Recent research has shown that even patients with mild symptoms of COVID-19 can experience an increased risk of developing heart disease and stroke. This risk is especially greater in older people who already have an accumulation of fat in their blood vessels.
Now, a pioneering study has found that the virus can directly infect the heart arteriesa revelation that not only surprises but also raises the alarm about long-term cardiovascular complications in recovered patients.
The investigation, led by cardiologist Chiara Giannarelli, from NYU Langone Health, found viral genetic material in coronary arteries months after recovery from COVID-19, suggesting that the virus is not only capable of infecting, but also of persisting in the cardiovascular system. This persistence could inflame atheroma plaques, increasing the likelihood of them rupturing and causing a heart attack or stroke.
SARS-COV-2 AND ARTERIAL INFLAMMATION
You macrophages – immune cells that normally protect the body from infections – can become a Trojan horse when loaded with cholesterol, transforming into foam cells that favor the formation of atherosclerotic plaques.
SARS-CoV-2 has demonstrated its ability to infect and grow within these cells in laboratory cultures, suggesting that the foam cells can act as reservoirs for the virus. This interaction between the virus and cells of the immune system not only increases the persistence of the virus but also exacerbates the severity of the disease.
Furthermore, when macrophages and foam cells are infected by the virus, they release cytokinessmall proteins that can increase inflammation and the formation of new plaque in arteries.
This phenomenon could explain the presence of long-term cardiovascular complications in recovered COVID-19 patients, establishing a direct link between the inflammation of atherosclerotic plaques and the virus.
TOWARDS A NEW UNDERSTANDING OF POST-COVID HEART DISEASE
While this study opens new avenues of understanding about how COVID-19 can alter heart health, more research is needed to fully understand the many ways the disease can alter heart function.
This study only analyzed 27 samples from eight deceased elderly patients, all of whom already had coronary artery disease and were infected with the original strains of the virus. Therefore, the results of this study do not necessarily apply to younger people without coronary artery disease, nor to new variants of the virus, which cause a slightly milder disease.
However, it is essential that people who have had COVID-19 remain aware of new symptoms, such as shortness of breath on exertion, chest discomfort, especially during physical activity, irregular heart rhythms and fainting. If these signs occur, it is essential to consult a doctor to evaluate the possibility of an underlying heart condition.