COVID-19 Infects Heart Cells: New Research Reveals Cardiac Complication Link

Researchers have demonstrated, using a novel human heart cell model, that the virus responsible for COVID-19 – SARS-CoV-2 – can directly infect heart tissue. The findings, published this week, offer new insight into the heart complications some individuals experience during and after a COVID-19 infection. This research builds on growing understanding of the virus’s potential to affect organs beyond the lungs, and could inform future treatment strategies.

Understanding the ‘Mini-Hearts’

The study, conducted by researchers at the Centenary Institute and the University of Technology Sydney (UTS), utilized what are being called ‘mini-hearts’ – technically known as cardiac spheroids. These aren’t literal miniature organs, but rather three-dimensional clusters of human heart cells grown in a lab. Crucially, these spheroids behave more like real human heart tissue than traditional two-dimensional cell cultures, offering a more accurate model for studying viral infection. The research, detailed in the journal Biofabrication, allowed scientists to observe how SARS-CoV-2 interacts with the heart cells directly.

Dr. Matt Johansen, a researcher at the Centenary Institute and UTS, explained that early in the pandemic, it wasn’t clear whether heart damage from COVID-19 was a direct result of the virus infecting heart cells, or an indirect consequence of the body’s inflammatory response. “Our results suggest that the virus can directly infect human heart tissue when the conditions are right, setting off damaging processes,” he said in a news release. This direct infection could explain why heart complications arise even in people without pre-existing heart conditions.

Who is at Risk?

Even as the study doesn’t pinpoint specific populations at highest risk of this direct heart tissue infection, broader data on COVID-19 suggests certain groups are more vulnerable to severe illness and therefore potentially more susceptible to cardiac complications. The Centenary Institute notes that older individuals, and those with chronic respiratory or cardiovascular disease, and diabetes, are more prone to severe outcomes from COVID-19. However, the new research emphasizes that even individuals without these pre-existing conditions can experience heart issues related to the virus.

As of early March 2026, Australia has reported over 185,000 COVID-19 cases in the past year, according to the Federal Government’s Notifiable Diseases Surveillance System. Globally, the virus continues to circulate, with ongoing variations and localized outbreaks. It’s essential to note that infection rates and the prevalence of specific variants fluctuate, and current public health guidance should always be consulted for the most up-to-date information.

What the Study Showed – and What it Didn’t

The researchers found that SARS-CoV-2 was able to infect and replicate within the 3D heart tissue model. This infection triggered inflammation and changes associated with impaired heart function. However, the study as well revealed an important nuance: the virus didn’t readily infect individual heart cells grown in isolation. This suggests that the structure and environment of the heart tissue itself play a role in the virus’s ability to infect cells.

It’s crucial to understand that this study was conducted in a laboratory setting, using a model of human heart tissue. While ‘mini-hearts’ are more representative than traditional cell cultures, they don’t perfectly replicate the complexity of a living human heart. Further research is needed to confirm these findings in human patients and to understand the long-term effects of viral infection on heart health. The study doesn’t establish a direct causal link between SARS-CoV-2 infection and specific heart conditions in all individuals; it demonstrates a potential mechanism for how such complications could arise.

Inflammation and the Heart: A Broader Context

The inflammation triggered by the virus is a key factor in the observed heart complications. Inflammation is a natural immune response, but when it becomes excessive or prolonged, it can damage tissues and organs. In the context of COVID-19, this inflammatory response – sometimes referred to as a “cytokine storm” – can affect multiple organ systems, including the heart. The direct infection of heart tissue, as demonstrated in this study, can exacerbate this inflammatory process.

What Happens Next?

This research is a stepping stone towards developing more effective treatments for COVID-19-related heart complications. The Centenary Institute is collaborating with the University of Sydney, UTS, and Sydney Local Health District (SLHD) to develop such treatments. Researchers are now focused on understanding the specific mechanisms by which the virus damages heart tissue, and on identifying potential therapeutic targets. This includes exploring antiviral medications, anti-inflammatory drugs, and other strategies to protect the heart from viral infection and inflammation. Ongoing surveillance of COVID-19 cases and their associated health outcomes will also be crucial for tracking the prevalence of heart complications and for evaluating the effectiveness of new treatments.

Further studies are planned to investigate the impact of different viral variants on heart tissue, and to assess the long-term effects of COVID-19 on cardiovascular health. Clinicians are advised to remain vigilant for signs of heart complications in patients with COVID-19, and to provide appropriate care and follow-up. Individuals concerned about their heart health should consult with a qualified healthcare professional.