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Severe COVID-19 increases risk of future cardiovascular events

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Severe COVID-19 increases risk of future cardiovascular events

Thus far, the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which is the virus answerable for the coronavirus disease 2019 (COVID-19), has infected over 603 million individuals and claimed greater than 6.4 million lives worldwide.

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

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

Background

Although multisystem inflammatory syndrome is probably the most common PASC syndrome in adults and youngsters, a wide selection of other symptoms, including sleep difficulties, persistent fatigue, type 1 diabetes, and neurological disorders, have been reported. The incidence of those symptoms varies from one person to a different based on their demographic and clinical characteristics.

Several studies have indicated the manifestation of multiple cardiovascular complications, akin to arrhythmia, hypertension, acute myocardial infarction, thromboembolism, and cerebrovascular accidents, in individuals who’ve recovered from COVID-19. Nevertheless, a limited variety of studies have confirmed that severe COVID-19 results in a high risk of cardiovascular diseases.

A recent Clinical Infectious Diseases journal study determines the connection between COVID-19 severity and risk of subsequent cardiovascular events (CVEs) in a big cohort.

Study findings

A retrospective cohort study was performed using nationwide health insurance claims data of adults from america Health Verity Real-Time Insights and Evidence database. Increased COVID-19 severity was found to reinforce the danger of developing subsequent CVEs amongst individuals with out a cardiac history in previous years. 

As in comparison with COVID-19 patients who required outpatient care, those that required hospital admission were more more likely to experience CVEs. Amongst COVID-19 hospitalized patients, those admitted to the intensive care unit (ICU) were almost 80% more more likely to develop CVEs than non-ICU hospitalized patients.

In truth, non-ICU hospitalized patients exhibited only a 28% possibility of experiencing CVEs thirty days after initial COVID-19 symptoms. Moreover, as in comparison with COVID-19 outpatients, hospitalized patients were more more likely to be admitted for a CVE after recovering from COVID-19.

In younger adults, the incidence of cardiovascular sequelae was lower as in comparison with older adults. Except for CVEs, other severe outcomes, akin to thrombotic events and cerebrovascular accidents, were observed in patients who recovered from severe COVID-19. Nevertheless, such observations were less likely in COVID-19 patients who required only outpatient care.

The study findings emphasize the importance of vaccination, as demonstrated by its ability to scale back severe disease. Similarly, prompt antiviral treatment of acute COVID-19 has been really useful, which might help reduce the potential for transition to severe illness.

Each COVID-19 vaccination and timely therapeutic interventions would alleviate the danger of severe COVID-19 and subsequently decrease the potential for experiencing CVEs.

The findings of the current study are consistent with previous research that has reported the next incidence of myocarditis and pericarditis in patients who recovered from severe SARS-CoV-2 infection. Nevertheless, it was observed that elevated cardiovascular risk after acute infection will not be exclusive to COVID-19.

In truth, another diseases which have been related to an increased risk of long-term CVEs are influenza and pneumonia bacteremia. Moreover, 22-65% of sepsis survivors are at an increased risk of CVEs.

The underlying mechanism answerable for the increased risk of CVEs 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 could remain persistent; subsequently, this interaction induces chronic inflammatory responses and subsequent tissue damage or fibrosis.

One other mechanism related to the event of CVEs following recovery from COVID-19 is an autoimmune response to cardiac antigens that causes delayed damage to cardiac tissues. Anti-heart antibodies also correlated with cardiovascular manifestation and COVID-19.

Viral toxicity is one other possible mechanism which may cause long-term cardiac damage or thrombosis in vasculitis. Nevertheless, in the longer term, more research is required to substantiate the mechanisms related to cardiac damage after SARS-CoV-2 infection.

Conclusions

As a result of the shortage of a COVID-19-negative control group, the authors didn’t quantify the elevated risk of CVEs in COVID-19 patients. The unwanted inclusion of patients with a history of CVEs could have overestimated the result as well. The impact of vaccination status on the incidence of CVE was not studied.

Despite these limitations, the current study strongly emphasized that patients who recovered from severe COVID-19 were at a greater risk of developing CVEs. As in comparison with COVID-19 patients who required outpatient care, those that were admitted to the ICU were at the next risk of experiencing CVEs.

The importance of COVID-19 vaccination in stopping severe infection was strongly emphasized on this study.

Journal reference:

  • Wiemken, L. T., McGrath, L. J., Andersen, K. M., et al. (2022). COVID-19 severity and risk of subsequent cardiovascular events. Clinical Infectious Diseases. doi:10.1093/cid/ciac661.

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