To date, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which is the virus responsible for coronavirus disease 2019 (COVID-19), has infected more than 603 million people and killed more than 6 .4 million deaths worldwide.

About 30% of COVID-19 survivors continue to experience a wide range of persistent symptoms for several weeks since their initial diagnosis. This condition is commonly referred to as post-acute sequelae of SARS-CoV-2 infection (PASC) or “long COVID”.

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


Although multisystem inflammatory syndrome is the most common PASC syndrome in adults and children, a wide range of other symptoms, including sleep disturbances, persistent fatigue, type 1 diabetes, and neurological disorders, have been reported. reported. The incidence of these symptoms varies from person to person depending on their demographic and clinical characteristics.

Several studies have indicated the occurrence of multiple cardiovascular complications, such as arrhythmia, hypertension, acute myocardial infarction, thromboembolism and stroke, in people who have recovered from COVID-19. However, a limited number of studies have confirmed that severe COVID-19 carries a high risk of cardiovascular disease.

A recent Clinical infectious diseases A journal study determines the relationship between the severity of COVID-19 and the risk of subsequent cardiovascular events (CVE) in a large cohort.

Study results

A retrospective cohort study was performed using national adult health insurance claims data from the United States Health Verity Real-Time Insights and Evidence database. The increased severity of COVID-19 has been found to increase the risk of developing later VECs in people with no heart history in previous years.

Compared to COVID-19 patients who required outpatient care, those who required hospitalization were more likely to experience VECs. Among hospitalized COVID-19 patients, those admitted to the intensive care unit (ICU) were nearly 80% more likely to develop CVE than non-ICU hospitalized patients.

In fact, non-hospitalized intensive care patients had only a 28% chance of experiencing CVEs thirty days after the first symptoms of COVID-19. Additionally, compared to outpatient COVID-19 patients, inpatients were more likely to be admitted for CVE after recovering from COVID-19.

In young adults, the incidence of cardiovascular sequelae was lower than in older adults. In addition to VECs, other serious events, such as thrombotic events and strokes, have been observed in patients who have recovered from severe COVID-19. However, such observations were less likely in COVID-19 patients who only needed outpatient care.

The results of the study underscore the importance of vaccination, as evidenced by its ability to reduce serious illnesses. Similarly, prompt antiviral treatment of acute COVID-19 has been recommended, which would help reduce the possibility of transition to severe disease.

Vaccination against COVID-19 and timely therapeutic interventions would mitigate the risk of severe COVID-19 and subsequently reduce the possibility of experiencing VECs.

The results of the present study are consistent with previous research that reported a higher incidence of myocarditis and pericarditis in patients who recovered from severe SARS-CoV-2 infection. Nevertheless, it has been observed that elevated cardiovascular risk after acute infection may not be exclusive to COVID-19.

In fact, some other illnesses that have been linked to an increased risk of long-term CVE are influenza and pneumonia bacteremia. Additionally, 22-65% of sepsis survivors are at increased risk for CVE.

The underlying mechanism responsible for the increased risk of CVE following SARS-CoV-2 infection has not been determined. SARS-CoV-2 infects cardiac myocytes through their interaction with the angiotensin-converting enzyme 2 (ACE-2) receptor, which may remain persistent; therefore, this interaction induces chronic inflammatory responses and subsequent tissue damage or fibrosis.

Another mechanism linked to the development of CVEs after recovery from COVID-19 is an autoimmune response to cardiac antigens that causes delayed damage to cardiac tissue. Anti-heart antibodies were also correlated with cardiovascular manifestations and COVID-19.

Viral toxicity is another possible mechanism that could cause long-term heart damage or thrombosis in vasculitis. However, in the future, more research is needed to confirm mechanisms related to cardiac damage after SARS-CoV-2 infection.


Due to the lack of a COVID-19-negative control group, the authors did not quantify the elevated risk of CVE in COVID-19 patients. The unwanted inclusion of patients with a history of CVE might also have overestimated the result. The impact of vaccination status on the incidence of VEC has not been studied.

Despite these limitations, the present study strongly emphasized that patients who recovered from severe COVID-19 were at higher risk of developing CVE. Compared to COVID-19 patients who needed outpatient care, those who were admitted to intensive care were at higher risk of experiencing VECs.

The importance of vaccination against COVID-19 in preventing serious infections was strongly emphasized in this study.

Journal reference:

  • Wiemken, LT, McGrath, LJ, Andersen, KM, et al. (2022). Severity of COVID-19 and risk of subsequent cardiovascular events. Clinical infectious diseases. doi:10.1093/cid/ciac661.