Severe COVID-19 increases risk of future cardiovascular events

To date, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the virus that causes coronavirus disease 2019 (COVID-19), has infected more than 603 million people worldwide, It has taken the lives of over 6.4 million people.

About 30% of COVID-19 survivors continue to experience a range of persistent symptoms for weeks after initial diagnosis. This condition is commonly referred to as acute sequelae of SARS-CoV-2 infection (PASC) or ‘prolonged COVID’.

study: Severity of COVID-19 and subsequent risk of cardiovascular events. Image Credit: Yurchanka Siarhei / Shutterstock.com

Background

Multisystem inflammatory syndrome is the most common PASC syndrome in adults and children, although a variety of other symptoms have been reported, including sleep disturbances, persistent fatigue, type 1 diabetes, and neuropathy. Incidence varies from person to person based on demographic and clinical characteristics.

Several studies have shown that individuals who have recovered from COVID-19 develop multiple cardiovascular complications such as arrhythmia, hypertension, acute myocardial infarction, thromboembolism, and cerebrovascular disease. However, a limited number of studies have confirmed that severe her COVID-19 increases the risk of cardiovascular disease.

Recent clinical infection A journal study determines the relationship between COVID-19 severity and subsequent cardiovascular event (CVE) risk in a large cohort.

Survey results

A retrospective cohort study was conducted using adult national health claims data from the US Health Verity Real-Time Insights and Evidence database. We found that increasing severity of COVID-19 increased the risk of developing subsequent CVE in individuals with no history of cardiac disease in the past few years.

Patients requiring hospitalization were more likely to experience CVE compared to COVID-19 patients requiring outpatient care. Among hospitalized patients with COVID-19, those admitted to the intensive care unit (ICU) were approximately 80% more likely to develop her CVE than those hospitalized outside the ICU.

In fact, non-ICU hospitalized patients were only 28% likely to experience a CVE after the first 30 days. COVID-19 symptomsAdditionally, compared to outpatients with COVID-19, inpatients were more likely to be hospitalized with CVE after recovering from COVID-19.

Young adults had a lower incidence of cardiovascular sequelae compared with older adults. Apart from CVE, other severe outcomes such as thrombosis and cerebrovascular accident were observed in the patient who recovered from her severe COVID-19. However, such observations were less frequent in her COVID-19 patients who required only outpatient care.

Research results underscore the importance of vaccination as demonstrated by its ability to reduce severe disease. Similarly, prompt antiviral treatment of acute COVID-19 is recommended, which can help reduce the likelihood of progression to severe disease.

Both COVID-19 vaccination and timely therapeutic intervention reduce the risk of severe COVID-19 and subsequently reduce the likelihood of experiencing CVE.

Our results are consistent with previous studies reporting higher rates of myocarditis and pericarditis in patients who recovered from severe SARS-CoV-2 infection. Nevertheless, we observed that elevated cardiovascular risk after acute infection may not be limited to COVID-19.

In fact, several other diseases that have been associated with an increased risk of long-term CVE are influenza and pneumoniae bacteremia. Additionally, 22-65% of sepsis survivors are at increased risk for CVE.

The underlying mechanisms responsible for the increased risk of CVE after SARS-CoV-2 infection have not been identified. SARS-CoV-2 infects cardiomyocytes through interaction with angiotensin-converting enzyme 2 (ACE-2) receptors. This interaction thus induces a chronic inflammatory response and subsequent tissue damage or fibrosis.

Another mechanism associated with the development of CVE after recovery from COVID-19 is an autoimmune reaction against cardiac antigens that causes delayed damage to cardiac tissue. Anti-cardiac antibodies were also correlated with cardiovascular symptoms and COVID-19.

Viral toxicity is another mechanism that can lead to long-term cardiac damage or thrombosis in vasculitis. However, in the future, more studies are needed to confirm the mechanisms associated with cardiac injury after SARS-CoV-2 infection.

Conclusion

The authors were unable to quantify the increased risk of CVE in COVID-19 patients, as there was no COVID-19-negative control group. Including patients with a history of CVE in the undesirable range may also have overestimated the results. The impact of vaccination status on CVE incidence has not been studied.

Despite these limitations, the present study strongly emphasized that patients who recovered from severe COVID-19 are at increased risk of developing CVE. Patients admitted to the ICU were at higher risk of experiencing her CVE compared to her COVID-19 patients who required outpatient care.

This study strongly emphasized the importance of COVID-19 vaccination to prevent severe infection.