Prof Eric Topol: COVID and the heart – so much we don’t know


The heart is a major target for the SARS-CoV-2 virus but its diverse effects through a range of mechanisms are still far from being understood, according to US cardiologist Professor Eric Topol.

Delivering the closing plenary address at CSANZ 2020 virtual meeting, he said that cardiac abnormalities in people with COVID-19 may occur as a result of vasculitis, myocarditis, arrhythmia, cardiomyopathy and immune system dysregulation.

A key feature of COVID-19 was the marked heterogeneity in individual susceptibility, organ manifestation and severity, said Professor Topol, director of the Scripps Research Translational Institute, San Diego.

While it was initially viewed primarily as a respiratory tract virus, it was now recognised as resulting in cardiac damage as well as affecting other organs including the liver, kidney, brain and GI tract. And although much attention has been put on severe COVID-19 disease, the viral infection may be asymptomatic in 30-40% of people and yet cause cardiac problems both in the short term and long term.

Prof. Topol noted that autopsies had shown unequivocally that COVID-19 could have cardiac involvement, and there was evidence that virus directly infected cardiomyocytes, entering the cell via the ACE-2 receptor and cell fusion.

The virus could also cause cardiac damage through indirect effects on coagulation and endotheliitis as well as systemic inflammatory responses.

In vitro investigations with stem cell derived cardiomyocytes showed that the virus resulted in apoptosis and/or arrhythmogenic effects.

And the damage caused was suggested by reports of myocarditis in autopsies and increases in rates of sudden cardiac death in areas with high COVID-19 case numbers, said Prof. Topol.

However he cautioned that it was difficult to ascertain the population level of cardiac abnormalities from selective case reports and autopsy studies.

“The true incidence of heart abnormalities is unknown but they can occur in healthy young individuals with only mild or even in the absence of symptoms,” he said.

Another cardiac aspect of COViD-19 was the impact of immune system dysfunction, as seen in the Kawasaki disease-like multisystem inflammatory syndrome in children. And in recent months there had been the emergence of ‘long COVID’ syndrome which may also have cardiac involvement, he noted.

“The propensity for cardiac involvement in individual isn’t understood, even in those who present exclusively with cardiac manifestations,” he said.

“Much more work needs to be done to get our arms around this,” he concluded.

In the meantime, Professor Topol said clinicians must promote the ‘Swiss Cheese’ model of COVID-19 prevention measures for both personal and shared responsibilities ranging from social distancing, mask wearing to test and trace systems and vaccination.

In a subsequent discussion, the prospect of success with a COVID-19 vaccine for people with cardiovascular disease was discussed by Professor Tony Cunningham, Director, Centre for Virus Research(WIMR), Sydney University.

Professor Cunningham said he was confident that the vaccines that had been developed in a very short time would be effective for a wide range of people, though there may need to be be tailored ‘second generation’ vaccines for susceptible groups such as the elderly and those who are immunocompromised.

“I can’t see any reason why with cardiac disease you will have a major problem with these vaccines – my only concern is with transplant patients, particular those with HSCT and haematological malignancies and HIV,” he said.

“We’re aiming for a vaccine like Shingrix where we can put T-cell adjuvants together and T-cell peptides and enhance immunogenicity in the [elderly patient].”

“When we did the Shingrix immunisation the co-morbidities just melted away – the efficacy was the same even in people with frailty, in people with six co-morbidities etc,” he said.

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