Jul 31, 2020 This Week in Cardiology Podcast

John M. Mandrola, MD


July 31, 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 July 31, 2020, John Mandrola, MD comments on the following news and features stories.

COVID Stats and a few Thoughts

Yesterday we hit 4.6 million cases in the United States. US deaths a week ago were 147,000 and this week they are 155,000, so the rate of rise of 1.05x is slightly up from last week’s 1.04x.

According to Johns Hopkins’ COVID site, Florida, California, and Texas have all seen spikes in cases, but 4 weeks on from the spike, there is very little change in death rates. Looking at cases form the four surging states (Arizona, Florida, California, and Texas) and at deaths per 1 million people, Arizona was highest with 500 deaths per million. But New Jersey, New York, and Massachussetts all had well over 1000 deaths per million, with New Jersey at nearly 1800 per million.

Internationally, Spain, France, Germany, and especially hunkered-down, law-abiding Australia are seeing rising cases. (Australia has had an 11-fold rise.) These data points bring me back to the words of Professor Hendrik Streeck of the University of Bonn who said in early May

“I am convinced that we are not going to get rid of SARS-COV-2, so it is going to become an endemic virus — which means it is going to live in our population, and we have to start living with it and find measures so that people are not dying of it but at the same time we can achieve normality.”

Barring a major breakthrough in vaccines, the professors’ words bear on huge societal decisions we must make--like getting kids back in schools. Case discovery will continue to increase as we test more and allow people to be increasingly human again. The key will not be total safety. The goal will be the best safety we can manage, given the tradeoffs. My colleague Eric Topol is Tweeting a lot about home testing. This seems like a hugely effective way to help slow the spread.

Cardiac Effects of COVID 19

JAMA-Cardiology published a highly circulated study looking at cardiac involvement of the heart in COVID disease. The headline of the paper and the news coverage scared people. A group from the University of Frankfurt, Germany, presented a cohort study of 100 patients recovered from COVID-19 who underwent cardiac magnetic resonance imaging (CMR) at weeks to months after recovery. The team then compared the scans of recovered patients with a nonrandomized group of healthy volunteers and a group of risk-factor-matched controls.

This was a nonrandomized comparison and a small number of patients. The main topline findings were that left ventricular ejection fraction (LVEF) was lower, and left ventricular volume and mass were higher in COVID patients vs risk-factor-matched controls. The problem was that LVEF was 56% in COVID-recovered patients and 61% in risk-factor matched controls. The p-value may be significant but is that really a clinically significant finding?

In all, 78/100 patients recently recovered from COVID-19 had abnormal CMR findings, including raised myocardial native T1 (n = 73), raised myocardial native T2 (n = 60), myocardial late gadolinium enhancement (n = 32), and pericardial enhancement (n = 22). But again, what does that mean? The authors explain that increased native T1 measures represent diffuse myocardial fibrosis and/or edema, whereas native T2 is specific for edema.

Venk Murthy wrote to me that T1 and T2 are tissue properties that may approximate measures of fibrosis and edema. He said the key was approximation. Cardiologist Will Watson wrote on Twitter that T1 and T2 are the times taken for hydrogen ions in a chunk of tissue to give back all their radiofrequency energy after you hit them with a radiofrequency pulse in an MRI scanner. If that chunk of tissue’s hydrogen ions is made up of a different chemical (a fat rather than water, let’s say), they will relax at different rates.

Another key limitation of this study was that many of these CMR features and lab values have overlap with the risk factor-matched controls.

The authors’ conclusions were that MR revealed cardiac involvement in 78 patients (78%) and ongoing myocardial inflammation in 60 patients (60%), independent of preexisting conditions, severity, and overall course of the acute illness, and time from the original diagnosis. These findings indicate the need for ongoing investigation of the long-term cardiovascular consequences of COVID-19.

But these problems are only the tip of the iceberg. On Twitter, Darrel Francis and Graham Cole found numerous problems with the presentation of the data.

We know that COVID 19 can affect the heart but this study should be interpreted with tons of caution. And once again, public and open peer review may have trounced the insular peer review of experts.

Atrial Fibrillation Ablation Safety

AF ablation is probably the most common electrophysiology procedure. One of the biggest concerns of the ablation is thermal damage to the esophagus, which sits precariously close to the posterior wall of the left atrium. If you have enough thermal damage to the esophagus from left atrial lesions, you can develop an atrio-esophageal fistula which is fatal in the vast majority of cases.

While the odds of having an esophageal injury during ablation are very small, the consequences of having it—a fatality—are huge. Everyone who does AF ablation worries about this risk.

At the virtual European Heart Rhythm Association meeting, a group from the United Kingdom tested an already approved cooling device (it’s used for cooling in cardiac arrest patients), for esophageal protection. The idea is if radio frequency heating damages the esophagus, then cooling from the inside may limit the damage.

The St. George’s group used an RCT design with 120 participants, half on standard care and half with cooling. They used a surrogate endpoint from post-procedure endoscopy: evidence of thermal injury on a 0-6 scale. Sadly but not surprisingly, 30% of both groups dropped out after refusing later endoscopies.

  • At 7 days, 93% of the protected group had no significant esophageal abnormality, compared with 70% of the control group (P < .001).

  • Any degree of mucosal injury occurred in 3.3% of protected patients and in 20.0% of control patients (P =.008)

  • There was a trend toward a lower incidence of gastroparesis among the protected group (2/60 vs 6/60, respectively; P = .27).

Esophageal protection is a hot topic in electrophysiology. But this is a small, nonpublished study and it’s pretty inconclusive.

Another SGLT2 Inhibitor Hits the Cardiac Radar

In a press release this week, we learned that the EMPEROR-Reduced outcomes trial of empagliflozin 10 mg daily vs placebo in patients with heart failure with reduced ejection fraction (HFrEF) with or without diabetes met its primary endpoint, which was time to first cardiovascular death or heart failure hospitalization. The multicenter trial sponsored by Boehringer Ingelheim will be presented at European Society of Cardiology. About 3700 patients are enrolled and followed for approximately 3.4 years.

This is now the second SGLT2i drug out for heart failure. Dapagliflozin earned US Food and Drug Administration labeling in May 2020 after DAPA-HF showed a highly significant 26% reduction in cardiovascular death or heart failure hospitalizations and a 17% reduction in all cause death. We will have to see the effect sizes of empagliflozin vs dapagliflozin but this looks to be another advance in cardiac therapeutics.


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