COVID-19 and Heart Disease: How the SARS-CoV-2 Virus Affects Your Cardiovascular System

Table of Contents

• Key Points
• Background: Why This Research Matters
• How the Virus Invades the Body (Pathophysiology)
• Three Clinical Stages of COVID-19 Infection
• How COVID-19 Affects the Heart: Key Cardiovascular Complications
• Cardiac Effects of COVID-19 Treatments
• How Doctors Manage Heart Patients With COVID-19
• Limitations of This Review
• Recommendations for Patients
• Frequently Asked Questions
• Source Information

Key Points

• COVID-19 can damage the heart, causing arrhythmias, heart failure, and sudden death, not just lung problems.
• In a 44,672-patient Chinese study, death rate was 10.5% with cardiovascular disease versus 2.3% overall.
• Do not stop ACE inhibitors or ARBs during COVID-19; evidence suggests they may be protective.
• Heart attacks in COVID-19 often involve inflammation or small clots, not blocked arteries; mortality was 72% in one 18-patient series.
• QT-prolonging COVID-19 treatments require daily ECG and electrolyte monitoring to prevent dangerous rhythms.

Background: Why This Research Matters

Coronavirus disease 2019 (COVID-19) is a serious illness caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The disease first emerged in Wuhan province, China, in late 2019. The virus is genetically related to the coronavirus responsible for the 2002 SARS outbreak, but it has spread far more widely.

On 11 March 2020, the World Health Organization (WHO) officially declared COVID-19 a global pandemic. Since that time, confirmed cases and deaths have risen daily — and it quickly became clear that this was not just a lung infection.

The symptoms of COVID-19 range from none at all (asymptomatic infection) to mild respiratory complaints and, in the worst cases, life-threatening heart and lung complications. Cardiac problems seen in COVID-19 patients include:

• Acute myocardial injury (damage to heart muscle cells)
• Arrhythmias (abnormal heart rhythms)
• Cardiogenic shock (when the heart cannot pump enough blood to the body)
• Sudden cardiac death

In a large analysis of 72,314 patients with COVID-19 in China, researchers classified the illness severity as mild in 81.4% of cases, severe in 13.9%, and critical in 4.7%. While respiratory failure is the primary cause of death, the authors emphasize that cardiac complications also contribute significantly to overall death rates — and in some patients, they are the main cause of death.

A study from New York found that the most common presenting symptoms of COVID-19 were cough (79.4%), fever (77.1%), shortness of breath (56.5%), muscle aches (23.8%), diarrhoea (23.7%), and nausea and vomiting (19.1%). Notably, many patients with heart involvement did not necessarily complain of chest pain first.

Underlying Heart Conditions Are Common and Dangerous

Pre-existing cardiovascular conditions are present in 8–25% of the overall COVID-19-infected population — and in a substantially higher proportion of those who die from the infection. A meta-analysis of eight studies from China involving 46,248 patients found that the most common pre-existing conditions among COVID-19 patients were:

• Hypertension (high blood pressure): approximately 17.7% of patients
• Diabetes mellitus: approximately 8.7%
• Cardiovascular disease: approximately 5.6%

Another large analysis from the Chinese Center for Disease Control and Prevention, covering 44,672 confirmed cases, compared death rates according to pre-existing medical conditions. The case fatality rates were striking:

• Cardiovascular disease: 10.5%
• Diabetes: 7.3%
• Chronic respiratory disease: 6.3%
• Hypertension: 6.0%
• Cancer: 5.6%
• Overall case fatality rate in the entire cohort: 2.3%

In other words, a patient with pre-existing heart disease was more than four times more likely to die from COVID-19 than the average infected person. This pattern makes understanding the heart–virus connection a medical priority.

How the Virus Invades the Body (Pathophysiology)

To understand how SARS-CoV-2 damages the heart, it helps to know how the virus enters cells. The virus contains four structural proteins: the spike (S) protein, envelope (E) protein, membrane (M) protein, and nucleocapsid (N) protein. Of these, the spike protein is the key that unlocks human cells.

The S protein binds strongly to angiotensin-converting enzyme 2 (ACE2) receptors — proteins found on the surface of cells in many organs, including the heart, kidneys, intestine, lungs, brain, and liver. This explains why COVID-19 produces such a wide range of symptoms beyond the lungs, including atypical gastrointestinal complaints, cardiac and kidney injury, and neurological problems.

Once the virus enters cells through ACE2 receptors, it actually down-regulates ACE2 expression — meaning the enzyme can no longer perform its usual organ-protective functions. This loss of protection may contribute to tissue injury in the heart and elsewhere.

What About Blood Pressure Medications?

A critical question early in the pandemic was whether ACE inhibitors (ACEI) and angiotensin receptor blockers (ARB) — common blood pressure medications — increased the risk of COVID-19 infection. These drugs are known to increase the number of ACE2 receptors on the surface of heart, lung, and intestinal cells, which raised a theoretical concern that they might give the virus more doorways into cells.

However, the evidence reviewed here suggests the opposite may be true. Experimental studies in mice showed that blocking the renin-angiotensin-aldosterone system (RAAS) reduced lung injury caused by the SARS-CoV-1 spike protein. Observational data in patients taking ACEI or ARB showed:

• A lower rate of severe COVID-19 disease
• Trend toward lower levels of the inflammatory marker interleukin-6 (IL-6)
• Increased CD3 and CD8 T-cell counts (immune cells) in the blood
• A decreased peak viral load

The authors note that ACEI/ARB therapy may therefore be protective, particularly in low-level viraemia. At the time of writing, trials of losartan (an ARB) in COVID-19 patients were ongoing. The authors advise patients not to stop these medications on their own.

The Autopsy Evidence

Examining heart tissue from COVID-19 patients who died revealed important clues. In one autopsy study, researchers found:

• Cardiomyocyte hypertrophy (enlarged heart muscle cells)
• Degeneration and necrosis (cell death) of cardiomyocytes
• Mild interstitial hyperaemia and oedema (excess fluid)
• Infiltration of lymphocytes, monocytes, and neutrophils (inflammatory immune cells)
• No virus particles found within the myocardial tissue itself

A second autopsy report showed scattered individual heart muscle cell death with lymphocytes located next to — but not surrounding — the dying cells, which may represent an early stage of viral myocarditis (inflammation of the heart muscle). The authors also explain that pericytes, cells that support tiny blood vessels, may become infected by the virus, leading to capillary endothelial dysfunction and individual cell death.

Three Clinical Stages of COVID-19 Infection

Researchers described the immune response to COVID-19 as multiphasic — developing in distinct stages that require different treatment approaches. This framework, originally proposed by Siddiqi and colleagues, helps doctors decide when to use supportive care versus more aggressive therapies:

1. Stage 1 — Viral response / early infection: Constitutional symptoms (fever, fatigue), mild respiratory or gastrointestinal symptoms. Laboratory findings may show mild leukopenia (low white blood cell count) and lymphopenia (low lymphocyte count), elevated prothrombin time, D-dimer, LDH, CRP, ferritin, and IL-6. Procalcitonin may be normal. Treatment focuses on antimicrobial therapy and reducing immunosuppressants if needed.
2. Stage 2 — Inflammatory / pulmonary phase: Shortness of breath and hypoxia (low oxygen levels), with a PaO2/FiO2 ratio below 300 and abnormal chest CT scans. Inflammatory markers and cardiac biomarkers (troponin, BNP) rise. Treatment shifts to supportive care, restrictive IV fluid strategy, antimicrobials, and immunotherapy as directed by infectious disease specialists.
3. Stage 3 — Hyperinflammatory / cytokine release storm: This is the most dangerous phase. Patients develop ARDS (acute respiratory distress syndrome), sepsis, systemic inflammatory response syndrome (SIRS), cardiac failure, multi-organ dysfunction, shock, and disseminated intravascular coagulation (DIC) — a condition in which blood clotting goes haywire. Inflammatory markers and cardiac biomarkers are markedly elevated. Patients require intensive care, often with ventilatory support and vasoactive medications.

The inflammatory cascade is closely linked to heart damage. Elevated levels of C-reactive protein (CRP), D-dimer, ferritin, IL-6, and lactate dehydrogenase (LDH) have been associated with higher mortality in COVID-19 patients, possibly due to a cytokine storm — an overwhelming, uncontrolled immune response — or secondary haemophagocytic lymphohistiocytosis (an extreme inflammatory syndrome).

How COVID-19 Affects the Heart: Key Cardiovascular Complications

Myocardial Injury, Acute Coronary Syndrome, and Myocarditis

Myocardial injury is defined as elevation of cardiac troponin (a protein released when heart muscle is damaged) above the 99th percentile of the upper reference limit. This finding has been observed in 7–17% of hospitalised COVID-19 patients. Importantly, the incidence rises dramatically with illness severity:

• About 22.2% of patients requiring intensive care showed myocardial injury
• 59% of patients who died had myocardial injury

The mechanisms behind this injury are likely multifactorial:

• Atherosclerotic plaque rupture (a cholesterol plaque breaking open)
• Coronary vasospasm (sudden squeezing of heart arteries)
• Hypoxic injury to the vasculature (damage from low oxygen)
• Direct endothelial injury (damage to blood vessel lining)
• Formation of microthrombi (tiny blood clots in small vessels)

The authors explain that myocardial injury and fulminant (sudden and severe) myocarditis can occur both from direct viral effects on heart muscle cells and from the body's exaggerated immune response to the virus.

Acute coronary syndrome (ACS) can be one of the initial presentations of COVID-19, ranging from ST-elevation myocardial infarction (STEMI) — the most severe type of heart attack — to Takotsubo cardiomyopathy (stress-induced "broken heart syndrome"). Myocardial ischaemia and infarction may result from plaque rupture triggered by the stress response to the virus, or from blood clots secondary to hypercoagulability. Type 2 myocardial infarction can also occur when there is a mismatch between oxygen supply and demand in the heart.

A striking case series of 18 COVID-19 patients in New York who experienced STEMI — 10 at initial presentation and 8 during hospitalisation — showed:

• Wide variability in how patients presented
• A high prevalence of non-obstructive coronary disease (33% of those who underwent cardiac catheterisation had no significant blockages)
• A remarkably poor prognosis: 72% mortality

This suggests that many "heart attacks" in COVID-19 patients are not caused by blocked arteries but by inflammation, spasm, or small-vessel clotting. Acute virus-negative lymphocytic myocarditis has also been associated with SARS-CoV-2 respiratory infection, and some reports showed improvement in cardiac biomarkers with lopinavir/ritonavir and hydroxychloroquine treatment.

The authors caution that any rise in troponin should be interpreted in the clinical context, and that invasive angiography or coronary CT angiography may be needed to distinguish between a classic heart attack and myocarditis.

Cardiac Arrhythmias (Heart Rhythm Problems)

Elevated cytokine levels trigger systemic inflammation and myocardial injury — both of which can set the stage for atrial and ventricular arrhythmias. New-onset, dangerous rapid rhythms, such as sustained monomorphic ventricular tachycardia (VT) and polymorphic VT, in a patient with elevated cardiac biomarkers should raise suspicion for myocarditis.

Specific data from the early studies included:

• Among 137 patients admitted for COVID-19 in Hubei province, heart palpitations were a presenting symptom in 7.3% of patients.
• In a study of 138 hospitalised COVID-19 patients, arrhythmia occurred in 16.7% — and was far more common in intensive care unit (ICU) patients than in non-ICU patients (44.4% vs 6.9%, p < 0.001).
• Complete heart block and atrial fibrillation have both been reported in COVID-19 patients.

The authors stress that these rhythm disturbances can be deadly, particularly when combined with the effects of COVID-19 therapies that prolong the heart's electrical recovery time (QT interval).

Heart Failure and Cardiogenic Shock

Increased inflammatory cytokines and respiratory distress can make pre-existing left ventricular (LV) dysfunction worse — or trigger a new-onset cardiomyopathy (weakening of the heart muscle). New LV dysfunction may represent myocarditis, stress cardiomyopathy, or myocardial ischaemia, all of which increase the risk of death.

In the study by Zhou and colleagues, the incidence of heart failure was significantly higher in patients who did not survive COVID-19 compared with survivors:

• Non-survivors: 52% developed heart failure
• Survivors: 12% developed heart failure
• Difference statistically significant at p < 0.0001

Right heart failure is also common in this setting, driven by elevated pulmonary artery pressure from lung complications. In early stages, worsening of heart failure with preserved ejection fraction (a form of heart failure where the pumping function looks normal but the heart is stiff) can occur due to aggressive IV fluid resuscitation. In later stages, as cytokine levels surge, acute systolic heart failure leading to cardiogenic shock has been reported.

The Threat of Blood Clots

COVID-19 strongly activates the coagulation (clotting) cascade. This leads to low platelet counts (thrombocytopaenia) and, in severe cases, dangerous hypercoagulability. Doctors have observed ischaemia of the fingers and toes — sometimes called "COVID toes" — as a result of small blood clots. There is a higher incidence of venous and arterial thromboembolism (blood clots in veins and arteries) despite patients receiving preventive anticoagulation. Contributing factors include excessive inflammation, hypoxia (low oxygen), immobilisation, and diffuse intravascular coagulation.

Some physicians have even used tissue plasminogen activator (tPA), a clot-busting drug, with some improvement in ARDS patients. This highlights how central blood clotting is to severe COVID-19 disease — and to its heart complications.

Cardiac Effects of COVID-19 Treatments

The medications used to treat COVID-19 can themselves put the heart at risk. The article notes that various antivirals, antimalarials, immunomodulating medications, glucocorticoids, and convalescent plasma from recovered patients have been used with variable results. The Infectious Disease Society of America (IDSA) published treatment guidelines that doctors were asked to follow.

Chloroquine and hydroxychloroquine — initially promoted as possible treatments — work by making the inside of cellular compartments (phagolysosomes) more alkaline, which prevents the virus from properly attaching to ACE2 receptors. However, both drugs can prolong the QTc interval, a measure of the heart's electrical recovery after each beat. A dangerously prolonged QTc increases the risk of a life-threatening rhythm called Torsades de Pointes.

Researchers highlighted two important clinical studies with sobering results:

First, a French study of 181 hospitalised COVID-19 patients with oxygen requirements found no evidence of clinical efficacy for hydroxychloroquine — despite earlier small studies suggesting it reduced viral carriage.

Second, a randomised trial of remdesivir in adult patients with severe COVID-19 admitted to Chinese hospitals found that the drug was not associated with a statistically significant difference in time to clinical improvement compared with placebo. (The original article text is cut off mid-sentence at this point, but this finding — later revised by additional trials — was the state of knowledge at the time of publication.)

Because COVID-19 therapies frequently interact with heart medications, doctors must check for drug–drug interactions, especially with antiplatelet agents, anticoagulants, and antiarrhythmic drugs.

How Doctors Manage Heart Patients With COVID-19

The review proposes a simplified management algorithm for cardiovascular disease in COVID-19 patients. Here are the key points translated for patients:

For Heart Attacks (ACS, STEMI, NSTEMI)

• NSTEMI (non-ST-elevation heart attack): Doctors check an ECG and troponin if acute coronary syndrome is suspected. Standard medications include aspirin, heparin (a blood thinner), statins (cholesterol-lowering drugs), and beta-blockers (if no slow heart rate or shock). Drug interactions are assessed. Cardiac catheterisation is performed if there is high suspicion of acute coronary blockage; otherwise, a coronary CT angiogram may be used in stable patients.
• STEMI (ST-elevation heart attack): Considered a medical emergency. Primary angioplasty (PCI) is the preferred treatment. Thrombolytic (clot-busting) therapy is controversial but may be used for lower-risk STEMI if an interventional cardiologist is not available. A bedside echocardiogram is recommended if there is any clinical uncertainty.
• If no angiographic disease is found: Patients are monitored and treated for myocarditis complications, including heart failure, arrhythmia, thromboembolism, and risk factor modification.

For Myocarditis and Myocardial Injury

• Echocardiogram to assess left ventricular function
• Troponin trend to distinguish from Type 1 heart attack and to assess prognosis (along with BNP)
• Arrhythmia monitoring, with electrophysiology (EP) consultation if dangerous rhythms appear
• Inotropes and vasopressors for haemodynamic instability with LV dysfunction
• Guideline-directed medical therapy for cardiomyopathy
• Exercise restriction for 3–6 months to prevent sudden cardiac death in patients recovering from myocarditis

For Heart Failure and Shock

• BNP, troponin, and echocardiogram to assess new-onset heart failure
• Telemetry (continuous heart monitoring) for arrhythmia detection
• Standard heart failure management: daily weight, input/output tracking, diuretics (water pills), and close monitoring of electrolytes and kidney function
• Restricted fluids and blood products due to high risk of cardiopulmonary decompensation; concentrated IV drips are preferred
• Avoid nonsteroidal anti-inflammatory drugs (NSAIDs)
• Continue ACE inhibitors, ARBs, or ARNI (heart failure medications) in otherwise stable patients who are at risk for, being evaluated for, or infected with COVID-19 — unless they become hypotensive (low blood pressure) or develop kidney failure

For Shock

• Shock is defined as systolic blood pressure below 90 mmHg for more than 15 minutes with impaired organ perfusion, or urine output below 30 mL per hour
• Doctors check mixed venous oxygen saturation to distinguish different types of shock
• Conservative fluid resuscitation with crystalloids preferred over colloids
• Norepinephrine is the first-line drug to stabilise blood pressure; transition to inotropes when clinically indicated
• Inhaled pulmonary vasodilators (such as inhaled nitric oxide) should be given through a closed system to prevent aerosolisation of the virus
• ECMO (extracorporeal membrane oxygenation) and mechanical circulatory support devices are reserved for highly selected cases

For Arrhythmias and QTc Prolongation

Many COVID-19 therapies prolong the QTc interval, so monitoring is essential. The authors provide specific thresholds and actions:

• Telemetry monitoring and at least daily QTc assessment for patients on high-risk therapy
• Keep blood potassium above 4.5 mEq/L and magnesium above 2.2 mg/dL
• If QTc is ≥470 ms in men or ≥480 ms in women but below 500 ms: close surveillance and stop QT-prolonging medications
• If QTc is >500 ms (or >550 ms in the presence of bundle branch block), or if QTc increases by more than 60 ms after starting a drug: apply pacer pads, stop the QT-prolonging medication, and maintain heart rate above 80 beats per minute with isoproterenol or dobutamine
• For Torsades de Pointes (TdP): IV magnesium 2–4 grams, maintain heart rate above 80 bpm (with beta-agonists or temporary pacing)
• For ventricular tachycardia (VT): amiodarone 150 mg IV bolus followed by infusion of 1 mg/min if QTc is below 450 ms; or lidocaine (bolus 75–100 mg, then infusion 0.5–2 mg/min) if QTc is above 550 ms
• For supraventricular tachycardia (SVT) including atrial fibrillation: adenosine 6–12 mg IV push for acute management; beta-blockers may be preferred over calcium channel blockers depending on LV function
• Lenient rate control is favoured — "permissive tachycardia" is acceptable in this setting

Cardiac Arrest in COVID-19 Patients

The authors emphasise addressing goals of care early and periodically with all patients. For cardiac arrest, standard advanced cardiac life support (ACLS) protocols should be followed, but with important pandemic-specific modifications:

• Use a mechanical CPR device if available
• Wear full personal protective equipment (PPE) per hospital protocol before starting resuscitation
• Minimise code team size to limit exposure of health care workers

Special Considerations for Transplant Patients

For heart transplant patients on immunosuppressive medications, doctors should discuss reducing immunosuppression — especially antimetabolites — due to the risk of severe infection. Patients on chronic steroids may need stress-dose steroids to prevent adrenal insufficiency.

Limitations of This Review

This article was written in the early phase of the pandemic (received for review April–May 2020, published online 5 June 2020), and the authors note that many treatment recommendations were based on limited data. Several important caveats apply:

• Much of the evidence came from observational studies and small case series, not large randomised controlled trials
• The benefits of hydroxychloroquine and remdesivir were still uncertain — later trials would go on to clarify (and often overturn) early impressions
• The long-term cardiac effects of COVID-19 in survivors were not yet known at the time of publication
• The interaction between ACE inhibitors/ARBs and COVID-19 risk was still being studied, with definitive trials pending

Despite these limitations, the core message has held up well: COVID-19 is a cardiovascular disease as much as a respiratory one, and pre-existing heart disease significantly worsens outcomes.

Recommendations for Patients

Based on this review, here is practical advice for patients concerned about COVID-19 and heart disease:

1. Do not stop your heart medications. If you take ACE inhibitors or ARBs for blood pressure or heart failure, continue them unless your doctor specifically tells you otherwise. Stopping them can cause rebound hypertension and increase cardiac risk.
2. Know the warning signs. Chest pain, palpitations, severe shortness of breath, fainting, or rapid heartbeats during a COVID-19 illness warrant urgent medical evaluation. Remember that in one series, heart attack was the first sign of COVID-19 in some patients.
3. Controlled heart disease makes a difference. The patients at highest risk are those with uncontrolled hypertension, diabetes, and established cardiovascular disease. Optimising these conditions — under medical supervision — may reduce your risk.
4. Recognise that COVID-19 treatment involves heart monitoring. If you are hospitalised and receive medications that prolong the QTc interval, expect daily ECGs and blood tests. This monitoring is designed to protect you from dangerous rhythm problems.
5. Recovery takes time. If you are diagnosed with myocarditis from COVID-19, plan for exercise restriction for 3–6 months to reduce the risk of sudden cardiac death — even if you feel better.
6. Prevention remains the most vital step. The authors remind readers that preventing the spread of infection through quarantine and personal hygiene is the single most important strategy, and this is especially true for patients with underlying heart disease.

Frequently Asked Questions

Can COVID-19 really affect the heart even if you don't have chest pain?

Yes. COVID-19 can cause heart muscle damage, abnormal heart rhythms, heart failure, and sudden death. In a New York study, the most common symptoms were cough, fever, and shortness of breath, not chest pain. Some patients had a heart attack as their first sign of COVID-19.

How much higher is the risk of dying from COVID-19 if you already have heart disease?

In a Chinese analysis of 44,672 confirmed cases, the death rate was 10.5% for people with cardiovascular disease, compared with 2.3% overall. That means someone with pre-existing heart disease was more than four times more likely to die from COVID-19 than the average infected person.

Should I stop taking my blood pressure medicine (ACE inhibitor or ARB) during the COVID-19 pandemic?

No. The article says patients should not stop these medications on their own. Evidence reviewed suggests ACE inhibitors and ARBs may actually be protective against severe COVID-19, possibly by reducing lung injury. Stopping them can cause rebound high blood pressure and increase cardiac risk.

What heart complications can happen in hospitalized COVID-19 patients?

Complications include myocardial injury (damage to heart muscle cells), arrhythmias, heart failure, cardiogenic shock, and blood clots. Myocardial injury was seen in 7–17% of hospitalized patients, but in 22.2% of ICU patients and 59% of patients who died. Dangerous rhythms were more common in ICU patients.

Why do COVID-19 patients get heart attacks even without blocked arteries?

In a New York series of 18 COVID-19 patients with ST-elevation heart attacks, 33% of those who had cardiac catheterization showed no significant blockages. The authors say inflammation, coronary spasm, or tiny blood clots in small vessels can cause heart muscle damage, not just plaque rupture. These patients had a 72% mortality rate.

Can the medications used to treat COVID-19 cause heart rhythm problems?

Yes. Drugs like chloroquine and hydroxychloroquine can prolong the QTc interval, which increases the risk of a dangerous rhythm called Torsades de Pointes. Therefore, hospitalized patients receiving these therapies should have daily ECGs and blood tests to monitor potassium, magnesium, and QTc.

Source Information

This patient-friendly article is based on a peer-reviewed scientific review:

Original title: "SARS-CoV-2 Infection and Cardiovascular Disease: COVID-19 Heart"

Authors: Bishnu P. Dhakal, MD; Nancy K. Sweitzer, MD, PhD; Julia H. Indik, MD, PhD; Deepak Acharya, MD, MSPH; Preethi William, MD — Sarver Heart Center, University of Arizona, Tucson, AZ, USA.

Publication: Heart, Lung and Circulation (2020), Volume 29, pages 973–987. Published by Elsevier on behalf of the Australian and New Zealand Society of Cardiac and Thoracic Surgeons (ANZSCTS) and the Cardiac Society of Australia and New Zealand (CSANZ).

DOI: https://doi.org/10.1016/j.hlc.2020.05.101

Note: This patient-friendly article is based on peer-reviewed research and is intended for educational purposes. It does not replace individual medical advice. Patients should always consult their own healthcare provider regarding their specific medical situation.