Cardiovascular Effects of COVID-19

It has been hypothesized that individuals who control their blood pressure using ACE inhibitors or ARBs are at a higher risk of contracting the disease and are at higher risk to develop adverse effects from it. It is important to debunk this myth because a large portion of the U.S. society is on those medications

Cardiovascular effects of COVID-19
There has been a great deal of discussion about the cardiovascular effects of COVID-19 on the general population because of trends suggesting a strong link between the two. It continues to look like the populations suffering from coronary heart disease and high blood pressure are more likely to develop severe symptoms from COVID-19 in comparison to those with benign cardiac history (1). Moreover, one study showed people who have never had previous cardiac problems can develop cardiovascular effects after contracting SARS-CoV-2 (2). It is not difficult to predict that individuals who have had some cardiac comorbidities face more detrimental short- and long-term prognosis after the virus is not contagious, in comparison to healthy people.

Cardiac conditions worsening COVID-19
The cardiac conditions that may worsen the effects of COVID-19, according to the literature, are: coronary artery disease, heart failure, hypertension, and cardiac arrhythmias (3). Early data from China suggests that these individuals are at higher risk of becoming infected and having worse outcomes. For example, in one study based on 416 patients admitted to the hospital, those with previous cardiac injury had a significantly higher in-hospital mortality rate (51.2%), compared to those without myocardial injury (4.5%) (1). Many patients who were diagnosed with COVID-19, and were without cardiac conditions but considered at risk, experienced an acute myocardial injury as evident by an increase in cardiac troponin levels (4). This discussion is still new and more data is needed but scientists link the response to the novel coronavirus with another previously reported coronavirus MERS-CoV, which seems to be similar to the COVID-19 in causing the same cardiovascular complications (5).

How blood pressure medications may affect the risk after a COVID-19 diagnosis
In order to understand how and why COVID-19 affects the lungs and heart, one might have to look more closely into mechanisms that happen within those body systems. Especially those relating to the angiotensin-converting enzyme-2 (ACE-2) and angiotensin receptors. Both are responsible for many physiological interactions within the cardiovascular system and play an essential role in the immune system (5). The same receptors that bind to ACE-2 also bind to the novel virus and, therefore, allow it to invade the organism. In other words, ACE-2 serves as a cellular entry point for the novel coronavirus. Another theory is that due to an initial imbalance and possibly injury within the cardiovascular organs, there is an imbalance in the immune system's response to the virus, which can cause secondary hypoxemia due to the respiratory dysfunction caused by COVID-19 (5). Interestingly, no correlation was found between the use of ACE inhibitors and ARBs and death rates among those diagnosed with COVID-19. It has been hypothesized that individuals who control their blood pressure using ACE inhibitors or ARBs are at a higher risk of contracting the disease and are at higher risk to develop adverse effects from it. It is important to debunk this myth because a large portion of the U.S. society is on those medications (6).

Stroke and coagulation concerns: the newest findings
Among some new findings related to cardiovascular issues surrounding COVID-19 cases are problems with coagulation causing subsequent strokes. According to some sources, the immune response during active phases of COVID-19 can be so severe, atherosclerotic plaque instability and rupture can occur (1). Either complication can lead to strokes or heart attacks. Moreover, there is increasing evidence that the novel virus can cause systemic coagulopathy, which can lead to microvascular thrombosis (7). From the different forms of altered coagulation described across the professional literature in COVID-19 patients, one can conclude that these are not predictable and are more likely to be fatal compared to thrombosis observed in patients without COVID-19 diagnosis (8). Therefore, as suggested in many sources, there is a need to prophylactically treat patients diagnosed with COVID-19. And in the condition of severe clinical presentation, the provider can decide to increase the frequency and dosage of anticoagulation therapy (7,8).