Why would a respiratory infection lead to increased risk of heart attack? In an article published last month in the Journal of the American College of Cardiology, Driggin^[1] and colleagues point to the severe hypoxemia (reduced oxygen in the blood) that develops due to lung compromise.  COVID-19 can cause pneumonia which in its worst state develops into something called adult respiratory distress syndrome (ARDS).  In ARDS there is fluid and inflammation in the lungs and oxygen simply can’t reach the blood.  When the blood serving the heart lacks oxygen the heart muscle can cease to function – this is also known as a heart attack.

COVID-19 can also cause severe systemic inflammation.  For people with underlying plaques within their heart arteries this can cause “unstable plaques,” which are prone to rupture.  When this happens, a clot can form at the site of rupture leading to complete blockage of the artery.  If not reversed quickly, the heart muscle served by that artery will die.

In the setting of a very high viral load, inflammatory cells can infiltrate the heart muscle and potentially weaken the tissue, leading to heart failure (inability of the heart to pump blood adequately).

As noted above, COVID-19 can cause widespread systemic inflammation and the release of many inflammatory proteins or cytokines including Interleukin 1 (IL1), Interleukin 6 (IL6), and tumor necrosis factor (TNF). This is also known as a “cytokine storm” which can lead to weakening of the heart muscle.

The heart needs oxygen. Hypoxemia (reduced oxygen in the blood) not only impacts the heart muscle (as outlined above), but also impacts the heart’s conduction, or electrical system. This can lead to an increased risk of arrhythmias, the change in rate of a heart beat.

COVID-19 can cause many metabolic and electrolyte abnormalities which can also predispose someone to cardiac arrhythmias.

In addition, not surprisingly, widespread systemic inflammation is also capable of triggering arrhythmias.

Finally, some of the medications that are being used experimentally to try to treat COVID-19 are capable of causing arrhythmias including: lopinavir/ritonavir (drugs commonly used to treat Human Immunodeficiency Virus (HIV)) and chloroquine (used to treat malaria).

It appears that COVID-19 patients are also at risk for venous thromboembolisms (blood clots that originate in the veins but can travel to the heart or lungs).

To date, there have been multiple reports of abnormalities in blood clotting (coagulation parameters) seen in persons infected with COVID-19.

Some people infected with COVID-19 develop disseminated intravascular coagulation (DIC) in response to widespread inflammation.  In DIC blood clots form inside multiple blood vessels. These clots use up all the blood’s clotting factors and ultimately lead to severe bleeding.

Just having FH should not make you more vulnerable to cardiac complications if you contract COVID-19. However, people with FH who were diagnosed as adults or have not been adequately treated may have “subclinical atherosclerosis” and may be at increased risk.  Subclinical atherosclerosis means that a person has plaque in their heart (and other) arteries but they have not yet had a cardiac event (heart attack, developed chest pain or required a stent or coronary artery bypass grafting (CABG)).

If you have FH and already have heart disease or other risk factors such as high blood pressure or diabetes, you are likely at increased risk for complications if you contract COVID-19.

Three FH specialists (Drs. Vuorio, Watts and Kovanen) recently published a Letter to the Editor of the Journal of Internal Medicine^[2] in which they asked just this question. They point out that, in previous studies, persons with FH who have been infected with Chlamydia Pneumonia (a common bacterial cause of community pneumonia) have an increased risk of subsequent cardiac events. While it is unknown if persons with FH will have a similar increase risk after a COVID-19 infection, it is crucial for patients and physicians to be aware of this possibility and to remain vigilant even post recovery.

They also point out that the Atherosclerosis Risk in Communities (ARIC) study found a link between cytomegalovirus antibodies (a herpes virus) and atherosclerosis in persons with elevated lipoprotein(a) or Lp(a). Persons with FH tend to have higher Lp(a). Again, it is unknown if there will be similar findings following COVID-19 infection in people with FH and elevated Lp(a).

Drs. Vuorio, Watts and Kovanen provide the following advice that we at the Family Heart Foundation completely agree with: If you have FH, make sure to take all your cholesterol medications without interruptions. It is possible that your health care provider may even want to intensify your treatment. the Family Heart Foundation outlined guidance for specific medications on this blog I wrote.

There is little doubt that avoidance of infection is very important. Frequent hand washing and following social distancing guidelines are of the utmost importance.