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Scientists have found out how the risk of thrombosis and myocarditis changed with new strains of COVID-19

Almost 7 years after the start of the pandemic, scientists recognized COVID-19 as a unique pathology - a vascular disease masquerading as a respiratory infection

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Scientists have found out how the risk of thrombosis and myocarditis changed with new strains of COVID-19

Cardiovascular complications of COVID-19 have been widely observed since the early days of the pandemic, when a small study in Wuhan reported myocardial damage in several patients. And then it turned out that up to 30% of patients admitted to intensive care units had myocardial damage. “In many ways, COVID-19 is a vascular disease masquerading as respiratory,” says University of Nottingham vascular biologist Andy Benest.

Although COVID-19 is transmitted as a normal SARS, most of the pathological processes develop in the vascular system. At the same time, microvascular damage, thromboinflammation and perfusion disorders are the basis of cardiac, pulmonary and neurological manifestations of the severe course of the disease. That is, the virus penetrates through the respiratory tract, but has a systemic effect through the blood vessels, which are a common denominator for the lungs, heart, kidneys and brain.

Cardiovascular complications are relatively common in the acute phase of COVID-19. Studies have shown that acute heart damage occurred in 6-25% of people hospitalized with COVID-19. A 2020 study found that 14.1 percent of people hospitalized with COVID-19 had some form of cardiovascular complications.

Why does COVID-19 affect the heart and cardiovascular system? At the beginning of the pandemic, there was a hypothesis that the walls of blood vessels could be directly infected by a virus that enters these cells through the receptors of the angiotensin-converting enzyme 2 (ACE2). Today, however, this hypothesis is increasingly being questioned. ACE2 receptors are virtually nonexistent in endothelial cells. Therefore, most likely, the effect of the virus on the vascular system is indirect - indirectly through inflammation, activation of the immune system and cascades of blood clotting, rather than through direct infection of the endothelium.

In the acute phase, COVID-19 can cause myocarditis, myocardial infarction, arrhythmias, heart failure, blood clots in the lungs (which can also affect the heart), and other complications. A large study based on data from the UK Biobank found that people infected with early variants of the virus had a doubled risk of cardiovascular disease. Those who had a severe form of infection requiring hospitalization had four times the risk of myocardial infarction and stroke than the control group. A 2022 study of nearly 154,000 U.S. veterans found a similar pattern. At least 30 days and no more than a year after infection, these veterans had a higher risk of developing cerebrovascular disorders, arrhythmias, coronary heart disease, pericarditis, myocarditis, heart failure and thromboembolic diseases than the two groups of more than 5 million controls. And while the increased risk was most significant in those hospitalized with COVID-19, even those with mild symptoms were more likely to develop cardiovascular complications than the control group.

Hypertension, diabetes, obesity and already existing cardiovascular disease (CVD) significantly increase the risk of severe COVID-19. The age of the patient increases vulnerability due to accumulated endothelial dysfunction and reduced vascular elasticity. Studies have also shown that existing risk factors for cardiovascular disease can be amplified when infected with COVID-19: diabetes and hypertension can aggravate the severity of the disease, as well as increase the risk of cardiovascular complications during and after acute infection.

In addition, we should not forget about longcovide, which also affects the cardiovascular system. Long-term COVID-19 is described as "a complex, multisystemic disorder that can affect almost all organ systems and lead to severe disability." According to data for 2024, it affected about 400 million (!) people worldwide. Cardiovascular symptoms are the third most common manifestation of the disease after neurological, neuropsychiatric and pneumological. Frequent vascular symptoms of prolonged COVID-19 are dysfunction of the autonomic nervous system and postural orthostatic tachycardia syndrome. People with a longcoid also complain of chest pain, heartbeat, shortness of breath and fainting. Studies show that people with longcoids are 1.6 times more likely to develop cardiovascular symptoms than people without the disease.

Do new COVID-19 variants cause more severe or milder cardiovascular disease? The good news is that thanks to vaccination and the accumulated immunity acquired after a previous infection, newer variants of the virus do not appear to carry the same risk of complications as earlier variants. The most “evil” and to this day is considered the variant “Delta”, which more often than others caused systemic inflammation, thrombosis and myocardial damage. Scientists note that in recent years, incredibly pathogenic variants have appeared, but they, fortunately, have not been as widespread as Delta or Omicron. Although there are no guarantees that there will be no new aggressive strains of covid in the future, and you need to be prepared for this.

Meanwhile, Moscow physician-therapist Natalia Lenskaya in 2020 said that we are not dealing with a respiratory virus, but with hemorrhagic vasculitis. The description of many hemorrhagic fevers is very similar to the course of the severe form of COVID-19. The use of recommendations for the treatment of hemorrhagic vasculitis in a number of hospitals at the beginning of the pandemic allowed to reduce mortality by 10 times, says Natalia Lenskaya.

Source: Московский комсомолец ↗

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