1.11 Localizing the Origin of VT and PVCs

[Music] This episode is about localizing the origin of ventricular tachycardia and premature ventricular contractions. This is, I think, one of the most interesting topics in cardiology, also definitely not straightforward at all. Let's jump right in. The most common type of adiopathic VT is outflow track VT. 70% of adiopathic VT is outflow track VT, actually. And among outflow track VT, the majority, 75%, originates from the RV outflow track. And that accounts for 60% of all adiopathic VTs. RVOT ablations have a 97% acute procedural success rate with less than 1% rate of procedural complications. The minority of outflow track VT, 25%, originates from the RV outflow track, accounting for 10% of all adiopathic VTs. RVOT ablations have a 94% acute procedural success rate with a 5% rate of procedural complications. The most common complication is pericardial effusion in 40%, followed by vascular axis complications in 8%, and injury to coronary arteries and 5%. Among RVOT VT, the most common sight of origin is the aortic root at the right and left aortic sinuses of Valsava, or the commissure between the two sinuses that accounts for 70% of LVOT VT, followed by the LV summit, which is 12% of LVOT VT, followed by the LV austiom, 5% to 10%, which consists of the aerodomicrile continuity, septal perihition area, and mitral anulus. The takeaway from this part so far is that the majority of adiopathic VT, 70% is outflow track VT, and both RV outflow track and LV outflow track VT is very ablatable with a very high success rate in the mid 90s. Apart from outflow track VT, adiopathic VT can also arise from the left anchiri or posterior fascicle. 10 to 15% of adiopathic VT arises from the left anchiri or posterior fascicle. This is the verapimel sensitive one. It can also arise from percange fibers, which accounts for less than 1% of adiopathic VT. This is the proprandal all sensitive one, pepillary muscles, which is 2 to 5% of adiopathic VT, and moderator band, which is 2.5% adiopathic VT, tricuspid anulus, 8% of adiopathic VT, micrallanulus, 5% of adiopathic VT, or from the epicarium, which makes up 2 to 9% of adiopathic VT. Categorized by the side of the heart, non outflow track causes of RV VT include those arising from the tricuspid anulus, papillary muscles, moderator band, and crux. Non outflow track causes of LV VT include those arising from the micrallanulus, left posterior or anterior fascicle, and papillary muscles. This episode will not cover non adiopathic causes of VT, such as scar mediated VT from prior coronary artery disease. Throughout this episode, the term ventricular arrhythmia, or VA, will be used to encompass both VTAC or PVCs, ventricular tachycardia or premature ventricular contractions. Here are some key principles. Ventricular arrhythmias coming from the outflow tracks above atroventricular valves, superior to inferior, will have a positive QRS in leads 2,3 and AVF. In contrast, ventricular arrhythmias coming from the inferior ventricles below the atroventricular valves, inferior to superior, will have a negative QRS in 2,3 and AVF. Ventricular arrhythmias coming from the left of chest midline will have a negative QRS in 1, ventricular arrhythmias coming from the right of the chest midline, in contrast, will have a positive QRS in 1. Most left ventricular structures are left of midline. As for the RV, the RVOT free wall is left of midline, so it will have a negative QRS in lead 1. But the RVOT septum is on the midline, and the right coronary cusp is right of the midline, so it will have a positive QRS in lead 1. Ventricular arrhythmias coming from the left ventricular free wall will have a right bundle branch block configuration, while ventricular arrhythmias coming from the right ventricle, or the interventricular septum will have a left bundle branch block configuration. Therefore, the mitral annular ventricular arrhythmias will have a right bundle branch block configuration, while RV outflow track free wall ventricular arrhythmias will have a left bundle branch block configuration. The pre-chordial transition occurs progressively earlier, and so this is transition from left bundle branch block to right bundle branch block, as we move from the RVOT free wall to the mitral annulus. Ventricular arrhythmias coming from basil and posterior sites will have positive pre-chordial concordance, while ventricular arrhythmias coming from apical and anterior sites will have negative pre-chordial concordance. The QRS transition varies with shifts in exit along a superior inferior axis, and also a right to left axis. Ventricular arrhythmias coming from the septum will have narrower QRS complexes than ventricular arrhythmias coming from the free wall, consistent with synchronous rather than sequential ventricular activation. Ventricular arrhythmias coming from the epicaridium, in non-ischemic cardiomyopathy, will have a slurred delayed upstroke of the QRS. These are the key principles to know when localizing VTN-PVCs. There are some things that just can't be explained in audio format for an more in-depth treatment of this topic with visual anatomical examples, please visit my YouTube channel. Next, how does knowing the VTN-PVC site of origin affect management other than eventual ablation? Well, RV-outflow track VTN-PVC can be treated with beta blockers, calcium channel blockers, type 1C anti-arithmic or catheter ablation. In contrast, mixillotine, which is a class 1B anti-arithmic, is used for re-entrant or scar mediate adventricular arrhythmias and has no effect on RV-outflow track VT. VT with a right-bondled branch block appearance and superior axis in a young person with no structural heart disease suggests idiopathic LV-VT. Likelyphysicular, which is a re-entrant tachycardia involving the left posterior fascial, usually, instead of anterior, giving a right-bondled branch block like appearance and superior axis. Idiopathic left ventricular vesicular VT is highly sensitive to verapimil. It is a low-risk tachycardia and can be completely cured by catheter ablation of the left posterior fascial. VT with a left-bondled appearance and inferior axis suggests right ventricular outflow track VT, which can be seen in structurally normal hearts and has a benign course that is responsive to catheter ablation. However, you need to get a resting ECG to see if there are T-wave inversions in the anterior pre-chordial leads, which would be concerning for ARVC, in which case you need to get a cardiac MRI. What do the guidelines say about VT for specific sites? According to the 2017 AHAACCHRS guideline for management of ventricular arrhythmias and the prevention of sudden cardiac death, for outflow track VT, in patients with symptomatic outflow track VA, in an otherwise normal heart for whom anti-rhythmic medications are ineffective, not tolerated, or not the patient's preference, catheter ablation can be useful. Class 1. In patients with symptomatic outflow track VT, in an otherwise normal heart, a beta blocker or calcium channel blocker is useful. Class 1. For papillary muscle VTAC, they say, "In patients with symptomatic ventricular arrhythmia arising from the papillary muscles, for whom anti-rhythmic medications are ineffective, not tolerated, or not the patient's preference, catheter ablation is useful." That's a Class 1 recommendation. Next, for adiopathic polymorphic VT or V5, in patients that are young, less than 40 years of age, with sudden unexplained sudden cardiac arrest, unexplained near drowning, or recurrent exertional syncopy, who do not have ischemic or other structural heart disease, further evaluation for genetic arrhythmias syndrome is recommended. Class 1. In patients resuscitated from sudden cardiac arrest due to adiopathic polymorphic VT or VF, and I see that in the video. CD is recommended if meaningful survival is greater than one year. Class 1. For patients with recurrent episodes of idiopathic V5 initiated by PVCs with a consistent QRS morphology, catheter ablation is useful. Class 1. For inter-physicular VT, the guidelines say, "In patients with verapimil sensitive idiopathic LV-VT related to the inter-physicular reentry for whom anti-irritmics are ineffective, not tolerated or not the patient's preference, catheter ablation is useful." Class 1. In patients with sustained hemodynamically tolerated verapimil sensitive idiopathic LV-T related to inter-physicular reentry, intravenous verapimil is recommended for VT termination. That's a class 1 recommendation. In patients with recurrent verapimil sensitive idiopathic LV-T, chronic therapy with aura verapimil can be useful. That's a class 2A recommendation. That is a summary of what we need to know for localizing the origin of VT and PVCs. Again, if you're interested in more granular specifics, you can check on my handout or YouTube channel. PVCs. I want to talk about PVCs, independent of localizing the origin of PVCs, since it's important to know and PVCs come on all the time, everyday on telemetry. In the absence of heart failure or a coronary artery disease, isolated PVCs have no impact on survival. But in the presence of MI, PVCs identify patients who are at increased risk for VTAC or sudden cardiac death. Not all PVCs are benign. If a PVC occurs right on the T of the EKG, it is bad. In the cast trial, the cardiac arrhythmias suppression trial, use of class 1C arrhythmias such as flecanine or end canine to suppress a symptomatic ventricular arrhythmias after MI actually increase the rate of death. So flecanine can no longer be used in patients with CAD. The frequency of PVCs increases over the first several weeks after MI and decreases about six months after MI. Indications for suppression of PVCs are significant symptoms, sustained VT or PVC-induced cardiomyopathy. PVC ablation can be considered if the PVC burden exceeds 15%. Pathetic ablation is effective in 60% to 90% of idiopathic PVCs or VT, depending on the site of origin. Ablation of RV outflow track PVCs has the highest success rate at 90%. Please remember that if the VTAC or PVC has a left bundle in ferriacismorphology, it is a right out, right ventricular outflow track VT or PVC, which is the more common one. If the VT or PVC has right bundle, superior access morphology, then it is a left ventricular outflow track VT or PVC, which is the less common one. When you see RV outflow track origin VT, you must think either idiopathic RVOTVT or ARVC, Arithmogenic Bright Ventricular Cardiomyopathy. What does the 2017 HAACCHRS guideline for management of patients with ventricular arrhythmias and prevention of sudden cardiac death say about PVC induced cardiomyopathy? For patients who require arrhythmias suppression for symptoms or declining ventricular function, suspected to be due to frequent PVCs, generally more than 15% of beats and predominantly one morphology. And for whom anti-arithmic medications are ineffective, not tolerated, or not the patient's preference, catheter ablation is useful. It's a Class I indication. In patients with PVC induced cardiomyopathy, pharmacologic treatments such as with a beta blocker or amyadurone is reasonable to reduce recurrent arrhythmias and improve symptoms and LB function, Class IIA. Can athletes with PVCs participate in competitive sports? According to the HAACCH 2015 scientific statement on eligibility and disqualification recommendations for competitive athletes with cardiovascular abnormalities, athletes with single PVCs and complex forms no greater than couplets at rest and during exercise testing without structural heart disease can participate in all competitive sports. The exercise testing protocol should be based on maximal performance rather than achieving 80% to 100% of the target heart rate to come as close as possible to the level of exertion achieved during the competitive sports, which is usually higher than the 85% target heart rate. Class I recommendation. Athletes with a PVCs at rest that increase in frequency during exercise or exercise testing and convert to repetitive forms should have further evaluation by appropriate imaging or monitoring strategies before clearance for participation in high intensity sports. If uncontrollable, exercise induced arrhythmias produce symptoms or light head of light headness or near-syncopy fatigue or dysnia. The athlete should be limited to competitive sports below the level at which market frequency increase or symptoms evolve during testing. Class I. Athletes with defined structural heart disease who are considered high risk based on the specific heart disease and who have PVCs with or without treatment should be limited to low intensity class Ia competitive sports. This statement applies whether or not PVCs in the setting are suppressed by drug therapy. Class I. Some degree of risk can still be present during class Ia sports however depending on the nature of the heart disease. Ablation of PVCs may be considered in symptomatic patients with frequent PVCs resistant to medical therapy that's class IIB. We should also know about ashman phenomenon. What is ashman phenomenon? It is intermittent right bundle branch block during a fib and aborin ventricular conduction due to a change in the heart rate or cures cycle duration. Whenever a long cycle is followed by a short cycle for example an a fib the beat of the short cycle often has a right bundle branch block morphology with an rsr prime bunny year in lead V1 because the impulses blocked in a right bundle branch. The wide complex aborin beat following the long cycle is an ashman beat. It is often mistaken for a PVC which is why I'm including it in the PVC section of the podcast. This is because the longer rr interval has a longer due action potential duration and longer refractory period. When a supra ventricular impulse reaches the hispricinjee system while one of the branches usually the right branch is still in the absolute or refractory period. After the left side fires normally the impulse eventually goes to the right side to fire in a delayed manner. It is why because it relies on cell to cell transmission outside the regular conduction system. That's why you get a morphology that is rsr prime. That's where the ashman beat comes from. Normally, the length of the refractory periods of the conduction system are as follows in the sending order. Right bundle branch followed by left bundle branch which is approximately the same as hr ventricular known followed by his bundle. That's the decreasing order of the length of the refractory periods in the conduction system. Therefore it would be unusual for the bundle of his to be a site of conduction delay in an ashman beat. The ashman beat usually has a right bundle branch block morphology. That's all for this episode on localizing the origin of ventricular tachycardias and PVCs as well as some tidbits on PVCs. This podcast is intended for qualified health care professionals and is designed for training purposes only. These materials should not be used for direct patient care or is a substitute for independent clinical judgment. For more educational content or to submit suggestions visit www.rayhu.com/meded. (upbeat music)