Quando procedere all’ablazione della tachicardia ventricolare
rinunciando al defibrillatore
Leonardo Calo’
Direttore U.O.C. Cardiologia
Policlinico Casilino -Roma
Low-voltage areas in pts from group A corresponded to echocardiographic/angiographic RV wall motion abnormalities and were significantly associated with myocyte loss and fibrofatty replacement at biopsy (P < 0.0001) and familial ARVC/D (P < 0.0001).
Circulation 2006;114:32-39
An example of CMR in a 64-year-old male patient with an inferior MI (white arrows), preserved LV systolic function (LVEF, 61%), and normal LV systolic volume index. The MI of this pt was characterized by a substantial peri-infarct zone (yellow region) with a %MDE periphery measuring 27%. The patient died 11 months after undergoing the CMR examination.
* *
AO Adx
Vdx TE
Vsn
TV IDIOPATICA DEL TRATTO DI EFFLUSSO SN
Cuspide coronarica sn - Cuspide coronarica dx-
Setto interventricolare
Origin of outflow tract ventricular arrhythmia
Yamada, JACC 2008; 52(2), 139–147
About 70% of outflow tract VA are from RVOT, inferior to the PV
Catheter Ablation - Outcome
Aliot EM,et al.: EHRA/HRS Expert Consensus on Catheter ablation of VA. Europace 2009, 11:771–817
• Acute success rate typically > 90%
• Recurrences occur in about 5% of cases
• Complications during ablation of idiopathic VTs are rare
– mainly related to vascular access
– tamponade or perforation occur in < 1% of the cases • Long-term follow-ups and larger sample sizes are still missing
Tachycardia-Related Cardiomyopathy
• TCM is caused by very frequent runs of VT as well as PVCs
• The threshold of ectopy needed to result in TCM has been evaluated by many authors:
– Yarlagadda et al. PVC > 17,000 daily
– Takemoto et al. PVC > 20% daily
– Baman et al. PVC > 24% daily
– Hasdemir et al. PVC > 16% daily
– Niwano et al. PVC > 31,268 daily
• Thus, patients likely need to have > 10,000 PVCs daily over a substantial period (≈4 years) to cause TCM
• TCM is uncommon and occurred in 5-6% of patients
Eric N. Prystowsky et al. J Am Coll Cardiol 2012;59:1733–44
Medical history
M.A. 59 years old female
Hypercholesterolemia; no other risk factors
Highly symptomatic for palpitations since several months
NYHA class II
Echo: Mitral valve prolapse with mild regurgitation; EF 46%; LVED 56 mm
On therapy with betablockers: persistence of symptoms
Holter: sinus rhythm; 34000 PVCs (two morphologies; one highly predominant); couplets; frequent runs of NSVT
Final ECG
Follow-up Bisoprolol was interrupted at 30 days follow-up
At 45 days follow up the patient is asymptomatic
24 hours Holter: normal sinus rhythm; 48 polymorfic PVCs
Echo: Slitght improvement of EF from 46% to 50% at 2 months
MRI late enhancement inferior basal wall
Athlete 35 y.o. male caucasian with 15000 polymorphic PVC, isolated, 228 couplets, 15 NSVT 4 beats
34 y.o. male caucasian with repetitive monomorphic NSVT No family history of heart disease
Symptomatic for palpitations, no syncope
34 y.o. male caucasian with repetitive monomorphic NSVT (GALLAVARDIN)
MRI: absence of cardiomyopathy
Holter monitoring:
27000 PVC, absence during sleep.
NSVT during Holter monitoring.
MRI absence of heart disease
EPS no inducibility of arrhythmias
No low voltage areas during electroanatomical mapping
Electrophysiological study:
mapping of right ventricular outflow tract (RVOT), inducibility of arrhythmias, RF ablation
MRI absence of heart disease
EPS no inducibility of arrhythmias
No low voltage areas during
electroanatomical mapping