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Dr. P. Pieragnoli Extrasistolia nel Cuore Sano Firenze, 8 Novembre 2014 Università degli Studi di Firenze.

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Presentazione sul tema: "Dr. P. Pieragnoli Extrasistolia nel Cuore Sano Firenze, 8 Novembre 2014 Università degli Studi di Firenze."— Transcript della presentazione:

1 Dr. P. Pieragnoli Extrasistolia nel Cuore Sano Firenze, 8 Novembre 2014 Università degli Studi di Firenze

2 D’Este et al, G Ital Cardiol 2010

3 Extrasistolia ventricolare che origina dal fascicolo posteriore della branca sinistra. Morfologia del QRS a tipo blocco di branca destra ed emiblocco anteriore sinistro. Extrasistolia ventricolare dal tratto di efflusso del ventricolo destro. Morfologia del QRS a tipo blocco di branca sinistra con asse verticale. D’Este et al, G Ital Cardiol 2010

4 Characteristic appearance of ectopy from the right ventricular outflow tract Giles et al, Canadian Journal of Cardiology 2013

5 Displasia aritmogena del ventricolo destro. Morfologia del QRS a tipo blocco di branca sinistra. Sindrome del QT lungo congenito. Allungamento dell’intervallo QT soprattutto nei battiti post- extrasistolici. D’Este et al, G Ital Cardiol 2010

6 Extrasistolia ventricolare in un caso di fibrillazione ventricolare idiopatica. Le extrasistoli sono precoci ed hanno morfologia bizzarra. D’Este et al, G Ital Cardiol 2010

7 Kennedy et al. NEJM 1985

8 Ataklte et al, Am J Cardiol 2013

9 Association of VPCs with risk for Sudden Cardiac Death

10 Ataklte et al, Am J Cardiol 2013 Association of VPCs with risk for Total Cardiac Death

11 Lee V et al, Heart 2012 Presence of PVCs is associated with a pooled OR of 1.72 (95% CI 1.28 to 2.31) of developing all-cause mortality, cardiovascular mortality, SCD or ischaemic heart disease when compared with patients without any PVCs.

12 Our paper has shown that the current evidence base on the exact prognosis of PVCs in structurally normal hearts is limited and has many flaws. Most studies on the prognosis of PVCs in normal hearts did not use advanced tests to rule out structural heart disease. Among these patients, PVCs are associated with a worse cardiovascular outcome, and this risk is correlated to the age and underlying cardiovascular risk of the patient population, suggesting that the poor prognosis studies may have inadvertently included patients with occult structural heart disease, the population in which PVCs are known to confer adverse outcomes. More studies are required. Lee V et al, Heart 2012

13 Giles et al, Canadian Journal of Cardiology 2013

14 Biffi et al. JACC 2002

15

16 Frequent and complex ventricular tachyarrhythmias are common in trained athletes and are usually unassociated with underlying cardiovascular abnormalities. Such ventricular arrhythmias (when unassociated with cardiovascular abnormalities) do not convey adverse clinical significance, appear to be an expression of “athlete’s heart syndrome,” and probably do not per se justify a disqualification from competitive sports. Biffi et al. JACC 2002

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18 Behavior of the median number of VPCs/24 hours during followup in subjects who continued sporting activity and in those who did not. The number of VPCs/24 hours decreased significantly in both groups. Median number of VPCs in the basal condition and during follow-up in subjects who had a normal (>55%) or abnormal (55%) EF at the end of follow up. Delise et al, Am J Cardiol 2013

19 The best cutoffs to predict low left ventricular EF at the end of follow-up, based on receiver operating characteristic curve analysis of the number of basal and final VPCs, were 5873 and VPCs/24 hours, respectively. Delise et al, Am J Cardiol 2013 Basal VPCs VPCs during Follow-up

20 Lee et al, Am J Cardiol 2014 The relation of VPC burden to (A) LVEF and (B) left ventricular end- systolic dimension (LVESD). Premature ventricular contraction (PVC) burden and its effect on LV function.

21 Lee et al, Am J Cardiol 2014

22 Kaplan-Meier survival estimates of PVC burdens. Significant difference among patient groups with PVC burden 10,000/24h

23 Lee et al, Am J Cardiol 2014 Kaplan-Meier survival estimates of PVC features. Survival rates were lower in patients with a PVC QRS duration of 150ms than those with a PVC QRS duration of <150ms (A) Survival rates were lower in patients with a PVC coupling interval of >480 ms than those with a PVC coupling interval of 480 ms (B).

24 Lee et al, Am J Cardiol 2014 Kaplan-Meier survival estimates of PVC origins. The comparison of survival rates between the VPCs originating from (A) OT and non-OT locations and (B) between the RV and the LV.

25 Ephrem et al Ann Noninvasive Electrocardiol 2013

26 Ephrem et al Ann Noninvasive Electrocardiol 2013 Time to adverse event by frequency Time to adverse event by pattern

27 Qureshi W et al, Am J Cardiol 2013

28 All-Cause Mortality Cardiovascular Disease Mortality Ischemic Heart Disease Mortality Qureshi W et al, Am J Cardiol 2013 APC VPC

29 These findings highlight the potential use of electrocardiography as a screening tool in asymptomatic patients to detect subclinical cardiac disease. Further studies are needed to validate our findings and evaluate the mechanisms by which APCs are associated with poor outcomes. Qureshi W et al, Am J Cardiol 2013

30 Heidbuchel et al, European Heart J 2003

31 Role of SEF

32 PVC-INDUCED CARDIOMYOPATHY Tachicardia Induced Cardiomyopathy Ventricular Dyssynchrony Increased Oxygen consumption Myocardial and pheripheral vascular autonomic dysregulation Alterations in heart rate dynamics Hemodynamic impairment Alterations in intracellulare calcium and membrane ionic currents Yong-Mei Cha et al, Circulation 2012

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34 Krittayaphong et al, Am J Cardiol 2014

35 Comparison of percent improvement of symptoms, PVC count, and average heart rate as measured by AECG, and QOL score be- tween the atenolol group and the placebo group (positive direction represents reduction in symptoms, PVC count, and heart rate, and an increase in QOL score) Krittayaphong et al, Am J Cardiol 2014

36 Minhua Zang et al, Heart Bmj 2014

37 Minhua Zang et al, Heart BMJ 2014

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39 Minhua Zang et al, Heart Bmj 2014 Change in LVEDd post-Ablation Change in LVEF post-Ablation Effect of Ablation

40 Miyamoto et al., Circ J 2010 Benigne PVC from RV Outflow Tract Surface EKGEndocardial Ablation

41 Benigne PVC from Outflow Tract Tanner et al., JACC 2005 Surface EKGEpicardic Ablation

42 Yokakawa et al., Heart Rhythm 2013

43 Wijnmaalen et al., Heart 2010 Conclusions: Frequent PVCs can induce subtle cardiac dysfunction detected by speckle tracking imaging analysis in patients without apparent cardiomyopathy. RFCA can successfully eliminate PVCs and improve cardiac function.

44 Baser et al., J Cardiovasc Electrophysiol 2014

45 Preablation and 3 months postablation PVC burden in patients with an acutely effective versus an acutely failed procedure. There was no significant difference in the PVC burden preablation. The PVC burden at 3 months postablation was significantly reduced. Site of origin of predominant PVCs. The numbers in parentheses indicate number of patients with success/failure at 3 months postablation.

46 Conclusioni 1  In assenza di una dimostrata cardiopatia di base i BPV frequenti non sembrano avere in sè una potenziale evolutività verso aritmie maligne e comportare quindi un più elevato rischio di morte improvvisa.  Un numero molto elevato di BPV nelle 24 ore (>2000) si accompagna più facilmente a polimorfismi e forme complesse, aspetti quest’ultimi caratterizzati da maggior prevalenza di cardiopatia.  È necessario che il cardiologo escluda con ragionevole sicurezza la presenza di una cardiopatia prima di assolvere i BPV dal sospetto di essere markers e spie di patologie latenti, subcliniche o molecolari.

47  Sotto il profilo terapeutico, solo la presenza di una cardiopatia giustifica provvedimenti farmacologici con antiaritmici, prescritti in modo personalizzato.  In casi altamente selezionati anche in questo campo risulta vantaggioso il ricorso alle tecniche di ablazione con radiofrequenza.  Per quanto riguarda gli atleti bisogna ricordare l’efficacia del detraining sul controllo dei BPV e l’importanza dell’indagine relativa all’assunzione di sostanze illecite, la cui sospensione è spesso sufficiente a risolvere il problema aritmico nei casi senza patologia cardiaca. Conclusioni 2


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