How COVID-19 Can Affect Your Heart

Most of the serious illness caused by the novel coronavirus (COVID-19) results from pneumonia, which in some cases can rapidly deteriorate to acute respiratory distress syndrome (ARDS). But doctors now recognize that in many patients COVID-19 becomes a systemic illness, and is not limited to causing pulmonary problems. Other organ systems that may be affected by COVID-19 include the vascular tree, the kidneys, the central nervous system, the skin—and the heart.

Cardiac problems are usually not among the most prominent features of COVID-19. But they are common enough, and potentially serious enough, that most people admitted to the hospital with COVID-19 are now being screened for heart muscle injury, and cardiologists often become part of their care team.

In many patients, heart involvement with COVID-19 is a relatively subtle condition, while in others it produces major and possibly fatal complications. While there are several potential causes of COVID-19-related heart muscle injury, the specific cause in a particular individual is often difficult to identify. Treatment is supportive and general rather than specific to COVID-19.

heart muscle injury and covid-19
​Verywell / Alex Dos Diaz

Prevalence of Heart Muscle Injury From COVID-19

Early studies have found that, among people sick enough to be hospitalized with COVID-19, evidence of cardiac muscle injury can be found in 8% to 12%. In people with milder forms of COVID-19, there is no evidence of heart muscle injury.

In most people with COVID-19 who have a detectable heart muscle injury, any resulting cardiac issues tend to be minor.


In hospitalized patients with COVID-19, any symptoms resulting from heart injury can be easily confused with the pulmonary symptoms caused by the virus. These symptoms may include:

  • Significant dyspnea (shortness of breath)
  • Cough
  • Fatigue
  • Weakness
  • Palpitations
  • Dizziness
  • Chest pressure or pain and
  • Syncope (loss of consciousness).

Because it is not easy to distinguish cardiac symptoms from symptoms caused by severe lung disease in people with COVID-19, doctors usually cannot rely on symptoms alone to alert them to the possibility that the virus also may be producing cardiac issues.

Causes and Risk Factors

The majority of people who develop heart muscle damage from COVID-19 have significant pre-existing medical conditions that predispose them to cardiac disease, including coronary artery disease, diabetes, obesity, or hypertension.

No single cause has been identified. There are several potential mechanisms that might produce this heart damage, and it is likely that all of them may play a role to one extent or another. These include:

  • Myocarditis: Heart muscle inflammation
  • Stress cardiomyopathy: Also known as "broken heart syndrome," this occurs in response to severe physical stress. A large portion of the heart muscle suddenly stops functioning, leading to acute heart failure.
  • Severe, generalized hypoxia: The absence of oxygen caused by overwhelming lung disease can damage the heart, especially in areas where the vascular supply to the muscle is already compromised.
  • Rupture of a pre-existing coronary artery plaque: Triggered by the inflammation produced by COVID-19, a rupture can lead to a heart attack or other forms of acute coronary syndrome.
  • Inflammatory damage to the small coronary arteries
  • Cytokine storm: This exaggerated immune response linked to COVID-19 can cause serious health problems, including direct damage to the heart. Low blood pressure caused by cytokine storm can also interfere with the heart's ability to pump.

Diagnosing Heart Muscle Injury From COVID-19

Especially because any cardiac symptoms that may be present can be masked by pulmonary symptoms in people with COVID-19, doctors now routinely screen for cardiac disease in patients hospitalized with this infection.

The most useful screening test is to measure blood levels of troponin. Troponin is a cardiac protein that is important for muscle contraction. Injured heart cells leak troponin into the bloodstream, so elevated troponin blood levels are an important indication that cardiac cell damage is occurring.

In addition to blood troponin levels, an electrocardiogram (ECG) and chest X-ray can also help screen for cardiac disease. If screening tests do suggest a heart problem, an echocardiogram can be helpful in determining the presence and the nature of any cardiac involvement with COVID-19. Invasive cardiac procedures, such as a heart catheterization, are avoided whenever possible in COVID-19 patients who are seriously ill.

Problems Caused by COVID-19 Heart Muscle Injury

Often, an abnormal troponin test is the only manifestation of cardiac muscle damage in people ill with COVID-19. But whether or not there are other symptoms of a cardiac problem, elevated troponin levels in patients hospitalized with COVID-19 are associated with an increased risk of mortality.

In some patients with elevated troponin levels, heart muscle injury is extensive enough to produce more obvious cardiac disease, which can complicate COVID-19 recovery.

Heart Failure

If the heart muscle is damaged severely enough, heart failure can occur. Heart failure is a serious problem in anyone; in a person ill with COVID-19, it is particularly dangerous.

In studies from Wuhan, China, heart failure was a prominent feature in many patients who became critically ill with COVID-19. In fact, heart failure was diagnosed in approximately half the patients with COVID-19 who died during their hospitalization. The large majority of patients diagnosed with heart failure during their illness had no prior history of heart failure, indicating that their cardiac problems apparently arose as a result of COVID-19.

Heart Attack

Heart attacks (myocardial infarctions) are also fairly common in people hospitalized with COVID-19. This is not unexpected, because it has long been known that influenza and other illnesses that cause pneumonia are associated with a higher risk of heart attacks.

There are at least two ways COVID-19 can trigger a heart attack:

  1. The increased cardiac workload, added to the hypoxia (low blood oxygen levels) caused by severe pulmonary illness, can lead to cardiac muscle damage in areas of the heart whose blood supply is compromised by diseased coronary arteries.
  2. COVID-19 may cause widespread vascular inflammation, which can trigger the rupture of a coronary artery plaque, occluding the artery and causing the death of cardiac muscle.


Several types of arrhythmias may occur in people hospitalized with COVID-19, but the most prominent are atrial fibrillation and ventricular tachycardia. In particular, these patients may develop a dangerous form of ventricular tachycardia called "torsades de pointes," or TdP.

TdP is seen when a QT interval is prolonged. (The QT interval is measured on the ECG, and represents the length of time it takes for electrolytes to cross back and forth across a cardiac cell membrane when a heart cell is stimulated to beat.) Because of the severity and complexity of their illness, the QT interval is often prolonged in people who are seriously ill with COVID-19.

Some of the medications that may be used to treat COVID-19 in a hospital setting, like hydroxychloroquine and azithromycin, can also prolong the QT interval, increasing the risk of TdP.


There is no specific treatment for the heart muscle damage caused by COVID-19. However, aggressive treatment is available for most of the consequences of this heart damage, such as heart failure, acute heart attacks, and cardiac arrhythmias. These treatments are the same as for patients who do not have COVID-19.

Heart Failure Treatment

When it is acute, heart failure treatment requires excellent fluid management (to keep excess fluid out of the lungs), restoring normal blood oxygen levels, and identifying underlying conditions amenable to treatment (such as cardiac ischemia).

Heart Attack Treatment

Acute heart attacks are generally treated the same in people with COVID-19 as they are in anyone else, with the exception that cardiologists are more likely to use fibrinolytic therapy ("clot busters") as primary therapy instead of stents. Surgery, like angioplasty, will be performed if the artery is totally blocked. Different types of medications may be administered, including medication to break up a clot (thrombolytic therapy), antiplatelet medications, blood thinners, beta-blockers, ACE inhibitors, and statins.

Cardiac Arrhythmia Treatment

Cardiac arrhythmias are also managed just as they are in people without COVID-19—from prescription drugs to pacemakers and ablation procedures. Anyone who is critically ill is prone to arrhythmias, and great emphasis should be placed on prevention. This means paying careful attention to fluid management, blood oxygenation, electrolyte balance, and avoiding (whenever possible) drugs that are known to prolong the QT interval on an electrocardiogram.

Seriously ill patients with COVID-19 will be placed on a cardiac monitor so that any acute arrhythmias can be dealt with quickly.

A Word From Verywell

In some people, cardiac involvement with COVID-19 does not play a major role in the course of their illness. In others, however, cardiac damage may be accompanied by heart failure, a heart attack, or serious cardiac arrhythmias.

Screening tests for heart injury should be performed in anyone admitted to the hospital with COVID-19. If such evidence is found, careful cardiac monitoring should be instituted.

The information in this article is current as of the date listed, which means newer information may be available when you read this. For the most recent updates on COVID-19, visit our coronavirus news page.

10 Sources
Verywell Health uses only high-quality sources, including peer-reviewed studies, to support the facts within our articles. Read our editorial process to learn more about how we fact-check and keep our content accurate, reliable, and trustworthy.
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By Richard N. Fogoros, MD
Richard N. Fogoros, MD, is a retired professor of medicine and board-certified in internal medicine, clinical cardiology, and clinical electrophysiology.