May 1, 2020 This Week in Cardiology Podcast

John M. Mandrola, MD


May 01, 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 May 1, 2020 John Mandrola, MD comments on the following news and features stories.


When I recorded last week, there were 880,000 COVID-19 cases. Today there are 1.1million cases. The rate of rise last week was 1.30x and this week it 1.25x, a decrease but given the massive ramp up in testing, an encouraging sign. The rate of deaths is also declining.

When I recorded last week there were 50,000 deaths in the United States, today are 63,000. The rate of rise last week was 1.6x but now it is 1.25x. The big news worldwide is that we now have more than million cases recovered.


This week our governor and hospitals in Kentucky have decided to start doing some semi-elective cases. That is good because our hospital sits about half empty; the number of COVID patients has declined as has the number in the ICU. UCSF also has decreasing numbers, and my friend Vinay Prasad tells me that his hospital in Oregon is more than half empty. My e-group with American electrophysiologists tells the same story. Even colleagues from New York City say things are much better.

So, we must start reframing things. The virus is not going to disappear. It’s a coronavirus. We will be dealing with this for years, perhaps, forever. It will always be dangerous to older people, and those with significant co-morbid conditions.

And I am not saying social distancing is wrong, or that we simply go back to pre-COVID days, but staying locked up and economically shut down as we are now is not sustainable without causing much more non-COVID morbidity and mortality.

I have a short column out today in which I discuss the harms of the intervention. In it, I cite a new preprint from Prof John McMurray’s group in Glasgow.


Results of two randomized controlled trials of remdesivir were released this week. The NIH sponsored double blind RCT, Adaptive COVID19 Treatment Trial (ACTT) began enrolling in Nebraska in February.

Patients who received remdesivir had a 31% faster time to recovery than those who received placebo (p<0.001). Results also suggested a survival benefit. One fly in the ointment, is that the outcomes measures for the trial were changed. The primary endpoint was originally an 8-point severity scale but two weeks ago was changed to time to recovery. Once this got on an Twitter, the NIH sent an explanation for the change, citing 1) little was known about the disease when the trial started, 2) concerns arose about relying on a single time point, 3) blinding remained from investigators.

Notably, Professors Rod Hayward from Michigan and Darrel Francis from London have both written that given the priors, the effect size, and the stature of the NIH researchers, they believe the drug has a real effect. But while a 3% effect size for mortality is indeed large, but a p-value of 0.06 raises the possibility that these results could have been observed by chance.

The second RCT, done in China, published in The Lancet had 237 patients but had to be halted due to lack of patients to recruit. Patients in this trial had 12 days of symptoms, confirmed viral infection, lung infiltrates, and O2 saturations less than 94%. This trial found no reduction in time to clinical improvement, and mortality was nearly identical. Chinese investigators checked the viral load and remdesivir had no effect compared with placebo.

So there you have it, the huge effect size in the NIH trial could be a type 1 error, a false positive, and the Chinese trial is accused of being a type 2 error, a false negative, conclusion.

Now to Cardiology

The QT interval is the time it takes for electrical relaxation, and if it gets too long, the heart can start having early afterdepolarizations, which are medical jargon for rapid ugly dangerous premature ventricular beats.

This week, the FDA put out a warning on the use of hydroxychloroquine (HCQ) and chloroquine in the treatment of patients with COVID-19. Many hospitals had codified use of HCQ and azithromycins in their COVID protocols. Equipoise was shredded and HCQ became standard of care.

But this week, after numerous reports of non-benefit and harm began surfacing, the US Food and Drug Administration updated safety communication saying that the drug should only be used in trials or on an emergency basis when trials were not available. And they urged close supervision for QT prolongation.

ECG Monitoring

Steve Stiles has a superb report on ECG monitoring of patients with COVID-19. One of the reports, from Canadian investigators, is especially interesting. This small prospective case series of 22 patients in a QT clinic studied the utility of a single lead recording from a handheld ECG, from the Kardia device, compared with a 12-lead ECG.

The study confirms that lead I alone, and therefore the single-lead KardiaMobile used as originally intended, is unreliable for measuring the QTc. "It suggests that you should do a multi-lead, and that lead II might be one of the more useful leads for measuring the QTc." Interestingly, Kardia now has a 6-lead ECG available from the device; this will surely be better than just one lead, but we need more data.

Thrombosis and Hemostasis in COVID-19

It is no small thing to intervene in the body’s delicate coagulation system balance, especially when it is immersed in an inflammatory storm.

Patrice Wendling has a comprehensive news recap on recent society publications on treatment of vascular complications in COVID-19. Given the confusion and heterogeneity of this condition, the only answer I see here are pragmatic trials. Lots of them.


Let’s talk low-surgical risk aortic stenosis patients and transcatheter-aortic valve replacement (TAVR). At the virtual ACC meeting, Michael Mack gave a report on two year outcomes of PARTNER 3.

In 2019, the reported results were 8.5% for death, stroke, or readmission at one year in the TAVR group as compared with 15.1% in the surgical aortic valve replacement (SAVR) arm. At 2 years, the difference in primary endpoints remained statistically significant, but the gap had closed: 11.5% with TAVR and 17.4% with SAVR, for a 37% relative risk reduction.

For stroke, the difference was no longer significant at 2 years, nor was the difference in mortality. Most notably, the cumulative incidence of valve thrombosis confirmed by CT or echocardiography was 2.6% in the TAVR arm, compared with 0.7% with SAVR, with most of these unwanted events coming in year 2.


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