Chapter 1: The COVID-19 Heart Dilemma

The new coronavirus has captivated attention in ways that most viruses do not, primarily because of its widespread impact.

Last Monday, I spoke with cardiologist Amy Kontorovich, who expressed her fatigue after a long day in her lab. “I’ve been infecting heart cells with SARS-CoV-2 since 6 a.m.,” she explained. This experimentation might seem peculiar for a virus known to spread through respiratory droplets and primarily affect the lungs. However, it has become evident that SARS-CoV-2 can also harm the heart. Early in the pandemic, it became apparent that some patients faced hospitalization due to respiratory issues and subsequently succumbed to heart failure. “Cardiologists have been pondering this since March,” Kontorovich noted, as data gradually emerged.

Autopsy reports have revealed the presence of the virus’s genetic material in heart tissues, alongside actual viral particles within heart muscle cells. Laboratory studies indicate that SARS-CoV-2 can damage cell cultures mimicking heart tissue. Research shows that approximately 10% to 30% of hospitalized COVID-19 patients exhibited elevated levels of troponin, a protein released when heart cells are compromised. Patients with elevated troponin levels tend to have poorer outcomes compared to those without signs of cardiac injury.

While this is concerning for those with severe symptoms, new studies suggest that even individuals with mild cases or those who have recovered could experience heart inflammation, or myocarditis. This revelation has sparked debate and worry, as myocarditis is often caused by viral infections and can lead to severe heart complications, including sudden death in young adults. Consequently, two collegiate football conferences, the Big Ten and the Pac-12, opted to cancel their fall seasons due to these concerns.

These findings have intensified the narrative surrounding COVID-19, framing it as an unusual virus that might not merely be a respiratory illness but rather a vascular one. However, many cardiologists and virologists argue that such views may be exaggerated. Although COVID-19 is a serious condition that warrants attention, it is not as unusual as it seems. The heightened focus is partly due to its novelty and the scale of its spread, capturing our attention in a way that most viral diseases do not. Extensive research is underway, with millions infected, leading to a multitude of studies and reports that amplify the urgency.

From the perspective of a virus, the heart is a dual-edged sword: it is accessible for infection due to its blood-collecting function and lack of a protective barrier like the brain, yet infecting it risks killing the host without the typical symptoms that facilitate virus transmission, such as coughing or diarrhea. This is why viruses that specifically target the heart "do not exist," according to virologist Efraín Rivera-Serrano from the University of North Carolina at Chapel Hill.

However, viruses can impact the heart indirectly. In Western nations, viral infections are a leading cause of myocarditis, with at least 20 known viruses capable of triggering this condition, including those responsible for influenza and Zika. Notably, the original SARS virus has also been linked to myocarditis. A study from Toronto identified its genetic material in autopsied hearts, while the new coronavirus presents a more complicated picture. Although it has been found in heart tissues, its role in causing significant heart damage remains uncertain.

Moreover, the virus doesn't need to infect the heart directly to cause damage; it can disrupt lung function, depriving the heart of oxygen, or provoke a systemic inflammatory response. Even viruses that primarily target the gut can lead to myocarditis through immune system reactions. For instance, Coxsackie B, predominantly a gut virus, can infect the heart indirectly, causing inflammation through immune responses.

“It’s an oversimplification to categorize a virus as cardiac, vascular, or respiratory,” states Paul Checchia, a cardiologist at Texas Children’s Hospital. “When any pathogen invades the body, the entire system reacts.” SARS-CoV-2 is no exception; its immune response can be delayed but becomes intense. This overreaction resembles responses to other respiratory viruses, albeit more severe, potentially putting the heart at risk.

Early in the pandemic, it appeared that heart injury risk was directly linked to illness severity, says Neel Chokshi, a sports cardiologist at the University of Pennsylvania. However, a study led by Valentina Puntmann at University Hospital Frankfurt, Germany, complicated this narrative. It revealed that 78% of individuals who had recovered from COVID-19, including many who were never hospitalized, displayed heart abnormalities detectable via MRI two months post-recovery, with about 60% showing signs of myocarditis.

The implications of this study were profound, generating widespread discussion about COVID-19’s potential for causing latent heart damage in seemingly healthy individuals. Criticism followed, highlighting methodological flaws, including missing data and incorrect analyses. Despite revisions, the Frankfurt team maintains that its core findings remain valid.

“I believe the data is sound,” says Tiffany Chen of Penn Medicine, who specializes in cardiac imaging. “These were mostly healthy individuals with mild cases, yet they exhibited numerous abnormalities, which is concerning.” However, the clinical significance of these findings—what they imply for COVID-19 patients with abnormal MRI results—is still unclear.

Viral myocarditis isn't always detrimental; many might have experienced it without realizing. While some recover, others may develop lasting scarring that weakens the heart, raising future health risks. A subset may experience rapid deterioration, leading to severe outcomes, including heart failure.

Determining accurate prevalence rates is challenging, Chokshi explains, as doctors typically identify viral myocarditis only when it manifests severely, necessitating diagnostic imaging. "We don’t perform MRIs on everyone with the flu, so we lack data on inflammation rates and long-term outcomes," adds Martha Gulati, chief of cardiology at the University of Arizona. For instance, Checchia found signs of heart damage in 40% and 55% of children hospitalized with RSV, a common respiratory virus, even though they seemed healthy upon discharge.

Given the limited data, the significance of the Frankfurt study and similar research remains ambiguous. While some patients exhibit myocarditis, the implications are unclear. How do these figures stack up against other respiratory viruses? Will COVID-19 patients with myocarditis fully recover, or will some face long-term issues? Is this virus behaving unusually, or are we simply studying it more rigorously than past infections? Currently, these questions linger.

The concern is that COVID-19's impact is magnified due to its scale. In contrast to the original SARS outbreak, which infected about 8,000 individuals, SARS-CoV-2 has reached over 31 million infections, resulting in nearly 1 million deaths. Even if its effects are comparable to other viral diseases, the sheer volume means that a small risk of severe long-term complications could affect a significant number of individuals.

Encouragingly, “there hasn’t been a noticeable increase in hospital admissions for unexplained myocarditis, despite the vast number of COVID-19 cases,” notes Venkatesh Murthy, a cardiologist at the University of Michigan. “I’m not convinced that significant clinically relevant myocarditis is prevalent in those feeling well.”

Nonetheless, experts agree on the need for long-term studies. “We’re still in the early stages,” Chen explains. “There’s no specific timeline for when we might observe heart failure, so we must monitor these patients over months or years.”

This uncertainty can be unsettling for those currently affected. Individuals suffering from long COVID symptoms are reacting to media interpretations of these findings, often leading to justified concern, according to Kontorovich, who works with long-haulers. However, she views myocarditis and long-hauler symptoms as distinct issues.

Some long-haulers have been diagnosed with dysautonomia—a collection of disorders impacting involuntary bodily functions, including erratic heart rates and blood pressure fluctuations. Yet, those with lingering heart issues post-viral myocarditis typically do not experience the chronic symptoms associated with long-haulers and often display measurable changes in heart function. “There may be a connection, but it remains unproven,” Kontorovich states.

College athletes are also facing immediate challenges. In recent months, two athletes—27-year-old Michael Ojo and 20-year-old Jamain Stephens Jr.—died from heart-related issues after recovering from COVID-19.

A recent study from Ohio State University examined the hearts of 26 college athletes who had mild or no COVID-19 symptoms. Of those, 15% displayed signs of myocarditis. However, the study lacked a control group of similar athletes without COVID-19. Additionally, even healthy athletes can experience heart changes due to training, which may resemble post-infection symptoms, according to Gulati.

If athletes develop clinical myocarditis, they must refrain from play for a minimum of three months to allow recovery. The pressing question now revolves around managing those with subclinical myocarditis, which goes unnoticed without diagnostic imaging. Chokshi suggests that the likelihood of these abnormalities leading to heart failure is very low, although the potential consequences are severe. The American College of Cardiology recommends that all athletes who test positive for COVID-19 rest for at least two weeks, regardless of symptoms.

Beyond myocarditis, preventing virus transmission among players remains crucial, especially as many colleges face outbreaks. “There are ample reasons to avoid playing football aside from this concern,” Murthy emphasizes. “We already have substantial evidence supporting the need to take COVID-19 seriously.”

As pandemics expand, they often appear more bizarre. The Ebola outbreak from 2014 to 2016 highlighted long-term complications that were previously underappreciated. Similarly, the 2015 Zika outbreak drew attention to its impact on fetal development. When millions become infected, rare occurrences can become common, making the disease seem stranger than it is.

COVID-19 is unique mainly because it is a new virus that everyone is encountering during a pandemic. The world has shifted from ignorance to a flood of information within a few months, leading to disconcerting revelations. The virus affects not only the heart but also other systems, leading to diverse symptoms, including a multisystem inflammatory syndrome in children and cases of reinfection. Some of these phenomena may be exclusive to SARS-CoV-2, while others would likely emerge if any new virus infected millions in a short time.

This is not to diminish the pandemic's severity. While some claims about COVID-19’s heart effects may be exaggerated, it does not imply that the virus is benign. Conversely, equating COVID-19 to the flu is clearly incorrect, but the reality lies somewhere in between. The ongoing crisis is dire, as reflected in the staggering number of infections, deaths, and lasting disabilities. “Finding a middle ground is challenging,” Rivera-Serrano points out. “This is not an apocalyptic virus that is drastically different from others, but we also must acknowledge the serious reality of its impact.”

Indeed, COVID-19 might enhance our understanding of viral diseases by illuminating aspects previously overlooked. The long-term implications of viral myocarditis, for instance, remain uncertain due to the difficulty of tracking individuals exposed to the same virus in a brief period. This challenge has been mitigated by the pandemic, which makes extensive studies feasible and highlights their importance. “We now recognize this is a problem worth addressing,” Murthy adds.

The heightened focus on COVID-19 fosters both sensationalism and critical attention on previously neglected phenomena. For instance, lingering symptoms in long-haulers resemble chronic conditions like dysautonomia and myalgic encephalomyelitis, which can be triggered by other viral infections. Historically dismissed and trivialized, these conditions have lacked adequate medical recognition. However, the pandemic could catalyze change as thousands with similar experiences emerge, advocating for acknowledgment and research. In a pandemic, once-ignored experiences gain visibility, suggesting they should have received attention all along.

The first video titled "Is COVID-19 a Heart Disease?" explores the implications of COVID-19 on heart health and the emerging research surrounding this topic.

Chapter 2: Lessons from the Pandemic

The second video, "Webinar: COVID-19 and public debate - Lessons learned and preparedness," discusses the broader impacts of the pandemic and insights into future preparedness.