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PVC & HEART FAILURE THERAPEUTIC OPTIONS AND NOVEL APPROACHES - PowerPoint PPT Presentation

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PVC & HEART FAILURE THERAPEUTIC OPTIONS AND NOVEL APPROACHES Alireza Ghorbani Sharif, MD Electrophysiologist Tehran arrhythmia Clinic May 2016 DEFINITION Premature ventricular contractions (PVCs) are early depolarization of the

  1. PVC & HEART FAILURE THERAPEUTIC OPTIONS AND NOVEL APPROACHES Alireza Ghorbani Sharif, MD Electrophysiologist Tehran arrhythmia Clinic May 2016

  2. DEFINITION • Premature ventricular contractions (PVCs) are early depolarization of the myocardium originating in the ventricle. • Traditionally they have been thought to be relatively benign in the absence of structural heart disease. Yong-Mei Cha, MD; Glenn K. Lee, MBBS; Kyle W. Klarich, MD; Martha Grogan, MD, (Circ Arrhythm Electrophysiol. 2012;5:229-236.)

  3. PVCS Compensatory Pause Interpolated PVCs

  4. ETIOLOGY • Causes: • Hypoxia • Myocardial Ischemia • Electrolyte Imbalance • Digitalis Toxicity • Congestive Heat Failure or CHF • Idiopathic

  5. PVCS AND VENTRICULAR TACHYCARDIA

  6. EPIDEMIOLOGY • PVCs are common with an estimated prevalence of 1 % to 4% in the general population. • In a normal healthy population PVCs have been detected in 1% of subjects on standard 12-lead electrocardiography and between 40% and 75% of subjects on 24- to 48-hour Holter monitoring. • Their prevalence is generally age-dependent ranging from 1% in children 11 years 7 to 69% in subjects 75 years. Yong-Mei Cha, MD; Glenn K. Lee, MBBS; Kyle W. Klarich, MD; Martha Grogan, MD, (Circ Arrhythm Electrophysiol. 2012;5:229-236.)

  7. PVC-INDUCED CARDIOMYOPATHY ( PVCI-CMP) • Commonly thought to be a benign entity the concept of PVC- induced cardiomyopathy was proposed by Duffee et a in 1998 when pharmacological suppression of PVCs in patients with presumed idiopathic dilated cardiomyopathy subsequently improved left ventricular (LV) systolic dysfunction. • It was only15 years ago that the term of (PVCi-CMP) emerged. Yong-Mei Cha, MD; Glenn K. Lee, MBBS; Kyle W. Klarich, MD; Martha Grogan, MD, (Circ Arrhythm Electrophysioloy. 2012;5:229-236.) Marie Sadron Blaye- Felice,MD et al, (Heart Rhythm2016;13:103 – 110 )

  8. MECHANISMS AND PATHOPHYSIOLOGY Yong-Mei Cha, Circ Arrhythm Electrophysiol. 2012;5:229-236 .

  9. WHICH CAME FIRST THE CHICKEN OR THE EGG?

  10. CLINICAL EVALUATION • Because a single 24-hour recording may not reflect the true PVC load due to day-to-day variability, a strong suspicion that frequent PVCs may be the cause of LV dysfunction may warrant extended Holter recordings of 48 to 72 hours or several 24-hour Holter recordings. • Echocardiographic features in PVC-induced cardiomyopathy include decreased LVEF, increased LV systolic and diastolic dimensions, wall motion abnormalities, which are often global as opposed to regional as well as mitral regurgitation (typically due to mitral annular dilatation) • Two-dimensional speckle tracking strain imaging detect subtle changes in the ventricles function whereas the LVEF remains preserved. Yong-Mei Cha, MD; Glenn K. Lee, MBBS; Kyle W. Klarich, MD; Martha Grogan, MD, (Circ Arrhythm Electrophysiol. 2012;5:229-236.)

  11. CLINICAL EVALUATION • Coronary angiography should be performed in every patient with reduced LV systolic function to exclude significant coronary artery disease except for those with a low cardiovascular risk. • Cardiac MRI may be warranted in detecting arrhythmogenic right ventricular cardiomyopathy with LV involvement and infiltrative disease when clinically suspected. Yong-Mei Cha, MD; Glenn K. Lee, MBBS; Kyle W. Klarich, MD; Martha Grogan, MD, (Circ Arrhythm Electrophysiol. 2012;5:229-236.)

  12. PARAMETERS SIGNIFICANTLY RELATED TO THE PVCI-CMP 1. PVC burden 2. Symptoms : Presence or absence of palpitation 3. Duration of symptoms 4. Age and gender 5. Morphology and Sit of origin Marie Sadron Blaye-Felice, MD, (Heart Rhythm2016;13:103 – 110)

  13. PVCS BURDEN • Majority of patients with frequent PVCs have a benign course whereas up to one third of them develop PVCi-CMP. • The prevalence of PVCi-CMP is estimated as only 5% to 7% among patients with a PVC burden 10%. • Baman and Fred Morady et al suggested that a PVC burden of 24% had a sensitivity and specificity of approximately 80% in separating the patient populations with impaired versus preserved LV function. Timir S. Baman, MD, Fred Morady et al, (Heart Rhythm 2010;7:865 – 869) Yong-Mei Cha, MD; Glenn K. Lee, MBBS; Kyle W. Klarich, MD; Martha Grogan, MD, (Circ Arrhythm Electrophysiol. 2012;5:229-236.)

  14. PVCS BURDEN • Takemoto et al analyzed the result of ablation with relation to 3 pre specified subgroups (<10%,10% – 20%, >20%) based on the burden of PVCs on 24-hour Holter monitoring the subgroup with >20% of PVCs at baseline had the most benefit from ablation with significant improvement in LVEF and LV dimensions • When the PVC burden was expressed in the absolute number of PVCs before RFA, the subgroup with >20 000 PVCs per day was shown to be associated with highest risk of LV dysfunction and heart failure. Clin. Cardiol. 38, 4, 251 – 258 (2015) A. Saurav et al: PVC-induced cardiomyopathy

  15. SYMPTOMS AGE AND GENDER • Absence of symptoms are independently associated with PVCi- CMP because diagnosis of PVCs is delayed in asymptomatic patients often made fortuitously over the course of the developing CMP • The duration of palpitations of 30 to 60 months specially more than 60 months • More common with increasing age and in males Fred Morady , MD, et al ,Heart Rhythm 2012;9:92 – 95 Marie Sadron Blaye- Felice, MD, (Heart Rhythm2016;13:103 – 110 )

  16. MORPHOLOGY AND SITE OF ORIGIN • Long PVC-QRS duration • Epicardial origin of the focus • Interpolated PVCs • LV origin of PVCs • Long PVC coupling interval • High PVC QRS amplitude • Presence of polymorphic PVCs

  17. MORPHOLOGY AND SITE OF ORIGIN • Longer PVC-QRS duration, especially in the presence of a LBBB participate in the alteration of LV function because of the electrical and therefore likely associated mechanical dyssynchrony. • Epicardial PVCs have longer PVC-QRS duration than other PVCs probably because of the paucity of Purkinje fibers in the epicardium. Marie Sadron Blaye- Felice, MD, (Heart Rhythm2016;13:103 – 110 )

  18. EPICARDIAL PVCS

  19. MORPHOLOGY AND SITE OF ORIGIN • Interpolated PVCs have a longer Ventriculo-atrial block cycle length compared with PVCs without interpolation. • The total PVC burden increased with interpolation Clin. Cardiol. 38, 4, 251 – 258 (2015) A. Saurav et al: PVC-induced cardiomyopathy

  20. INTERPOLATED PVCS Clin. Cardiol. 38, 4, 251 – 258 (2015) A. Saurav et al: PVC-induced cardiomyopathy

  21. MORPHOLOGY AND SITE OF ORIGIN  LV origin of PVCs  Long PVC coupling interval  High PVC QRS amplitude  Presence of polymorphic PVCs Fred Morady, MD et al, (Heart Rhythm 2011;8:1046 – 1049 ) Marie Sadron Blaye-Felice, MD, (Heart Rhythm2016;13:103 – 110 )

  22. TREATMENT OPTIONS • Medical Therapy • Catheter Ablation

  23. MEDICAL THERAPY • Anti-Failure therapies • Typically, in mildly symptomatic patients with mild LV dysfunction a trial of β -blockers or a nondihydropyridine calcium channel blocker should be considered as first-line therapy. • Class Ic and III antiarrhythmic agents such as flecainide and sotalol are effective but with significant adverse effect. • These agents, with the exception of amiodarone, should not be used in patients with sever LV dysfunction. Fred Morady, MD et al, (Heart Rhythm 2011;8:1046 – 1049 )

  24. CATHETER ABLATION • There are growing evidence in favor of catheter ablation for PVCs especially in the presence of LV dysfunction. • Multiple studies demonstrating high efficacy of catheter ablation of PVCs with success rates ranging from 80% to 100%. • Procedural success may be dependent on the site of origin with lower efficacy for epicardial foci or multiple PVC morphologies. • Major complications occur in approximately 3% of cases including death stroke myocardial infarction cardiac perforation with or without pericardial tamponade pericardial effusion and blood vessel dissection or stenosis. A. Saurav et al: PVC-induced cardiomyopathy Clin. Cardiol. 38, 4, 251 – 258 (2015)

  25. CATHETER ABLATION Ablation of frequent PVCs in patients meeting criteria for primary prevention ICD implant: • In patients with frequent PVCs and PP-ICD indication ablation improves LVEF and, in most cases, allows removal of the indication. • Withholding the ICD and reevaluating within 6 months of ablation seems to be a safe and appropriate strategy Heart Rhythm. 2015 Dec;12(12):2434-42. doi: 10.1016/j.hrthm.2015.09.011. Epub 2015 Sep 15 .

  26. CATHETER ABLATION How many PVCs are too many in post-MI patients: • Sarrazin et al considered frequent PVCs to be 5% of the beats observed on a 24-hour monitor. • Our data suggest that despite the presence of scar tissue in post infarction patients a component of reversible cardiomyopathy may be present in patients with frequent PVCs. • A low ejection fraction with a small amount of scar tissue may suggest a potentially reversible cardiomyopathy. Renee M. Sullivan, MD, Brian Olshansky, MD, FHRS doi:10.1016/j.hrthm.2009.08.029

  27. PVC MEDIATED CARDIOMYOPATHY • Ablation of PVC in patient in presence of structural heart disease • Reverse or stop of progression of LV dysfunction

  28. CATHETER ABLATION Effect of ablation of in patients with nonischemic cardiomyopathy: • Frequent PVCs to be 4-5% of the beats observed on a 24-hour monitor • In patients with frequent PVCs and nonischemic cardiomyopathy EF and functional class can be improved but not always normalized by successful PVC ablation

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