Those living with hypertension, arrhythmias, poor circulation, diabetes, and dyslipidemia are significantly more susceptible to blood clots, stroke, and inflammation of the heart (aka pericarditis) after infection with COVID19.
But how does the SARs-CoV2 virus exert this effect?
To thrive in a host environment, a virus must first find a molecule on the cell surface to hijack in order to gain entry to the cell. In the case of SARs-CoV2, it hijacks the ACE2 transporter which can be found in cells of our heart, lung, kidneys, nose, mouth, and intestines causing ACE2 enzyme levels to go down. Some major roles of the ACE2 enzyme include keeping our blood pressure tightly regulated and heart beating strongly. Low ACE2 levels can therefore contribute to weakened heart contractions, poor circulation to the heart’s ventricles, and worsened diastolic hypertension.
Once entry into the cell is achieved, the virus causes a cascade of inflammation which drives the production of reactive oxygen species (ROS). ROS can be damaging to the cells, and this is especially true for the cells that line our blood vessels. Injury to the blood vessel causes the vessel walls to constrict, leading blood pressure to go up. Clotting factors also become activated in an attempt to heal the injured tissue, and platelets are made in greater numbers to help fight off the infection. Both clotting factors and platelets thicken the blood and slow circulation with goal of forming a clot. On the skin surface this process would look like the formation of a scab. To coat and reinforce the damaged blood vessel itself, cholesterol and immune cells also come together to lay a fatty steak foundation that sets off the process of atherosclerosis and plaque formation. Together, these processes increase the risk of stroke and heart attack.
Finally, the heart cells themselves can become injured after infection which can be seen from testing markers of cardiac inflammation such as D-dimer, fibrinogen, prothrombin time, and troponin T levels.
Although most people recover once the infection is cleared, some have a hard time overcoming the inflammatory response. In the short term, inflammation plays a protective role to help us fight the virus and activate the immune system. But inflammation in the long term can become detrimental and shows in the cardiovascular system as hardening of the heart muscle, atherosclerosis, altered coordination of nerve signals that regulate the heart’s rhythm, or postural orthostatic tachycardia syndrome (PoTS). There is a lot we still need to learn about what leads one person to respond so differently than another to a SARs-CoV2 infection, so hopefully future research will be able to speak to these knowledge gaps.
In the meantime, naturopathic medicine has a major role to play in supporting and preventing cardiovascular risk factors by means of dietary counseling (especially around antioxidants!), lifestyle changes, use of botanical medicines, and targeted nutritional supplementation.
Interested in learning more? Let’s chat!
- Danilczyk U, Penninger JM. Angiotensin-converting enzyme ii in the heart and the kidney. Circulation Research. 2006;98(4):463-471.
- Raisi-Estabragh Z, Cooper J, Salih A, et al. Cardiovascular disease and mortality sequelae of COVID-19 in the UK Biobank. Heart. 2023;109(2):119-126.
- Cenko E, Badimon L, Bugiardini R, et al. Cardiovascular disease and covid-19: a consensus paper from the esc working group on coronary pathophysiology & microcirculation, esc working group on thrombosis and the association for acute cardiovascular care (Acvc), in collaboration with the european heart rhythm association(Ehra). Cardiovascular Research. 2021;117(14):2705-2729. – Picture