Feature BMJ 2026; 392 doi: https://doi.org/10.1136/bmj.s31 (Published 09 February 2026) Cite this as: BMJ 2026;392:s31
Covid-19 is not just a respiratory infection. Cardiovascular symptoms are seen in both acute and long covid. Katharine Lang reports on what we’ve learnt since the onset of the pandemic
Cardiovascular complications from covid-19 have been seen widely since the early days of the pandemic, when a small study in Wuhan reported myocardial injury in several patients.1 Soon after, studies found that up to 30% of those admitted to intensive care units showed myocardial injury.23
“In many respects covid-19 is a vascular disease masquerading as a respiratory one,” says Andy Benest, vascular biologist at the University of Nottingham.
Although covid is transmitted through the respiratory system, much of the pathology unfolds in the vascular system, with microvascular damage, thromboinflammation, and dysregulated perfusion underpinning the cardiac, pulmonary, and neurological manifestations of severe disease.
“The virus enters through the airways but exerts its systemic effects through the vasculature, the common denominator in the lungs, heart, kidneys, and brain,” Benest tells The BMJ.
Cardiovascular complications are relatively common in the acute phase of covid. Studies have found that acute cardiac injury occurred in 6-25% of people admitted to hospital with covid.4 One 2020 study reported that 14.1% of people admitted to hospital with covid experienced some type of cardiovascular complication.5
Why does covid-19 affect the heart and cardiovascular system?
Early studies suggested that the endothelium could be directly infected by the virus, as it enters these cells through angiotensin-converting enzyme 2 (ACE2) receptors.6 Benest suggests, however, that this may not be the case. “The notion that endothelial cells express ACE2 at meaningful levels is increasingly questioned. Transcriptomic and protein data suggest ACE2 is present in perivascular and smooth muscle cells, but largely absent in true endothelial cells,” he says.
This does not mean the endothelium is unaffected, Benest points out. Rather, it implies that the viral effects on the vasculature are mostly indirect, through inflammation, immune activation, and coagulation cascades rather than direct endothelial infection.
“Covid’s hallmark vascular features—endothelial activation, microthrombosis, and barrier dysfunction—likely arise from cytokine driven injury, platelet-leukocyte interactions, and altered coagulation rather than primary viral cytopathy,” he told The BMJ.
What are the cardiovascular symptoms of covid-19?
In the acute phase covid-19 can cause myocarditis, myocardial infarction, arrhythmias, heart failure, blood clotting in the lungs (which can also affect the heart), and other complications, says Ziyad Al-Aly, professor of medicine at Washington University in St Louis in the US.
A large study, using data from UK Biobank, found that those infected by early variants had a doubled risk of cardiovascular events. For those with severe infection requiring hospital admission, the risk of myocardial infarction and stroke was four times that of controls—an equivalent increase in risk to having coronary artery disease.7
A 2022 study of almost 154 000 US veterans told a similar story. At least 30 days, and not more than a year, after infection, these veterans had a greater risk of cerebrovascular disorders, dysrhythmias, ischaemic and non-ischaemic heart disease, pericarditis, myocarditis, heart failure, and thromboembolic disease than two groups of more than 5 million contemporary and historical controls.8 The increased risks were greatest in those who had been admitted to hospital with covid, but those who had had mild symptoms were still more likely to experience cardiovascular complications than controls.
Who is at greatest risk of heart problems after covid-19 infection?
Benest says that hypertension, diabetes, obesity, and pre-existing cardiovascular disease (CVD) all magnify post-covid risk, emphasising how underlying cardiometabolic health has a major influence. “Age adds vulnerability through accumulated endothelial dysfunction and reduced vascular elasticity,” he says.
Several factors increase a person’s risk of cardiovascular complications following covid-19, but severity of the acute infection is one of the clearest indicators. “People requiring admission to hospital or intensive care units show the highest rates of subsequent vascular and cardiac events,” he says, adding that even mild cases carry a small, measurable increase in risk.
Studies have also shown the pre-existing risk factors for CVD can be amplified by covid infection: diabetes and hypertension may increase the severity of covid, as well as raising the risk of cardiovascular complications during and after acute infection.9
What do we know about long covid’s effect on the heart and cardiovascular system?
Long covid has been described as a “complex, multisystem disorder that can affect nearly every organ system and can be severely disabling,” and in 2024 it was reported to be affecting around 400 million people worldwide.10 The cardiovascular system is commonly affected, with cardiovascular symptoms being the third most frequent manifestation of the condition after neurological-neuropsychiatric and pneumological symptoms.11
Al-Aly points out that one of the characteristics of long covid is dysautonomia and postural orthostatic tachycardia syndrome.
A systematic review found that chest pain, palpitations, dyspnoea, and syncope were common in people with long covid.12 Another, that people with long covid were 1.6 times as likely as those without long covid to experience cardiovascular symptoms.8
As with acute covid, the more severe the initial infection, the more likely the person is to experience cardiovascular complications as part of long covid.
Do new variants of covid-19 cause worse or milder cardiovascular effects?
With the availability of vaccines, and some immunity from previous infection, newer variants do not seem to carry the same risk of complications as earlier ones.
“Variant differences appear to reflect severity rather than biology,” Benest says. “Earlier variants like delta caused more intense systemic inflammation and higher rates of thrombosis and myocardial injury.”
So far, no variant has shown unique tropism for the vasculature or heart, he says, adding that the intensity of the host’s inflammatory and coagulative response remains the key determinant of cardiovascular outcome.
“There have been incredibly pathogenic variants that did not appear to take hold in the same way as delta and omicron did, which means it’s critical we understand more about how those variants might have impacted the cardiovascular system differently, to be awake to more emergent variants,” Benest says.
The best preventive measure is vaccination
While some antivirals (nirmatrelvir/ritonavir and molnupiravir) have proved effective at reducing the risk of heart and vascular complications, others, such as remdesivir and baricitinib, are thought to increase risk.13
Both Al-Aly and Benest say that the best way to minimise the risk of cardiovascular complications is to prevent severe infection through vaccination.14
And it is not only covid-19 vaccination that appears to give protection against further cardiovascular complications in people with CVD. One large study found that both covid and flu vaccinations have a protective effect in people with CVD, post-covid and with long covid.15
“Vaccination substantially reduces both acute and long term cardiovascular complications by blunting systemic inflammation. And, finally, lifestyle factors such as good blood pressure, lipid control, and regular exercise remain protective; covid-19 tends to magnify existing vascular risks rather than create new ones,” Benest says.
Footnotes
Commissioned, externally peer reviewed.
Competing interests: None.