Management of Non-Sustained Ventricular Tachycardia Troy Hounshell, DO Iowa Heart Center Heart Rhythm Center

Disclosures Harvard Clinical Research Institute Medtronic Milestone Pharmaceuticals, Inc. St. Jude Medical Employee-Iowa Heart Center/Mercy-Des Moines

Objectives Discuss NSVT and its relation to different clinical etiologies To discuss NSVT risk in relation to SCD Discuss treatment of NSVT in its presenting clinical setting

Definition The Concern There can be many different definitions Nonsustained ventricular tachycardia (NSVT) is defined as 3 (sometimes 5) or more consecutive beats arising below the atrioventricular node with a heart rate of >100 beats/min and lasting <30 s. The Concern In several clinical settings, NSVT is a marker of increased risk for subsequent sustained tachyarrhythmias and sudden cardiac death (SCD), whereas it may have no prognostic significance in others. Eur Heart J 2004;25:1093–9

Goal in Managing NSVT Detect those apparently healthy individuals in whom NSVT represents a sign of occult disease, and to risk stratify patients with known disease who present with this arrhythmia to provide therapy that mitigates associated risks.

NSVT with Normal Heart How to Evaluate History (Age/PMHx/FMHx/Medications) 12 Lead ECG Channelopathy (Brugada/Long QT/Early Reoplarization/ARVD/etc) How does it respond to exercise? Suppression with exercise is a marker of benign clinical course** NSVT during recovery is a better predictor if increase mortality than NSVT during exercise only* NSVT in athletes is benign and has no adverse prognostic significance (assuming a structural normal heart and channelopathies are excluded)** * > 7 ventricular ectopic beats per minute was frequent *N Engl J Med. 2003;348:781–90. **J Am Coll Cardiol 2002;40:446 –52 **Eur Heart J 2008;29:71– 8 **Am J Cardiol 2008;101:1792–5.

J Am Coll Cardiol 2012;60:1993–2004

Idiopathic VT Typically referred to as outflow tract tachycardia's Benign arrhythmia May be sustained or repetitive monomorphic NSVT Usually a result of triggered activity from heightened intracellular calcium Usually a LBBB (RVOT) inferior axis with transition usually occurring around V4 Can be RBBB (LVOT) with inferior axis. Transition usually occurring around V1-V2 Treatment aimed at symptoms and typically occurs with BB, CCB. Many times BB with Class IC antiarrhythmic are used for efficacy

Idiopathic vs Arrhythmogenic Right Ventricular Dysplasia Idiopathic VT ARVD RBBB or LBBB Inferior Axis Transition at V4 or V1-2 QRS Lead I >120ms Earliest-onset QRS V1 QRS notching Transition V5 or later The distinction must be made between the two as ARVD has a malignant clinical course Both do or can arise from the RVOT/LVOT and may appear similar at ECG J Am Coll Cardiol 2011;58:831– 8

JACC Vol. 58, No. 8, 2011

Twelve-lead electrocardiograms from patients with right ventricular outflow tract tachycardia (RVOT-VT) (A to C) and arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVD/C) (D to H) showing characteristic features. (A) RVOT-VT from an anterior-septal location showing precordial transition at V2 and narrow QRS duration in lead I (78 ms). (B) RVOT-VT originating superior to His bundle region showing precordial transition at V4, positive R-wave in aVL, and narrow QRS in lead I (86 ms). (C) RVOT-VT from a posterior-septal location showing precordial transition at V3 and narrow QRS duration in lead I (118 ms). (D) ARVD/C ventricular tachycardia (VT) showing late precordial transition V5, wide QRS duration in lead I (124 ms), and earliest onset QRS in V1 (vertical line). (E) ARVD/C-VT shows very late precordial transition V6 and wide QRS duration in lead I (126 ms). (F) ARVD/C-VT shows very late precordial transition V6 and wide QRS duration in lead I (150 ms). (G) ARVD/C-VT shows late precordial transition V5, wide QRS duration in lead I (160 ms), and notching of the QRS (II, III, aVF, V4 to V6). (H) ARVD/C-VT shows wide QRS duration in lead I (128 ms) and notching of the QRS (II, III, aVF, V4 to V6). JACC Vol. 58, No. 8, 2011

NSVT with Hypertension and Valvular Heart Disease Burden closely correlates with LVH No convincing evidence to suggest increased risk of SCD Should have evaluation for IHD Treat hypertension aggressively High correlation between NSVT and VHD NSVT marker of LV pathology No evidence to suggest NSVT predicts SCD even after valve replacement Treat valve disease NSVT in this population correlates with LV remodeling (hypertrophy and subendocardial fibrosis) Am J Cardiol 1992;69:913–7 Circulation 1997;96: 500–8 Am Heart J 1987;113:1298-307 N Engl J Med 1987;317:787–92

NSVT and Coronary Artery Disease NSTEMI NSTEMI Am J Cardiol 2011;108:1373–81

NSVT and Coronary Artery Disease After the reperfusion era evidence now exists to suggest that NSVT no longer carries independent risk death in IHD once other factors like EF are taken into account* CARISMA study showed EF <40% with NSVT (> 125 BPM >16 beats <30s) showed no association with cardiac death over 2 years after multivariable analysis** *Circulation 1997;96:1888 –92 *Circulation 1993;87:312–22 *J Am Coll Cardiol 1999;33:1895–*902 *Circulation 2001;103:2072–7 *Eur Heart J 2005;26:762–9 **Circulation 2010;122:1258–64

NSVT and Coronary Artery Disease When to study? MUSTT trial (EF <40%) Evaluated in hospital vs post hospital presentation of NSVT* Patients post surgical revascularization with NSVT showed worse outcomes when NSVT occurred late after surgery vs early* An exception seems to be patients with early NSVT post surgery with sustained VT at EPS. These patients had poor outcomes** Other modalities Heart rate variability, T-Wave alternans Not well delineated to warrant routine use *J Am Coll Cardiol 2001;38:1156–62 *J Cardiovasc Electrophysiol 2002;13:757– 63 **J Cardiovasc Electrophysiol 2002;13:342– 6

NSVT and LV Dysfunction/ Congestive Heart Failure NSVT in this population is common and can be as high as 80% Two studies CHF-STAT and PROMISE failed to show NSVT to predict SCD or total mortality* Only in the recovery period of exercise does “severe ectopy” show adverse prognostic significance** In patients with idiopathic dilated cardiomyopathy NSVT and LVEF <30% showed 8 fold increase in arrhythmia risk compared to other groups. NSVT by itself was not predictive.*** Triplets or worse was severe NSVT *N Engl J Med 1995;333:77– 82 *Circulation 2000;101:40–6 **J Am Coll Cardiol 2004;44:820–6 ***Circulation 2003;108:2883–91

Special Populations HOCM Incidence of 20-30% Appears to be related to myocardial fibrosis as MRI delayed enhancement and echo strain relate to presence of NSVT Associated with worse LVH and more symptomatic HCM High risk factors Syncope Frequent NSVT FMHx SCD young age Severe LVH (Wall thickness >30mm) Abnormal BP response to exercise Zero to one risk factor shows ~1% risk SCD (low) 2 or more risk factors have high SCD risk NSVT <30 years old significant predictor of SCD. Did not hold up for >30 years old NSVT was associated with greater left ventricular hypertrophy (p 0.01) and severe symptoms (New York Heart Association functional classes III and IV) (p 0.04); SVT occurred more commonly in patients with outflow obstruction (p 0.02). Over a follow-up of 5.5 3.4 years, 11 (6%) patients died suddenly (annual mortality rate, 1.1%) including 5 patients with NSVT. For sudden death, NSVT on Holter ECG had negative and positive predictive values of 95% and 9%, and sensitivity and specificity of 45% and 69%, respectively. J Am Coll Cardiol 2003;42:873–9 J Am CollCardiol 2005;45:697–704 Heart 2004;90:570–575

Giant Cell Myocarditis Special Populations ARVD Giant Cell Myocarditis A condition of fibrofatty infiltration of the myocardium classically in the right ventricle (can be left ventricle) resulting in cardiomyopathy and eventual RV dyfunction Increased risk for SCD Patient can present with asymptomatic NSVT and be at increased risk for SCD NSVT may be monomorphic or Polymorphic Usually sustained arrhythmias with high SCD risk Repaired TOF 50% will have NSVT with 4-14% prevalence of sustained VT Inducible Sustained VT is marker of subsequent events