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In This Week’s Podcast
For the week ending April 22, 2022, John Mandrola, MD comments on the following news and features stories.
VT Ablation
I want to revisit the comments I made last week on ventricular tachycardia (VT). If you haven’t listened, you might do that first.
I misspoke slightly in my review of the PARTITA study of early VT ablation vs standard care after an implantable cardioverter defibrillator (ICD) shock. The trial found that VT ablation reduced the primary endpoint of death or hospitalizations for heart failure (HHF). I criticized it on many fronts. One was that VT ablation improved overall mortality but did not really reduce VT.
I said this: “Cardiac death, recurrent VT, VT with anti-tachycardia pacing (ATP), or VT with shocks did not differ.”
The last phrase – VT with shocks — was actually lower in the ablation arm; two vs 10 patients, with a P of 0.039. Thanks to Dr. Dimitris Tsiachris for listening so carefully.
Sorry for the mistake. My criticisms still stand: recurrent VT of any type, of which there were more events, did not differ. Again, the primary endpoint of this trial, which had 23 patients in the ablation arm and 24 getting standard care, had a positive endpoint driven by non-cardiac deaths, which could not have been affected by either arm.
I also received an extremely kind email from one of the SURVIVE VT investigators. He disagreed with many of my criticism of SURVIVE VT, a trial conducted in Spain, that compared early VT ablation with substrate ablation and antiarrhythmic drugs (AAD) in patients with ischemic cardiomyopathy (CM) who had an ICD shock.
This trial included 144 patients and a primary endpoint of cardiovascular (CV) death, ICD shock for VT, HHF, or severe treatment-related complications. I want to review some of his most important responses to my criticisms.
First, he took issue with my citation of a 14% complication rate. In the supplement they broke down complications into major and minor and here there were eight major complications in seven patients, which is 10%. Two of these were slow VTs that, if excluded, would result in an 8% complication rate. He also points out that AAD also have complications.
My response: Okay, but 8% to 10% is still a high complication rate, especially considering the trial is conducted in super-expert centers on carefully selected patients.
Second point of contention: he took issue with my comment that VT ablation should reduce the primary endpoint via reduction of VT. Again, in SURVIVE, rates of ICD shocks, CV deaths, total deaths, and any VT were all similar.
He said, “You made it sound like VT ablation is a curative procedure and I don’t think that is the case. VT ablation is an adjuvant therapy to ICD aimed at reducing VT recurrent events; the more you reduce them, the better, but I think it is unrealistic to believe that VTs can be eliminated.”
That’s fair, but keep in mind, these were patients who had undergone one ICD therapy or one episode of sustained VT.
He also took issue with my critique of calling sinus bradycardia and hypothyroidism severe complications, which made the AAD arm look worse. His rebuttal was that the hypothyroidism was symptomatic and led to discontinuation of amiodarone. And both cases of sinus bradycardia and dyspnea were symptomatic.
That is also fair, but still, none of these are akin to stroke or pericardial tamponade.
A fourth disagreement centered on my comments that slow VTs in the AAD arm are not severe complications because part of the efficacy of AAD is to slow VT and if recurrent it can be ablated.
My gracious colleague from Spain wrote: “AADs slow conduction velocity, but the reason we use them is not to slow VTs, it is to prevent them, right? Suffering a slow VT (undetected and untreated by the ICD) led these patients to the hospital because they were symptomatic, many of them with VT lasting hours and requiring cardioversion. Additionally, five out of these 15 patients (33%) had incessant VT defined as a VT that recurs promptly despite repeated interventions for termination over several hours, and this is a serious condition that may require urgent VT ablation.”
There were some other more minor points of disagreements.
I want to say how much I love these comments and interactions. I learn from them and I hope you can too. I also want to re-iterate strongly that my critical appraisal of a trial is never meant to be personal. I’ve gotten involved in trials and now understand firsthand how damn hard they are to do. This week, I heard results of an NIH trial I was part of, and as proponents of the thing we were studying, we had hoped for stronger results. So, I get it.
My aim here is never to diminish the work of generating evidence. My aim is to help clinicians appraise the evidence in a neutral way and to be able to better translate it to the bedside. And it is true that I have biases. I have lived through many periods of irrational exuberance in cardiology — especially electrophysiology (EP). In large part this happened because we were too easily bamboozled. We were unable to critically appraise the evidence for ourselves. These experiences have led me to becoming medically conservative. So, part of my aim is to provide a cautious approach to new therapies.
American College of Cardiology (ACC): More to Come
I’ve spent two weeks reviewing the ACC meeting. I did not get to all the studies. There are still some more noteworthy topics to sort out from ACC.
One is renal denervation, the SPYRAL-HTN – On Med follow-up study, for instance. I am in a journal club on this next week and will let you know more on this study coming soon. Renal denervation is making a comeback, there are many studies in this space, using different study designs and different devices vs the SYMPLICITY III days. It’s super complicated.
European Heart Rhythm Association (EHRA) Meeting
As ACC was on, the EHRA meeting happened in Copenhagen. It’s quite unfortunate that the two meetings overlapped. I hope that changes in the future.
At EHRA, a number of studies addressed three white-hot topics in EP. I realize EP is a sub-specialty so I will attempt to keep it interesting for a broad audience.
Pulsed-Field Ablation (PFA)
First is a new ablation energy called PFA.
PFA works via electroporation, a technique that involves applying electrical current to the heart, which then disrupts current flow across the cardiac cell membrane. This results in pore formation and cell death.
Recall that the very first ablation was DC shock to the atrioventricular (AV) node. PFA is a super-controlled form of DC shocks. Patients have to be under anesthesia to have it. The main upside of PFA is its cardio-selectivity; it purportedly does not harm the adjacent phrenic nerve or esophagus. It’s also fast. There is much excitement in the EP community about this technique.
Vivek Reddy presented results of a large European experience with the first generation PFA system. It earned the Conformitè Europëenne (CE) Mark about 11 months ago, and Reddy had a survey from 24 European centers and 1700 patients. The study was called MANIFEST PF. The results were mixed.
Patients in this retrospective observational survey were typical of an ablation cohort; about 62 years old with a mean CHADSVASC of 2 and normal ejection fractions (EF).
All patients had one transseptal puncture, the mean procedure time was 65 minutes (range, 38 to 215 minutes), mean fluoroscopy time was 12.7 minutes (range, 4.5 to 33 minutes), and 16% of patients were discharged the same day.
I want to stop there and say that this is not much different than my radiofrequency (RF) ablation procedures and probably longer than my colleagues’ cryoballoon procedures.
The success rate using PFA was similar to standard; 99.9% of PVs were isolated.
In this survey, there were no esophageal fistulas or pulmonary vein (PV) stenoses. However, there was one (transient) phrenic nerve (PN) injury and coronary vasospasm. The PN injury was very short lived but again, PFA is supposed to be cardio-specific.
There was a 1% rate of pericardial tamponade; 17 of 1700. Four required surgery.
There were seven strokes, one fatal; incidence 0.4%.
There were 56 vascular complications, the majority were hematomas, for a rate of 3%
Reddy presented another slide comparing major vs minor adverse events (AE) and the major AE rate was 1.6%. Minor was 3.9%.
Another finding of note was that 114 patients (of 1750) had magnetic resonance (MR) brain imaging post procedure and the rate of “positive MRIs” or silent cerebral ischemic events was — get this — 17.5%. I worry a lot about these ischemic spots on MR with this procedure. PFA is known to create significant bubble formation in the left atrium (LA).
British EP doc David Tomlinson and I wrote an editorial in the Journal of the ACC on an early PFA study primarily because it was missing data on post procedure brain scans.
While this type of study is not a randomized controlled trial, it is important data. Observational registry-like data tells us what we are actually doing. Europe has a head start with PFA because of the lower regulatory standard there. Good on the investigators for reporting this data.
In sum, PFA has great potential. Early studies look promising. But, as Vivek Reddy pointed out, a painfully small number of patients have been studied. And this early data from Europe shows procedure, xray times, and complication rates not much different from contemporary atrial fibrillation (AF) ablation. We have little to no randomized data. I am glad the US regulators have not approved this energy source. It may be great. It’s likely to be great. But we have far too little data to embrace it yet.
High Power Short Duration Ablation
Another hot topic in EP and another way to ablate the LA is the use of high-power short-duration radiofrequency (RF) energy. The core issue with AF ablation is doing enough ablation to durably isolate pulmonary veins but not so much to perforate the heart or do damage to the esophagus or phrenic nerves.
The concept of high-power short duration (HPSD) vs standard lower power longer duration (LPLD) hinges on physics. Heating tissue from a catheter results in immediate resistive heating and then later conductive heating. Low power longer burns leads to more resistive heating, which can go deeper. HPSD results in more conductive heating which leads to less depth but greater size.
The three goals of HPSD are:
safety, as less depth of the lesions may spare the esophagus;
efficacy, as larger lesions may make for durable ablation lines; and
speed, as short burns make for faster procedure times than longer lesions.
There have been many studies comparing HPSD to standard RF but these are small and often single center studies. At EHRA, Prof Jose Merino presented results of the PW Fast III trial conducted in Spain.
The study included 267 patients with AF for less than 1 year at 12 centers in Spain. LPLD patients received 25 to 40 Watts, according to lesion size and ablation indices, and HPSD patients received 70 Watts for 9 to 10 seconds. Endpoints were efficacy and safety. Safety included acute esophageal injuries noted on post-procedure endoscopy, which all patients underwent.
For efficacy, first pass PV isolation, that is, getting isolation on your first lesion set, was better in the standard ablation arm. First pass isolation is thought to correlate with better durability of PV isolation. Professor Merino went quickly over that slide but it’s surprising.
For acute PV reconnections, there were no significant differences but there were numerically more reconnections with HPSD. Again, surprising given the use of 70 watts (American machines only go to 50 watts).
Procedure times were not significantly different.
For safety and esophageal lesions there were no differences: 6.5 vs 7.5% of patients had some post-procedural esophageal lesions noted on EGD. This is good and bad news. You’d like HPSD to be lower but at least it wasn’t worse.
For total complications, such as pericardial effusion and bleeding and stroke, there were no significant differences, but there were trends against HPSD.
1 effusion vs 4 in the standard vs HP arm
0 strokes vs 3 strokes in the standard vs HP arm.
Professor Merino concluded that the techniques were similar, but he did note the trends against HPSD.
This trial is not yet published, but this is sobering data. I’ve not adopted HPSD. It scares me. This data finds less acute efficacy and strong trends for less safety. I’ve adopted a cautious approach on the posterior wall of the LA. I’ve ablated AF for 16 years and I’ve been lucky enough to avoid a catastrophic atrioesophageal fistula. It’s reassuring that Power FAST III did not find a higher rate of esophageal lesions, but I think we need a lot more data before we adopt more aggressive ablation strategies.
LBBB Area Pacing
Because I grew up in the heyday of ablation, I used to feel pacemakers were boring. Now, with age, I’ve come to love the purity of pacing. Patients are sick or dying and pacers make them well. It’s one of medicine’s most beautiful therapies. But even better, we now have conduction system pacing.
First there was His-bundle pacing and now there is left bundle pacing. These can be lumped into “conduction system pacing” and the promise is that if you pace the rapidly conducting His-Purkinje system, you avoid muscle-to-muscle slow conduction, those ugly wide-paced QRS complexes, and the dyssynchronous conduction of standard right ventricle (RV) pacing.
You might wonder, with the left bundle is on the left side of the septum, how do you get a pacing lead there from the RV? I wondered that too. This may sound a bit peculiar, but the way you do it is to place the lead on the mid-septum, and screw it like a screwdriver, through the septum a few millimeters until the tip gets close to but not through the septum.
The tip of the lead now captures the left bundle, or the area of the left bundle, and the conduction spreads down the left bundle branch (LBB) first and results in rapid LV activation and a right BB (RBB) morphology QRS. Recall that in RBB block (RBBB), left ventricular activation is not delayed. Also recall that the LBB arborises quickly into fascicles after the proximal LBB. So we often capture fascicles of the LB when on the left side of the septum.
At EHRA, one of the most active conduction system pacing (CSP) experts, Dr. Marek Jastrzebski presented results from the MELOS study, a massive European effort from 14 centers and 2533 patients; 27% had heart failure and 22% had LBBB.
Some of the interesting findings of this observational real-world data:
There is a big learning curve—plateau is reached after 150 cases. Success rate for bradycardia was 92%, however for use in cardiac resynchronization therapy (CRT) it was 77%.
Pacing parameters with LBBB is far better than His bundle pacing and this study shows it:
Pacing threshold 0.77v.
Sensing: huge R raves of 10 mV and paced QRS durations of 136 to 145.
Importantly the R-wave peak time in V6, a measure of lateral LV activation, was low at 77 to 83 msec.
Complications: Septal perforation rate was 3.7% (not the same as cardiac perforation where there is bleeding into the pericardium). When this happens, you pull back and reposition; the lead is extremely low profile.
There are the normal complications seen with other pacers but there are some specific-to LBB area pacing, such as coronary artery injury.
Total complications were 8% and this is similar to standard pacing. Many of these included transient septal perforation, which is not known to be a severe complication.
Comments: I have moved to almost 100% LBB area pacing when doing a standard brady pacer. The learning curve is substantial. However, once you get it, it becomes much easier – 10 times easier than His-bundle pacing. What I like about it is the pacing parameters are amazing, you are working in the septum so perforation leading to tamponade is less likely, you get amazing QRS complexes, and avoid the dyssynchrony of RV pacing. I also love that the lead we use for this has been around for years and years and has an excellent track record.
Yet I agree that we need more data, especially when using this for correction of LBBB and CRT. If you don’t know how to do it, you can’t easily use it as a bailout for CRT. The potential downsides extend beyond MELOS data. This includes long-term performance of a lead with a hinge point in the septum.
I also admit the bias of beauty. I went into cardiology largely based on the magnificence of the electrocardiogram (ECG). The ECG of LBB capture is truly a thing of beauty. I’ve had multiple calls from nurses on the floor who are concerned that they can’t tell the heart is paced. I tingle with delight, because that means the ’paced‘ QRS is so natural. Like it was when we came out of our moms!
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Cite this: Apr 22, 2022 This Week in Cardiology Podcast - Medscape - Apr 22, 2022.
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