ventricular tachycardia: the beat of your heart

Ventricular TachycardiaThe beat of the heart

Yasmin S Hamirani, MDCardiology

www.SpringfieldClinic.com/DoctorIsIn

Why do we need to know about Ventricular tachycardia

• Asymptomatic

• Palpitations

• Shortness of breath • Syncope

• Sudden cardiac death

Outline Electrical activity of the Heart What is Ventricular Tachycardia Causes of Ventricular Tachycardia Structural Heart Disease Non-structural Heart Disease Symptoms of Ventricular Tachycardia Treatment of Ventricular Tachycardia

https://www.youtube.com/watch?v=te_SY3MeWys

Definition• VT: ≥3 consecutive ventricular beats @ ≥100 bpm

• Nonsustained VT: VT lasting ≥3 beats, <30 secs and not requiring intervention for termination • Sustained VT: VT lasting ≥30 secs or requiring

intervention for termination.

Specific VT Syndromes• Structural Heart Disease:

Ischemic Cardiomyopathy

Non-ischemic Cardiomyopathy

Arrhythmogenic Right ventricular Dysplasia

Hypertrophic Cardiomyopathy

Sarcoidosis

• No significant structural heart disease:

Normal Hearts – “Idiopathic” VTs Outflow Tract VTs LV fascicular VTs

PMVT TdP/LQTSCPVT

Brugada’s Syndrome

Specific VT Syndromes• Structural Heart Disease:

Ischemic Cardiomyopathy

Non-ischemic Cardiomyopathy

Arrhythmogenic Right ventricular Dysplasia (ARVC)

Hypertrophic Cardiomyopathy (HCM)

Sarcoidosis

• Early (<48 hrs p MI)– ↑d in-hospital mortality– Acute therapy: shocks, AADs, treat metabolic

imbalances, recurrent or ongoing ischemia • Long term

– Risk Stratification (Frequent PVCs, NSVT, VT/VF >48 hrs p MI; LVEF; EPS)

– Role of ICD therapy • Beta-blockers and ACE inhibitors have been

associated with improved survival in many studies

Ischemic Cardiomyopathy

Nonischemic Cardiomyopathy

• VT/Vf cause of death in~8-50%. • Risk Assessment: Holter• Treatment

Primary prevention of high risk pts: ICD (SCDHeFT, DEFINITE) ß-blockers AADs, ablation adjunctive

• Secondary vs. primary prevention of sudden death

Primary prevention of sudden cardiac death in both ischemic and non ischemic CMP

• Ischemic – CAD, post MI– LVEF≤ 30%, 1 mo p MI, 3 mo p revasc ICD ⇒

(MADIT II)– LVEF≤35%, NYHA II, III ICD (SCDHeFT)⇒– LVEF≤40%, NSVT EPS±ICD (MADIT,MUSTT) ⇒• Nonischemic

– LVEF≤35%, NYHA FC II, III ICD (SCDHeFT) ⇒• Don’t forget about beta blockers

Role of antiarrhythmic drugs and ablation in both ischemic and non ischemic CMP

• Empiric suppression of PVCs/NSVT with AAD– Generally NOT indicated, unless symptoms, ICD shocks– potential for ↑d mortality– possible exception: amiodarone • Catheter ablation for VT

– Generally adjunctive for reduction of symptoms, ICD shocks

ECG in ARVC

MRI in ARVC

Arrhythmogenic Right ventricular Dysplasia (ARVC)

• Predominant RV cardiomyopathy– Fibrous, fatty infiltration, thinning or hypokinetic areas of the RV – May involve the LV • Strong familial transmission (>50%ofpts) – Autosomal dominant, variable penetrance– Mutations in desmosomal genes

• Presentation with symptomatic ventricular arrhythmias or sudden death

– Cause of ventricular arrhythmias in pts with apparently normal LV – Cause of SCD in athletes (4% US, 22% N Italy) – VTs generally with multiple LBBB morphologies, often precipitated by exercise

ARVC Therapy• ICD

– Cardiac arrest, spontaneous or inducible rapid VT, depressed LV function – Familial ARVD at high risk of SD • Drug therapy and catheter ablation – adjunctive for increased VT frequency – Antiarrhythmic drugs (Sotalol, Amiodarone, beta blockers, IA, III) – Catheter Ablation • adjunctive, multiple VT circuits and progressive disease common

Hypertrophic Cardiomyopathy (HCM)• Most common genetic cardiovascular disease (1:500) • • Autosomal dominant transmission

• Caused by mutations in any of genes encoding protein components of the cardiac sarcomere• Genetically and phenotypically heterogeneous

• Highly variable clinical course and expression • Sudden cardiac death Most frequent in asx young patients (<35 yrs) May occur in young athletesMay be the initial presentation of HCM • Symptoms may also result from diastolic dysfunction and outflow

obstruction in ~1/4 of cases • Compatible with normal longevity

• Risk for sudden cardiac death:• Prior VT/VF/cardiac arrest • Recurrent syncope • Strong FH of SCD • Failure to raise BP on exercise • Very thick ventricle (e.g. 3 cm septum) • NSVT • High risk genotype (esp. β myosin HC, cardiac troponin T, α-

tropomyosin)

• Indications for ICD • HCM with high risk = Class IIB • Prior cardiac arrest, sustained VT/spontaneous VF

= Class I

HCM sudden cardiac death risk factors

• ACC AHA ESC guidelines 2006• Major Risk Factors:• CardiacArrest• Spont.SustainedVT • FamHxofSCD• UnexplainedSyncope • LV>30mm• ExerciseBPdrop• NonsustainedVT

• Possible Risk Factors:• AF • Myocardial ischemia • LV outflow obstruction • High-risk mutation • Competitive physical activity

• No significant structural heart disease:

Normal Hearts – “Idiopathic” VTs Outflow Tract VTs LV fascicular VTs

PMVT TdP/LQTSCPVT

Brugada’s Syndrome

No SHD, but may have tachycardia-induced CM Asymptomatic or symptomaticAss’d with ↑d sympathetic tone • Stress, exercise, high catecholamine states, caffeine,

premenstrual period, menopause, gestation • Adenosine or vagal maneuvers may suppress Treatment • β-blockers, CCB, 1C AADs• Catheter ablation – success rate ~90%+

Fascicular VTach• Paroxysmal VT • Reentry involving calcium dependent Purkinje-fascicular fibers • Not typically precipitated by exercise, but may be potentiated • RBBB morphology

• No definite structural heart disease; negative SAECG • Terminated or suppressed by verapamil or diltiazem • NOT usually adenosine sensitive• Ablation: sites where the VT is preceded by a Purkinje/fascicular

potential• Most common site – LV inferior septum (mid-apical

Long QT syndrome• Inherited ion channel disorder (Na and K channels) • Autosomal dominant inheritance most common • Places patient at risk for TdP which may cause

syncope and sudden death • Clinical features can vary with genetic mutation • Variable expression of severity • Syncope and sudden death have an increased

frequency in adolescence Moss JAMA 2003

Long QT syndrome evaluation• History (QT prolonging drugs etc) • ECG • Holter monitor (TdP) • Exercise testing (diagnostic value not well defined) • No role for EP testing • Genetic testing now available on a commercial

basis

Prognosis: Risk factors for cardiac events

• History (QT prolonging drugs etc) • ECG • Holter monitor (TdP) • Exercise testing (diagnostic value not well defined) • No role for EP testing • Genetic testing now available on a commercial

basis

Treatment of Torsades• Avoid offending agents • Correct electrolyte imbalances • Potential acceleration of the HR (e.g. isoproterenol

or pacing) • Intravenous magnesium • Consider lidocaine, mexiletine, phenytoin

Polymorphic V tach not associated with long QT

• May be associated with ischemia or electrolyte abnormality

• Often degenerates to VF • Catecholaminergic PMVT with/without ARVD • Mutations in genes controlling intracellular Ca++ • Ryanodine release channel (RYR2)• Calsequestrin (CASQ2)

• Beta blockers effective (~60%) • Less/Not effective • – Calcium channel blockers – Na channel blockers

– Amiodarone • • Re-exercise stress test

• ICDs for recurrent cardiac arrest

Indication for ICD• Prior cardiac arrest • Syncope • Uncertain if asymptomatic pts should undergo ICD • Prognostic value of EP testing controversial