VENTRICULAR TACHYCARDIA IN THE ABSENCE 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
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 Idiopathic left VT Left posterior fascicle Left anterior fascicle High septal fascicle Others Mitral annulus Tricuspid annulus Papillary muscle Perivascular epicardial
ANATOMIC CORRELATES RVOT is bounded by pulmonary valve superiorly and superior aspect of tricuspid apparatus inferiorly RVOT is leftward and anterior to LVOT RVOT 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 (Holter Arrhythmia burden monitorting) 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
ELECTROPHYSIOLO GIC MECHANISM Re-entrant mechanism Orthodromic limb -zone of slow, decremental conduction 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 44A Merliss 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. Histological characteristics of cryothermal and radiofrequency ablation lesions 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) 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. Paul Khairy et al. Circ Arrhythm Electrophysiol. 2011;4:211-217 Copyright American Heart Association, Inc. All rights reserved.