ventricular tachycardia: the beat of your heart
TRANSCRIPT
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