Aug 21, 2020 This Week in Cardiology Podcast

John M. Mandrola, MD


August 21, 2020

Please note that the text below is not a full transcript and has not been copyedited. For more insight and commentary on these stories, subscribe to the This Week in Cardiology podcast.

In This Week’s Podcast

For the week ending August 21, 2020, John Mandrola, MD comments on the following news and features stories.

COVID-19, Briefly

Yesterday we hit 5.7 million cases in the United States. US deaths two weeks ago were 170,000 and this week they are 176,000; so the rate of rise has fallen slightly, to 1.03x. The bad news is with schools, colleges particularly. Numerous schools have tried to bring in students but had to go virtual due to clusters of cases.

But today I will offer a bit of good news. My colleague and editor-in-chief at Medscape, Eric Topol, Tweeted this week that SARS-COV-2 is evolving very slowly, meaning neutralizing antibodies and vaccines have a better chance to succeed; all of the recent reports support a solid B (antibody) and T cell immune response; and there are no documented reinfections. Professor Natalie Dean from the University of Florida noted that serious illness in kids is very rare.

On the home front, our hospital has not seen a significant rise in admissions and the mortality rate is plummeting. We see fewer older and more vulnerable patients, presumably because we have learned how to protect them. My colleagues in the ICU think steroids are helping and possibly remdesivir.


My trusted editor of many years Tricia Ward has an outstanding Q & A with interventional cardiologist Quinn Capers from Ohio State. Dr Capers isn't just an interventional cardiologist, he was also dean of admissions at the OSU College of Medicine and has been a leader in promoting diversity in medical education.

My favorite quote from Dr. Capers is:

There has never been any evidence that somebody who gets 90% of those questions right will be a better cardiologist or surgeon or family physician than somebody who gets 80% of those questions correct. So when they say I just want the best, they're clinging to a metric that doesn't measure who is the best.

In the interview, Dr. Capers explained the retraction of Dr. Norman Wang's paper on diversity in the Journal of the American Heart Association. Capers noted that the article was not retracted because the author's views are controversial or hurt people's feelings. The bar for retraction is that that author falsified data.

Clinical Research in the COVID Era

I don't know how it is at your place, but recruitment for clinical trials is harder during the pandemic. A research letter published in the Journal of the American College of Cardiology confirmed that our experience is typical. The authors, led by heart surgeon, Mario Gaudino from Cornell, used data from to study the effect of COVID19 on ongoing non-COVID trials.

On average about 640 trials per month were stopped in the 3 years before the pandemic. During the pandemic it was nearly 9-fold greater at 5800 trials stopped per month. More than 95% of the trials that were stopped during the COVID pandemic had non-governmental (primarily industry) funding. According to study co-author Dr. Dheepak Bhatt, "It may be a while before we fully appreciate just how much information was lost and how much might be salvaged."

Of course, the interruption of and termination of trials is problematic because of the lost information. But a contrarian view of this would be that the pandemic may help trim the fat from dubious research. As the late statistician Doug Altman famously said: We need less research, better research, and research done for the right reasons.

The Subcutaneous-ICD – PRAETORIAN Trial

At the virtual Heart Rhythm Society meeting in May, the PRAETORIAN trial investigators presented the first RCT of the Boston Scientific subcutaneous implantable cardioverter defibrillator (S-ICD) as a late-breaking clinical trial. I covered it then on the podcast, but earlier this month, the New England Journal of Medicine published the results.

A quick review: The S-ICD has a lead outside the ribs and a can in the left lateral chest. The lead is close enough to the heart to sense the cardiac signals. In the event of V-tach or V-fib, defibrillation occurs with energy from the can to the leads. The point of the S-ICD is that it has no leads in the veins or the heart and thus, theoretically avoids lead complications like infection, threshold rises, fractures, insulation breaks, and recalls. But without a lead in the heart there can be no bradycardia pacing, no overdrive anti-tachycardia pacing, and sensing is more challenging for the extra-thoracic system. Double counting of R and T waves have been noted.

PRAETORIAN used a noninferior design and a safety primary endpoint—a composite of lead complications and inappropriate shocks—to compare the S-ICD with the transvenous ICD (TV-ICD).

The topline results were that the identical number of patients in each group had a primary safety outcome. This met noninferiority but not by much. The two components of the safety endpoint diverged. Lead complications favored the S-ICD but inappropriate shocks favored the TV-ICD. Appropriate antitachycardia pacing was delivered in 13% of the patients in the TV-ICD group and successfully terminated 55% of all treated episodes of V-tach. The authors concluded the two devices were noninferior

My written commentary on this study will be coming out soon on Medscape. But briefly, why study just safety? We know TV-ICDs reduce mortality, but the S-ICD is dissimilar enough to warrant an efficacy study. A recent German study found that 1 in 5 patients with an S-ICD did not defibrillate when tested at generator change. One theory as to why defibrillation thresholds increased is that a gain in fat could increase the impedance enough. Another issue: Is a lead complication such as dislodgment the same as wide awake shocks? I would argue that shocks are worse.

In a study that barely met noninferiority, 38 patients were lost to follow up; I know the fragility index is in disfavor but this many missing in a close call is not nothing. The biggest weakness of the trial is that it was 4 years long. The S-ICD is promoted for its ability to prevent long-term complications. There is nothing in PRAETORIAN that supports that contention.


Two news stories published on the | Medscape Cardiology highlighted the past and present of the ECG. The first news story covered a report on a foolproof way to diagnose narrow-complex SVT on an ECG from hospitalist Meghan Mary Walsh.

I saw the word foolproof in the headline and wondered what her technique was. Turns out it was good old classic systematic thinking. Start with the rate, then regularity, then p-wave axis, then use these to narrow the differential diagnosis. It sounds simple but more and more I see people not follow the basic approach.

No, it is not AF if there are organized p-waves. No, it is not sinus tachycardia if the p-wave axis is superior, it's probably atrial flutter. What's more, an older patient does not have a resting rate of 120 bpm. Dr. Walsh has a beautiful algorithm. The only thing I would add to it is this: don't look at the computer read until after you have read the ECG. So often, the computer leads people astray.

If Dr. Walsh's technique rekindles the past, the second study, published in Circulation: Arrhythmia and Electrophysiology, signals the future. Mayo docs studied 1600 patients who came to the emergency department for dyspnea. They applied an AI ECG algorithm to identify left ventricular systolic dysfunction on an echocardiogram within 30 days of presentation. Get this: the AI program identified low ejection fraction with an AUC of 0.89 and an accuracy of 86%. This actually outperformed BNP.

While a contrarian might say one doesn't need AI to predict a bad ejection fraction, you could just do an echo, or soon, a point of care bedside echo to learn the EF. Yes, now that is true. But this is the beginning of the AI work on ECG. You have to open your mind to what is possible with further iterations.


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