8/11/20 COVID Update: Sports, COVID and heart issues

You know, six months later and I’m still not a doctor. And if you would’ve told me on New Year’s Eve that I was going to spend most of 2020 with my nose in medical journals I would’ve been incredibly confused. Meteorology journals? Sure. Medical journals? Not so much.

But here we are!

Some troubling new evidence is starting to surface regarding how the body recovers from COVID-19 that may help to explain why many college campuses are debating canceling fall sports. Some already have, sure. But this may help to explain the reasoning.

And no, it isn’t “The media” influencing University presidents, as some people have tried to claim. It is more likely to be the threat of dead players.

Michael Ojo, a former Florida State basketball player, is a visible example. He died of a heart attack at 27. He was reported to have recovered from COVID-19. And some doctors, based on new research, are drawing a connection between COVID-19 and heart attacks in people without previous underlying conditions.

Again, that is just a visible example. But we have to turn to science to see if one example is a piece of a trend, or an outlier.

Be warned… there are a lot of words, and not many pictures in this post!

New Research

New heart-related problems

Perhaps this isn’t news, but there is some new information along the heart-COVID connection. In an editorial posted to JAMA Cardiology titled, “Coronavirus Disease 2019 (COVID-19) and the Heart—Is Heart Failure the Next Chapter?” the authors wrote that, “Multiple data sets now confirm the increased risk for morbid and mortal complications due to coronavirus disease 2019 (COVID-19) in individuals with preexisting cardiovascular diseases including hypertension, coronary artery disease, and heart failure.1,2 These salient observations have strengthened preventive strategies and undoubtedly have resulted in lives saved.”

The authors pointed to a different paper as an example of how COVID-19 can affect the heart. The paper, titled, “Association of Cardiac Infection With SARS-CoV-2 in Confirmed COVID-19 Autopsy Cases” highlights 39 autopsy cases of patients with COVID-19. There were 39 people in this study, so it wasn’t very large. But the authors did notice a few trends.

The authors found that 35 of 39 died from “pneumonia.” And in of the 39 total, there was evidence of virus present in the heart of 24 of 39 patients. And a viral load of more than 1,000 copies per microgram of RNA in 16 of those 24 patients.

So often, we think of this as a lung-and-nose infection. But in this case, the virus spread to the heart.

The authors wrote:

In situ hybridization suggested that the most likely localization of the viral infection was in interstitial cells or macrophages infiltrating the myocardial tissue rather than localization in the myocytes themselves. Further using a panel of 6 proinflammatory genes, the investigators demonstrated increased activity among hearts with evidence of viral infection compared with hearts with no SARS-CoV-2 viral infection detected.4 These new findings provide intriguing evidence that COVID-19 is associated with at least some component of myocardial injury, perhaps as the result of direct viral infection of the heart.

The last line says it all. New evidence of direct infections to the heart. Authors of the research – and the authors of the editorial agreed that future study was necessary to evaluate the long-term ramifications of being infected with COVID-19.

Ventricle problems

Another paper published recently titled, “Spectrum of Cardiac Manifestations in COVID-19” looked at patients’ hearts as they were admitted to the hospital. One-hundred “consecutive patients” diagnosed with COVID-19 underwent a complete echocardiographic evaluation. That means they weren’t picking who gets one and who doesn’t. If people were diagnosed, they got one. For 100-new-cases in a row.

The authors wrote:

“The most common cardiac pathology was [right ventricle] dilatation and dysfunction (observed in 39% of patients), followed by [left ventricle] diastolic dysfunction (16%) and LV systolic dysfunction (10%). Clinical deterioration occurred in 20% of patients.

In these patients, the most common echocardiographic abnormality at follow-up was RV function deterioration (12 patients), followed by LV systolic and diastolic deterioration (in 5 patients). Femoral deep vein thrombosis was diagnosed in 5 of 12 patients with RV failure.”

Researchers found that after a COVID-19 infection, the left ventricle emptying wasn’t as affected as the left ventricle filling. The researchers also noted that right ventricle function was impaired. Elevated troponin and poorer clinical grade tended to go hand-in-hand with a worse right ventricle function. And when people were still having heart issues during the follow-up, “acute [right ventricle] dysfunction, with or without deep vein thrombosis,” was more common, but “acute [left ventricle] systolic dysfunction” was noted in about 20-percent of patients.

Looking at the heart of people who’ve recovered

I probably shouldn’t have buried this one so deep, because it probably is the best example of how new research is working to find out what COVID-19 really does to the heart. The authors of a paper titled, “Outcomes of Cardiovascular Magnetic Resonance Imaging in Patients Recently Recovered From Coronavirus Disease 2019 (COVID-19)” looked a relatively small group of people – 100 in total – to find out how the heart had changed after infection.

Since researchers didn’t have access to a MRI of patients hearts before infection, they used proxies. Researchers compared the findings to other non-infected people of similar age, sex, race and underlying conditions as those in the study.

The authors found…

Of the 100 included patients, 53 (53%) were male, and the median (interquartile range [IQR]) age was 49 (45-53) years. The median (IQR) time interval between COVID-19 diagnosis and CMR was 71 (64-92) days. Of the 100 patients recently recovered from COVID-19, 67 (67%) recovered at home, while 33 (33%) required hospitalization.

At the time of CMR, high-sensitivity troponin T (hsTnT) was detectable (3 pg/mL or greater) in 71 patients recently recovered from COVID-19 (71%) and significantly elevated (13.9 pg/mL or greater) in 5 patients (5%). Compared with healthy controls and risk factor–matched controls, patients recently recovered from COVID-19 had lower left ventricular ejection fraction, higher left ventricle volumes, higher left ventricle mass, and raised native T1 and T2.

A total of 78 patients recently recovered from COVID-19 (78%) 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). There was a small but significant difference between patients who recovered at home vs in the hospital for native T1 mapping (median [IQR], 1122 [1113-1132] ms vs 1143 [1131-1156] ms; P = .02) but not for native T2 mapping or hsTnT levels.

None of these measures were correlated with time from COVID-19 diagnosis (native T1: r = 0.07; P = .47; native T2: r = 0.14; P = .15; hsTnT: r = −0.07; P = .50). High-sensitivity troponin T was significantly correlated with native T1 mapping (r = 0.35; P < .001) and native T2 mapping (r = 0.22; P = .03). Endomyocardial biopsy in patients with severe findings revealed active lymphocytic inflammation.

Native T1 and T2 were the measures with the best discriminatory ability to detect COVID-19–related myocardial pathology.

In English? Cardiovascular Magnetic Resonance, CMR, revealed 78 patients (78%) with some type of heart issue. In 60 people, “ongoing myocardial inflammation” was occurring. And researchers say that the findings were “independent of preexisting conditions, severity and overall course of the acute illness, and time” from the original diagnosis.

Researchers from this study also suggested further study of the long-term cardiovascular consequences of COVID-19.

The Bottom Line

There are already no easy answers with COVID-19. And these new findings about how COVID-19 affects the heart are far from conclusive. A lot of questions still. I have to give credit to a lot of the people “in charge” recently for recognizing this, too. Nothing with this virus is easy.

The problem with this new heart research is that it raises more questions than it answers. And since the science of COVID-and-the-Heart is still in the identification stages of things, it is still too early to make determinations about who is at more risk and who is not.

And that is a big problem. Especially for those who must make decisions about the welfare of large populations. Because this potentially latent problem could manifest itself with some deadly consequences. To who? When? How? Why? Science hasn’t determined yet.

While no one wants to contract or pass along COVID-19, because the illness may have deadly consequences, itself… This new line of evidence suggests another layer of potential problems. The illness is bad enough. And we have talked recently about long-term lung damage. Now new evidence of lingering, long-term heart problems, too.

Coming full circle for a moment, this is the more likely explanation for the hesitancy of sports being played. Not media pressure. This is also a reasonable explanation as to why this COVID-19 threat isn’t likely to “end after the election,” as some have claimed.

via GIPHY

Like I’ve said since the beginning, I’m not here to tell you what to think or how to feel. All I can do is present information.

But, it is important to recognize that reinforcing information to a held belief feels good. Our brains like it! But just because fact-based evidence disputes a held belief does not make that evidence faulty. It is still evidence. Based in reality and fact.

It may feel good to say “the media” is at fault or that COVID “won’t be a problem by December” but scientific evidence would disagree with those claims. I won’t stop your speculation. But as Tuvok, from Star Trek, pointed out in the GIF above: Speculation is not evidence.

And the available evidence to date does not seem to support those claims.