agents during the
first 1 to 3 months
Post-AF ablation Long term
• Patients may present left AF or AFl during the first 3 months, not associated to subsequent recurrene.
• The most severe complication: atrioesophageal fistula (0.01%). It appears between the first and second week: fever, bacteriemia, leukocytosis, epigastric pain, neurological focus=hospitalization=NMR or CT=NON-endoscopic surgery or contrast study.
• PV stenosis: around 1%: between the 2nd and 5th months: dyspnea, cough, hemoptysis, chest pain
• Severe stenosis of a vein or multiple veins
• Angioplasty with stent
Post-AF ablationLong term
AF ablation: Who are the main candidates?
• PAROXYSMAL or PERSISTENT AF <1 year, symptomatic, recurrent with drugs.
• Age <65 years old
• Minimal or no heart disease
• Left atrium <50 mm
CONCLUSIONS
• The patients with paroxysmal forms of AF and with minimal heart disease obtain the greatest results with radiofrequency ablation.
• Those wiht persistent forms greater than 1 year or permanent, require more prolonged procedures and frequently require a second ablation.
CONCLUSIONS
• Although the information comes from observational studies, those with AF + left ventricular dysfunction present an improvement in ejection fraction
• Currently, studies on heart failure and ventricular impairment are being developed to assess this phenomenon.