Approaching ventricular arrhythmias in a structurally normal heart

SNOWMASS, COLO. – Two generally benign forms of ventricular arrhythmia identifiable by their characteristic signatures on an electrocardiogram – and readily curable by catheter ablation – are ventricular tachycardia originating in the right ventricular outflow tract and premature ventricular contraction–induced cardiomyopathy, Dr. Samuel J. Asirvatham said at the Annual Cardiovascular Conference at Snowmass.

"I think these are two patterns of the ECG that you have to commit to memory. These are two patterns of ventricular tachycardia that are readily treatable, generally benign, and found in structurally normal hearts," said Dr. Asirvatham, professor of medicine and pediatrics at the Mayo Clinic in Rochester, Minn.

• Right ventricular outflow tract (RVOT) ventricular tachycardia (VT): This arrhythmia arises in patients with no coronary artery disease and no valvular disease – in short, no structural heart disease at all. It is often exercise-provoked in males, and can be either exercise-provoked or hormonally cyclic in females. The common symptoms include palpitations and dizziness.

Dr. Asirvatham provided three ECG clues to the diagnosis. One is a negative V₁ lead, indicative of delayed left ventricular activation, as seen in left bundle branch block. The second clue is a strong inferior axis, with the II and III aVF leads being positive. The third giveaway is negative leads at I aVR and II aVL, which indicates the impulse originated in the right ventricle and is simultaneously moving away from these two superior leads.

"You can sometimes treat RVOT VT with beta-blockers or calcium channel blockers, but very often ablation is a better idea for these patients in order to save them from lifelong medications and breakthroughs. Usually if a single source in the ventricle is identified, ablation is a curative procedure," the cardiologist explained.

A caveat: The presence of a little R wave in V₁ is a clue that the anatomic location of that patient’s premature ventricular contractions (PVCs) is likely going to make ablation challenging. The little R wave in V₁ suggests the presence of a deep-tissue focus that needs to be targeted for ablation. It means the patient doesn’t have a complete left bundle branch block, perhaps because the origin of the impulse lies in remnants of embryologic conduction tissue located in the outflow tract, or in a sleeve of myocardium extending up the pulmonary artery. Addressing such a focus successfully via catheter ablation requires an advanced skill set.

• PVC-induced cardiomyopathy: This condition features PVCs plus runs of nonsustained VT and a depressed left-ventricular ejection fraction (LVEF).

"We have a classic chicken versus egg situation here: We know that when the heart is bad you get ventricular arrhythmias, but now we also understand that when you have ventricular arrhythmias it can make the heart bad. It’s our job to tease out which one is the primary culprit," according to Dr. Asirvatham.

The distinction is critical. If the arrhythmias are secondary to a bad heart, the patient should be directed down the pathway of heart failure management and possibly eventual transplantation. But if the cardiomyopathy is due to PVCs, it’s a condition that’s curable through ablation. In making the distinction, Dr. Asirvatham leans heavily on several factors: PVC morphology and coupling interval on the ECG, and total PVC burden over the course of 24 hours on Holter monitoring.

If the PVC morphology looks exactly the same beat after beat, chances are that the impulses are coming from one potentially ablatable spot, and that the ventricular dysfunction followed from the frequent PVCs. In contrast, if the impulses are multimorphic and arise from numerous locations, the likelihood is that the culprit is primary heart disease.

A VT rate in excess of 200 bpm is generally malignant, as is a coupling interval of less than 200 ms between the VT and the preceding normal QRS. Those, along with poly- or multimorphic VT, are worrisome features. In their absence, the key factor in determining whether PVCs are the cause of the patient’s cardiomyopathy or vice versa is how many PVCs there are.

"There’s no definite number, but in general it’s unusual to get cardiomyopathy in someone who has less than 10,000 PVCs per day. It’s more common when you get beyond 20,000 per day, and certainly beyond 30,000. Those are good numbers to keep in mind. The more PVCs you have per day, the more likely you are to get ventricular dysfunction. The corollary is also true: If ventricular dysfunction has occurred with frequent PVCs, once you get rid of the PVCs, in the vast majority of patients the ventricular function improves," according to the electrophysiologist.

On occasion, and with careful informed consent, it’s helpful to turn to empiric amiodarone to help sort out if a patient truly has PVC-induced cardiomyopathy.

"No one likes to prescribe amiodarone in a young patient with cardiomyopathy because amiodarone can produce bad things even when used for 3-6 months. But amiodarone is like an eraser for PVCs, and if, once the PVCs are gone, the ventricular function is still bad, then don’t waste time and put the patient at risk for the possibility of complications by doing a complex ablation. On the other hand, if, after giving amiodarone and the PVCs are gone the ventricular function normalizes, that’s very good evidence that ablation is worth the risk," he explained.

The results of catheter ablation of PVC-induced cardiomyopathy are often spectacular. Dr. Asirvatham recounted the story of a young adult patient whose LVEF had dropped to as low as 6%-8%. After ablation, it’s now 65%-plus and the patient is now an active surgical resident.

Dr. Asirvatham reported serving as a consultant to close to a dozen pharmaceutical and medical device companies.

bjancin@frontlinemedcom.com

SNOWMASS, COLO. – Two generally benign forms of ventricular arrhythmia identifiable by their characteristic signatures on an electrocardiogram – and readily curable by catheter ablation – are ventricular tachycardia originating in the right ventricular outflow tract and premature ventricular contraction–induced cardiomyopathy, Dr. Samuel J. Asirvatham said at the Annual Cardiovascular Conference at Snowmass.

"I think these are two patterns of the ECG that you have to commit to memory. These are two patterns of ventricular tachycardia that are readily treatable, generally benign, and found in structurally normal hearts," said Dr. Asirvatham, professor of medicine and pediatrics at the Mayo Clinic in Rochester, Minn.

• Right ventricular outflow tract (RVOT) ventricular tachycardia (VT): This arrhythmia arises in patients with no coronary artery disease and no valvular disease – in short, no structural heart disease at all. It is often exercise-provoked in males, and can be either exercise-provoked or hormonally cyclic in females. The common symptoms include palpitations and dizziness.

Dr. Asirvatham provided three ECG clues to the diagnosis. One is a negative V₁ lead, indicative of delayed left ventricular activation, as seen in left bundle branch block. The second clue is a strong inferior axis, with the II and III aVF leads being positive. The third giveaway is negative leads at I aVR and II aVL, which indicates the impulse originated in the right ventricle and is simultaneously moving away from these two superior leads.

"You can sometimes treat RVOT VT with beta-blockers or calcium channel blockers, but very often ablation is a better idea for these patients in order to save them from lifelong medications and breakthroughs. Usually if a single source in the ventricle is identified, ablation is a curative procedure," the cardiologist explained.

A caveat: The presence of a little R wave in V₁ is a clue that the anatomic location of that patient’s premature ventricular contractions (PVCs) is likely going to make ablation challenging. The little R wave in V₁ suggests the presence of a deep-tissue focus that needs to be targeted for ablation. It means the patient doesn’t have a complete left bundle branch block, perhaps because the origin of the impulse lies in remnants of embryologic conduction tissue located in the outflow tract, or in a sleeve of myocardium extending up the pulmonary artery. Addressing such a focus successfully via catheter ablation requires an advanced skill set.

• PVC-induced cardiomyopathy: This condition features PVCs plus runs of nonsustained VT and a depressed left-ventricular ejection fraction (LVEF).

"We have a classic chicken versus egg situation here: We know that when the heart is bad you get ventricular arrhythmias, but now we also understand that when you have ventricular arrhythmias it can make the heart bad. It’s our job to tease out which one is the primary culprit," according to Dr. Asirvatham.

The distinction is critical. If the arrhythmias are secondary to a bad heart, the patient should be directed down the pathway of heart failure management and possibly eventual transplantation. But if the cardiomyopathy is due to PVCs, it’s a condition that’s curable through ablation. In making the distinction, Dr. Asirvatham leans heavily on several factors: PVC morphology and coupling interval on the ECG, and total PVC burden over the course of 24 hours on Holter monitoring.

If the PVC morphology looks exactly the same beat after beat, chances are that the impulses are coming from one potentially ablatable spot, and that the ventricular dysfunction followed from the frequent PVCs. In contrast, if the impulses are multimorphic and arise from numerous locations, the likelihood is that the culprit is primary heart disease.

A VT rate in excess of 200 bpm is generally malignant, as is a coupling interval of less than 200 ms between the VT and the preceding normal QRS. Those, along with poly- or multimorphic VT, are worrisome features. In their absence, the key factor in determining whether PVCs are the cause of the patient’s cardiomyopathy or vice versa is how many PVCs there are.

"There’s no definite number, but in general it’s unusual to get cardiomyopathy in someone who has less than 10,000 PVCs per day. It’s more common when you get beyond 20,000 per day, and certainly beyond 30,000. Those are good numbers to keep in mind. The more PVCs you have per day, the more likely you are to get ventricular dysfunction. The corollary is also true: If ventricular dysfunction has occurred with frequent PVCs, once you get rid of the PVCs, in the vast majority of patients the ventricular function improves," according to the electrophysiologist.

On occasion, and with careful informed consent, it’s helpful to turn to empiric amiodarone to help sort out if a patient truly has PVC-induced cardiomyopathy.

"No one likes to prescribe amiodarone in a young patient with cardiomyopathy because amiodarone can produce bad things even when used for 3-6 months. But amiodarone is like an eraser for PVCs, and if, once the PVCs are gone, the ventricular function is still bad, then don’t waste time and put the patient at risk for the possibility of complications by doing a complex ablation. On the other hand, if, after giving amiodarone and the PVCs are gone the ventricular function normalizes, that’s very good evidence that ablation is worth the risk," he explained.

The results of catheter ablation of PVC-induced cardiomyopathy are often spectacular. Dr. Asirvatham recounted the story of a young adult patient whose LVEF had dropped to as low as 6%-8%. After ablation, it’s now 65%-plus and the patient is now an active surgical resident.

Dr. Asirvatham reported serving as a consultant to close to a dozen pharmaceutical and medical device companies.

bjancin@frontlinemedcom.com

SNOWMASS, COLO. – Two generally benign forms of ventricular arrhythmia identifiable by their characteristic signatures on an electrocardiogram – and readily curable by catheter ablation – are ventricular tachycardia originating in the right ventricular outflow tract and premature ventricular contraction–induced cardiomyopathy, Dr. Samuel J. Asirvatham said at the Annual Cardiovascular Conference at Snowmass.

"I think these are two patterns of the ECG that you have to commit to memory. These are two patterns of ventricular tachycardia that are readily treatable, generally benign, and found in structurally normal hearts," said Dr. Asirvatham, professor of medicine and pediatrics at the Mayo Clinic in Rochester, Minn.

• Right ventricular outflow tract (RVOT) ventricular tachycardia (VT): This arrhythmia arises in patients with no coronary artery disease and no valvular disease – in short, no structural heart disease at all. It is often exercise-provoked in males, and can be either exercise-provoked or hormonally cyclic in females. The common symptoms include palpitations and dizziness.

Dr. Asirvatham provided three ECG clues to the diagnosis. One is a negative V₁ lead, indicative of delayed left ventricular activation, as seen in left bundle branch block. The second clue is a strong inferior axis, with the II and III aVF leads being positive. The third giveaway is negative leads at I aVR and II aVL, which indicates the impulse originated in the right ventricle and is simultaneously moving away from these two superior leads.

"You can sometimes treat RVOT VT with beta-blockers or calcium channel blockers, but very often ablation is a better idea for these patients in order to save them from lifelong medications and breakthroughs. Usually if a single source in the ventricle is identified, ablation is a curative procedure," the cardiologist explained.

A caveat: The presence of a little R wave in V₁ is a clue that the anatomic location of that patient’s premature ventricular contractions (PVCs) is likely going to make ablation challenging. The little R wave in V₁ suggests the presence of a deep-tissue focus that needs to be targeted for ablation. It means the patient doesn’t have a complete left bundle branch block, perhaps because the origin of the impulse lies in remnants of embryologic conduction tissue located in the outflow tract, or in a sleeve of myocardium extending up the pulmonary artery. Addressing such a focus successfully via catheter ablation requires an advanced skill set.

• PVC-induced cardiomyopathy: This condition features PVCs plus runs of nonsustained VT and a depressed left-ventricular ejection fraction (LVEF).

"We have a classic chicken versus egg situation here: We know that when the heart is bad you get ventricular arrhythmias, but now we also understand that when you have ventricular arrhythmias it can make the heart bad. It’s our job to tease out which one is the primary culprit," according to Dr. Asirvatham.

The distinction is critical. If the arrhythmias are secondary to a bad heart, the patient should be directed down the pathway of heart failure management and possibly eventual transplantation. But if the cardiomyopathy is due to PVCs, it’s a condition that’s curable through ablation. In making the distinction, Dr. Asirvatham leans heavily on several factors: PVC morphology and coupling interval on the ECG, and total PVC burden over the course of 24 hours on Holter monitoring.

If the PVC morphology looks exactly the same beat after beat, chances are that the impulses are coming from one potentially ablatable spot, and that the ventricular dysfunction followed from the frequent PVCs. In contrast, if the impulses are multimorphic and arise from numerous locations, the likelihood is that the culprit is primary heart disease.

A VT rate in excess of 200 bpm is generally malignant, as is a coupling interval of less than 200 ms between the VT and the preceding normal QRS. Those, along with poly- or multimorphic VT, are worrisome features. In their absence, the key factor in determining whether PVCs are the cause of the patient’s cardiomyopathy or vice versa is how many PVCs there are.

"There’s no definite number, but in general it’s unusual to get cardiomyopathy in someone who has less than 10,000 PVCs per day. It’s more common when you get beyond 20,000 per day, and certainly beyond 30,000. Those are good numbers to keep in mind. The more PVCs you have per day, the more likely you are to get ventricular dysfunction. The corollary is also true: If ventricular dysfunction has occurred with frequent PVCs, once you get rid of the PVCs, in the vast majority of patients the ventricular function improves," according to the electrophysiologist.

On occasion, and with careful informed consent, it’s helpful to turn to empiric amiodarone to help sort out if a patient truly has PVC-induced cardiomyopathy.

"No one likes to prescribe amiodarone in a young patient with cardiomyopathy because amiodarone can produce bad things even when used for 3-6 months. But amiodarone is like an eraser for PVCs, and if, once the PVCs are gone, the ventricular function is still bad, then don’t waste time and put the patient at risk for the possibility of complications by doing a complex ablation. On the other hand, if, after giving amiodarone and the PVCs are gone the ventricular function normalizes, that’s very good evidence that ablation is worth the risk," he explained.

The results of catheter ablation of PVC-induced cardiomyopathy are often spectacular. Dr. Asirvatham recounted the story of a young adult patient whose LVEF had dropped to as low as 6%-8%. After ablation, it’s now 65%-plus and the patient is now an active surgical resident.

Dr. Asirvatham reported serving as a consultant to close to a dozen pharmaceutical and medical device companies.

bjancin@frontlinemedcom.com