ventricular tachycardia in the absence of … · ventricular escape rhythms are defined as slower...

VENTRICULAR TACHYCARDIA IN

THEABSENCE OF

STRUCTURAL HEART DISEASE

Dimosthenis Avramidis, MD.Consultant Mitera Children’s Hospital Athens Greece

Scientific Associate 1st Cardiology Dpt Evangelismos

Hospital Athens Greece

• Accelerated idioventricular rhythm

Ventricular escape rhythms are defined as slower than sinus rhythm

Idioventricular rhythms are similar to sinus rhythm and

Accelerated idioventricular rhythms are slightly faster than sinus rhythm, defined as within 10% of the underlying sinus rate.

Benign phenomenon - Temperature - Metabolic and electrolyte abnormalities

Monomorphic ventricular tachycardias

• Classified on basis of site of origin

• Most common sites are ventricular outflow tracts and left ventricular fascicles

• Idiopathic left VT

• Left posterior fascicle

• Left anterior fascicle

• High septal fascicle

• Others

• Mitral annulus

• Tricuspid annulus

• Papillary muscle

• Perivascular epicardial

Outflow tract VT

Right ventricular outflow- 80%

Pulmonary artery

Left ventricular outflow-10%

Aortic sinus of Valsalva

Aortic cusps

Area of aortomitral continuity

Superior basal septum near His bundle(Peri His bundle)

Epicardial surface of outflow tracts

ANATOMIC CORRELATES

RVOT is bounded by pulmonary valve superiorly and superior aspect of tricuspid apparatus inferiorly RVOT is leftward and anterior to LVOTRVOT is a muscular infundibulum circumferentially

Upper part of septal wall is the conus arteriosus, bordered below by supraventricular crest

LVOT is region of LV between anterior cusp of mitral valve and ventricular septum

Large of part of right and some part of left aortic sinuses of Valsalva overlie muscular LVOT

ELECTROPHYSIOLOGIC MECHANISM

• Outflow tract VT is due to triggered activity • Secondary to cyclic AMP mediated DAD• Release of calcium from sarcoplasmic reticulum and DAD • Tachycardia may terminate with Valsalva maneuvers, adenosine, BB or

CCB• Rare cause automaticity, micro-re-entry

Non-coronary cusp and posterior aspect of left coronary cusp are continuous with fibrous aortomitral continuity

Explain lack of VT related to the non-coronary cusp

VT from aortic sinuses of Valsalva arise from muscular extensions of the LVOT to areas above the base of the aortic valve cusps

These muscle fibers often exhibit slow conduction and fractionated electrograms.

Localization of site of VT origin can be predicted using QRS morphology on surface ECG and anatomic relationships help to explain shared ECG patterns and subtle differences

Proximity of RCC to RVOT- ECG based differentiating algorithms may not be consistently accurate

Must be based on the earliest intracardiac activation or on pace mapping

Epicardial foci of VA

OTVT originate from epicardial locations

9%–13% of idiopathic VT

Cluster along the course of the anterior interventricular vein and at its junction with great cardiac vein

Q wave in lead I and terminal S wave in V2(Paper speed 100 mm/s).

Clinical characteristics

• The most common variant consists of frequent PVCs or non sustained monomorphic VT occurring at rest or in the recovery period after exercise

• The less common variant manifests as longer runs of monomorphic VT triggered by exercise or stress

Natural history

Symptoms

• Palpitations

• Syncope is uncommon and should raise the suspicion of an alternative diagnosis or an associated cardiomyopathy

Electrocardiography

Baseline ECG

• Exclude LQTS, Brugada syndrome, ARVC, and short QT syndrome, as well as the cardiomyopathies

• Electrolyte abnormality, myocarditis, or hypertrophy

• Preexcitation or bundle branch block may lend weight to the diagnosis of supraventricular tachycardia

• Conduction delay may also be a marker of an underlying pathologic condition (e.g., sarcoid and ARVC)

Exercise testing

• Is especially useful when trying to distinguish patients with CPVT or LQTS from others with apparent structurally normal hearts

Cardiac imaging

• Echocardiogram to rule out structural heart disease (Evaluation should include wall thickness assessment, quantitation of systolic function, measurement of indices of diastolic function, and exclusion of

valvular lesions, coronary artery anomalies, and cardiac tumors)• Excludes the diagnosis of any form of

cardiomyopathy or overt ARVC• Developed cardiomyopathy owing to a high

burden of frequent ventricular arrhythmias• MRI late gadolinium enhancement may suggest

areas of scarring or fibrosis exclude coronary anomalies or tumors

• Laboratory testing assessment for acute inflammation as seen in myocarditis and to exclude drug toxicity and metabolic or electrolyte disturbance.

• Genetic testing used to evaluate a molecular diagnosis of LQTS, short QT syndrome, CPVT, and Brugada syndrome.

Ambulatory monitoring (Holtermonitorting)

• Arrhythmia burden

• The distinction of monomorphic from polymorphic ventricular ectopy

• Efficacy of therapy

• Prolonged monitoring with event monitors in evaluating sporadic episodes and correlating them with symptoms

ASSOCIATION BETWEEN CARDIOMYOPATHY AND PVC

• QRS duration

• Epicardial origin

• Persistence of PVCs or frequent monomorphic VT

• Longer duration of palpitations (in symptomatic patients).

TREATMENT

Idiopathic left VT

• Three varieties

• left posterior fascicular VT -RBBB and LAD (90%)• left anterior fascicular VT -RBBB and RAD • high septal fascicular VT -relatively narrow QRS

and normal axis

15 to 40 years

More in men (60%)

Usually paroxysmal

Incessant forms leading to TCM are described

ELECTROPHYSIOLOGIC MECHANISM

Re-entrant mechanism

Orthodromic limb -zone of slow, decrementalconduction in intraventricular left septum proceeding from base to apex

Lower turnaround point is toward the apex

Retrograde limb is formed by Purkinje network

VT originates from a false tendon extends from posteroinferior left ventricle to basal septum

Resection of tendon or ablation at septal insertion site eliminate tachycardia

Exact role tendon is unclear

Specificity is low

Gallagher JJet al. AJCardiol 1988;61(2):27A–44AMerliss AD, Seifert MJ, Collins RF, etal Electrophysiol 1996;19(12 Pt 1):2144–6.Thakur RK, Klein GJ, Sivaram CA, et al.Circulation 1996;93(3):497–501.

Short-coupled torsade de pointes

ARVD VS IVT

1. Exertional

2. Abnormal baseline ECG

3. Worrisome family history of sudden death in the young

4. Unlike RVOT tachycardia ,VT associated with ARVC is usually due to reentry and is not typically responsive to adenosine or vagal maneuvers

5. Multiple QRS morphologies

F/U

• Complications during outflow tract VT ablation are rare

• RBBB (1%)

• Cardiac perforation

• Damage to the coronary artery (LAD) - cusp region ablation

• Overall recurrence rate is approximately 10%

Epicardial surface 1 year after ablation.

Paul Khairy et al. Circ Arrhythm Electrophysiol.

2011;4:211-217

Copyright © American Heart Association, Inc. All rights reserved.

Conclusions— Ablation lesions produced by cryothermal energy in immature atrial and ventricular myocardium enlarge to a similar extent to radiofrequency ablation. In contrast, AV groove lesion volumes do not increase significantly with either energy modality.

Lesion volumes increased 3.3-fold in atria (95% confidence interval [CI], 2.3 to 4.3; P=0.001) and 2.2-fold in ventricles (95% CI, 1.4 to 3.0; P<0.0001)

Histological characteristics of

cryothermal and

radiofrequency ablation lesions