The Cardiac Impacts of COVID

Disclaimer: Some of what will be discussed in this post is theory and opinion with no high level of evidence being available. More and more research is being conducted each day with new information being discovered. Some of the information provided in this post may become obsolete. You have to take some of it with a grain of salt. Continue to conduct your own research and stay up-to-date.

I was listening to an Amal Mattu lecture the other day and he highlighted some very valid COVID related points. Is it possible that for many years we’ve underappreciated the affects that different viruses have on the heart?It’s been studied over the past couple of decades that viruses have a very powerful and direct influence on the heart. He mentioned a study published in 2018 that found there was a six-fold increase in AMI in the first seven days after the diagnosis of influenza (Influenza B > Influenza A) (Kwong, et al. NEJM 2018; Mattu, COVID and the Heart).

Viruses can produce adverse affects on the heart through an inflammatory response. It’s probably safe assume that COVID has a more profound inflammatory response than other viruses such as Influenza A and B. Two questions being asked right now are: How likely is the virus to indirectly affect the heart by exacerbating already existing conditions? Does the virus have a propensity to directly attack the heart by infecting myocites?

First lets define a couple types of AMI. I’m including this because you’ll frequently hear these terms used in the discussion of the possible cardiac affects of COVID.

Type 1 AMI refers to a primary coronary event such as an atherothrombotic plaque rupture. Think of this as the unstable plaque that ruptures, invites its platelet friends to the party, and forms a clot that blocks the artery.

The definition of type 2 AMI is often viewed as unsatisfactory. It’s not really defined by what it is but rather by what it’s not. Type 2 AMI is caused by an imbalance between myocardial oxygen demand and supply which ultimately leads to myocardial ischemia. It’s not due to plaque rupture and can exist in patient’s with and without coronary artery disease.

From the link above: The imbalance may be attributable to reduced myocardial perfusion in the context of fixed coronary atherosclerosis (without plaque disruption), coronary artery spasm, microvascular dysfunction, coronary embolism, dissection, or systemic causes such as hypoxemia, anemia, hypotension, or bradyarrhythmia, or increased myocardial oxygen demand attributable to tachyarrhythmia or severe hypertension

Some Current COVID Theory on Endothelial Damage and Thrombosis

Now let’s talk about some of the processes that are thought to possibly contribute to COVID related thrombosis secondary to endothelial damage. Note: everything I’m about to say below is a simplified version of a very complex process. If you want to know more see some of the links I’ve included.

I want you to recall your knowledge on the renin-angiotensin-aldosterone system (RAAS). I’ve included an image as a reference point and a great video below.


Corona virus uses the ACE 2 receptor on type 2 pneumocytes for entry. Angiotensin II is pro-inflammatory while another hormone called angiotensin 1,7 reduces inflammation. Further explained, when ACE-2 binds with angiotensin II it converts it to angiotensin 1,7. This binding is good because it reduces the amount of angiotensin II. It’s possible that when the Corona virus invades the ACE-2 receptor, it essentially leaves angiotensin II with no enzyme to convert it to angiotensin 1,7 (this increases angiotensin II and decreases angiotensin 1,7). Neutrophils are recruited and superoxide creation is increased. The increase in superoxide creation is thought to cause endothelial cell dysfunction, increases in the activity of Von Willebrand factor (VWF) (up to 500% increase), and increased chances of thrombosis around sites of inflammation.


In a patient that already has oxidative stress secondary to disease (cardiovascular disease, diabetes, obesity etc.), could push them over the edge? We know that the immunocompromised population is at an increased risk of mortality.

Here’s a fantastic video by Dr. Roger Seheult that will provide you with much more information on the suspected causes of COVID-19 blood clotting.

Potential Cardiovascular Affects of COVID

We’ve learned over the years that inflammation is a pretty large risk factor for the development of plaque rupture. As discussed earlier, COVID has been shown to have a profound inflammatory affect. Among other factors, inflammation can decrease the level of plaque stability. When the plaque turns from stable to unstable it runs the risk of rupturing, developing a thrombus, and ultimately causing Type 1 MI to occur.

Earlier we discussed hypercoagulability as it relates COVID. States of hypercoagulation secondary to endothelial damage can lead to the development of coronary embolisms which can affect the balance between myocardial oxygen demand and supply. The development of a pulmonary embolism secondary to a hypercoagulable state can also affect the heart. A variety of other lung related conditions are known to result in hypoxia/hypoxemia which in more severe states can lead to myocardial ischemia/injury. Excess sympathetic stimulation from viruses can cause an increase in myocardial oxygen demand and make the patient more proarrhythmic. Hypertrophy developing secondary to sympathetic surge can decrease the hearts ability to overcome peripheral vascular resistance. Viruses themselves can invade the myocites and cause direct injury to the myocardium.

Myocarditis is an inflammation of the myocardium, the middle of the three layers forming the outer wall of the heart. It’s possible that Myocarditis can affect the heart muscle and the heart’s electrical conduction system. Myocarditis is most often caused by a viral infection but it can result from drug reactions or be part of a more general inflammatory condition. In more severe cases, myocarditis can lead to cardiomyopathy and sudden death. Interestingly, up to 5% of people with any sort of acute viral infection may have some form of myocarditis. Age and comorbidities (HTN, diabetes, hyperlipidemia, CAD) have been shown to be risk factors. Cardiac manifestations of the corona virus could certainly be due to myocarditis but could also be a number of many other things. Dr. Richa Gupta from Vanderbilt University Medical Center came up with a short list of etiologies which ties back into some of the things we previously discussed:

  • Is it true myocarditis?
  • Is it a stress-induced inflammatory myopathy?
  • Could there be coronary endothelial dysfunction?
  • Is it hypoxia-mediated cardiac injury?
  • Is it myocardial depression due to cytokine storm?

An additional question Dr. Gupta posed was “could there be overlapping of the previously stated conditions?” Check out Dr. Gupta’s videos:

With Prehospital ECG Changes Suggestive of Injury Should I Call a STEMI Alert or Not?

With or without COVID, the previously stated conditions can result in ECG manifestations that may mimic the ECG manifestations associated with Type 1 AMI. It can be extremely difficult at times to differentiate between the sub-types of AMI. I’ve recently heard about cases where the cath lab was activated only to find clean coronaries. I also recently heard about a case where they delayed taking the patient to the cath lab for 2 days due to suspected COVID only to find that the patient had a 100% LAD occlusion and a resulting ejection fraction of 30%.

If you suspect that the ECG changes are occurring outside of a Type 1 AMI plaque rupture then you should start by trying to fix what you feel might be the underlying problem. There have been step-wise approaches developed for pericarditis but unfortunately nothing for myocarditis. Even in cases of pericarditis, Dr. Steven Smith (Dr. Smith’s ECG Blog) says you should diagnose at your own peril. There are no reliable ECG methods to distinguish myocarditis from STEMI! Some of the potential but certainly NOT definitive clues of myocarditis are as follows.

The cardiac cells that are most susceptible to the initial inflammatory problem associated with myocarditis are the cells of the right bundle branch. What starts to happen is conduction through the right bundle branch begins to slow significantly. In fact, it can slow so much that it looks like damage is occurring to the right ventricle. The depolarization of the right ventricular cells now has to come through the left ventricular cells. The right bundle branch cells are slowed and are becoming activated in a much more delayed process. This could cause the axis to shift rightward, cause RBBB morphologies to occur, and cause ST elevation in AVR.

I’m a believer in coupling history with ECG findings to make a well thought out and calculated decision that leads to either calling or not calling a “STEMI Alert.” Just because myocarditis mimics STEMIs and has been shown to be present in COVID positive patient’s doesn’t mean that they might not be suffering from a variety of other cardiac related conditions caused directly or indirectly by the virus. Additionally, many patient’s were at high risk of AMI before the pandemic and will continue to be high risk throughout and after the pandemic. Exercise good clinical judgement and do what’s right for your patient’s. If you’re ever unsure, there’s no shame in transmitting your ECG, consulting with the receiving facility, and working together to accomplish what’s best for the patient. Always follow your clinical guidelines/protocols.

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Scopeducation Team (Ryan FP-C, CCP-C)


1. Kwong JC, Schwartz KL, Campitelli MA. Acute Myocardial Infarction after Laboratory-Confirmed Influenza Infection. N Engl J Med. 2018;378(26):2540‐2541. doi:10.1056/NEJMc1805679

2. Oxidative Stress in Endothelial Cell Dysfunction and Thrombosis

3. Assessment and Treatment of Patients With Type 2 Myocardial Infarction and Acute Nonischemic Myocardial Injury.

4. Amal Mattu. COVID and the Heart.

5. Coronavirus Virus Pandemic Update 67 with Dr. Seheult

6. Weston T. Harkness; Mary Hicks. Right Bundle Branch Block


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