Yes, COVID-19 can affect your heart. The virus is capable of directly infecting heart tissue, triggering inflammation, damaging blood vessels, and promoting blood clots. Most people recover without lasting cardiac problems, but the risk is real: a large NIH-supported study found that people who had COVID-19 early in the pandemic had double the risk of heart attack or stroke compared to those who were never infected, and that elevated risk persisted for up to three years. Severe cases requiring hospitalization carried nearly four times the risk.
How the Virus Reaches Your Heart
The coronavirus enters human cells by latching onto a protein called ACE2, which sits on the surface of cells throughout the body. ACE2 is found on the lining of blood vessels in the heart and kidneys, not just in the lungs. Once the virus binds to ACE2, a second protein on the cell surface helps it break through and get inside. This means the heart’s blood vessels are a viable target, especially in severe infections where the virus spills into the bloodstream.
When the virus infects these cells, it reduces the amount of ACE2 available on the surface. That matters because ACE2 plays a protective role in regulating blood pressure and inflammation. With less of it functioning, the balance tips toward constriction of small blood vessels, increased inflammation, and a greater tendency for blood to clot. Researchers have actually found viral particles inside the cells lining the heart’s tiny blood vessels, confirming that the virus doesn’t just cause collateral damage from afar. It can directly injure the heart’s plumbing.
Inflammation of the Heart Muscle
Myocarditis, or inflammation of the heart muscle, is one of the most talked-about cardiac complications of COVID-19. The CDC reported that infection with the virus increases the risk of myocarditis roughly 16-fold, from about 9 cases per 100,000 people to around 150 per 100,000. A meta-analysis covering more than 20 million people found that myocarditis occurred in about 2 out of every 10,000 COVID-19 survivors, compared to roughly 1 out of every 10,000 in uninfected people. Within a year of infection, survivors had more than five times the risk of developing myocarditis compared to people who never had COVID.
Those numbers make myocarditis relatively uncommon in absolute terms, but it’s a serious condition when it does occur. Symptoms can include chest pain, shortness of breath, fatigue, and a feeling that your heart is racing or pounding. Some people develop it during the acute infection, while others notice symptoms weeks later. The American College of Cardiology recommends that anyone diagnosed with myocarditis avoid exercise for three to six months, though some patients with rapid symptom resolution may be reassessed as early as one month after diagnosis.
For context, the risk of myocarditis from COVID-19 infection is about seven times higher than the risk from mRNA vaccination. A large meta-analysis of 58 million people found that vaccination roughly doubled the background risk of myocarditis, while infection increased it by a factor of 15.
Blood Clots and Vascular Damage
COVID-19 pushes the body into a hyperinflammatory, clot-prone state. The virus injures the inner lining of blood vessels, triggering a cascade: the immune system releases inflammatory signals, damaged vessel walls activate the clotting system, and small clots can form in vessels throughout the body, including those feeding the heart.
Among people hospitalized with COVID-19, roughly 9% developed a blood clot (including deep vein thrombosis, pulmonary embolism, or clots in arteries) within 90 days. The broader category of cardiovascular events, which includes clots, heart failure, new irregular heart rhythms, and cardiovascular death, affected about 16% of hospitalized patients in the same timeframe. For those admitted to the ICU, the numbers were far worse: 1 in 5 had a clot, and nearly 1 in 3 experienced a cardiovascular event.
This vascular damage can also affect the smallest blood vessels in the heart, a condition sometimes called coronary microvascular dysfunction. Even when the large arteries look fine, the tiny vessels that deliver oxygen to the heart muscle can become inflamed, constricted, or partially blocked by micro-clots. This may explain why some people develop chest pain or exercise intolerance after COVID without any obvious blockages on standard cardiac testing.
Heart-Related Symptoms in Long COVID
Some people continue to experience heart-related symptoms for months after their initial infection. One of the most common is a condition called postural orthostatic tachycardia syndrome, or POTS, in which your heart rate jumps abnormally when you stand up. The diagnostic threshold is a heart rate increase of at least 30 beats per minute when going from lying down to standing, lasting for at least three months, without a drop in blood pressure that would explain it.
People with post-COVID POTS often describe dizziness, brain fog, fatigue, and a pounding heartbeat when doing simple things like standing in line or taking a shower. In studies of long COVID patients, those with POTS had significantly higher heart rates during a six-minute walk test and covered less distance than other long COVID patients without the condition. The good news is that POTS is treatable with a combination of increased fluid and salt intake, compression garments, and a carefully graded exercise program, though recovery can take months.
Even mild COVID can leave subtle signs on the heart. One study of outpatients with mild to moderate infections found measurably elevated levels of troponin, a protein released when heart muscle cells are stressed or damaged. These elevations were small, often below the threshold used to diagnose a heart attack, but they were more frequent in COVID patients than expected and were most common in older men. Even very low-level troponin increases are associated with a higher long-term risk of cardiovascular events.
Who Faces the Highest Risk
Severe COVID-19 carries the greatest cardiac risk. People who were hospitalized, especially those in the ICU, had the most dramatic increases in heart attacks, strokes, clots, and heart failure. But milder infections are not risk-free. The NIH study found that even non-hospitalized COVID patients had double the cardiovascular risk of uninfected individuals over the following years.
Blood type appears to play a role. Hospitalization for COVID-19 more than doubled the risk of heart attack or stroke among people with A, B, or AB blood types, but not in those with type O, which was associated with a lower risk of severe disease overall. Pre-existing heart disease, present in about 11% of the study population, amplified risk further but was not a prerequisite. Many of the people who developed cardiac complications had no prior heart problems.
Returning to Exercise Safely
Current guidance from the American College of Cardiology says that the old recommendation to avoid all exercise for 10 days after COVID is no longer necessary. Instead, everyone recovering from COVID should use a graded approach: start light, increase gradually, and pay attention to how you feel. If you notice chest pain, unusual shortness of breath, a racing or irregular heartbeat, or lightheadedness during or after exercise, those symptoms warrant cardiac evaluation before pushing further.
For people diagnosed with myocarditis, the standard recommendation remains three to six months of complete exercise abstinence, with heart imaging and monitoring before clearance. Athletes with rapid symptom resolution may be reassessed earlier, but no sooner than one month. Cardiac MRI is the most useful tool for evaluating whether inflammation has fully resolved, particularly when initial screening tests are abnormal or symptoms persist. Repeat testing for people who get COVID again is only recommended if new heart or lung symptoms develop.