Respiratory Diseases Roundup

Metabolic, Cardiovascular, and Infectious Sequelae of COVID-19

Miranda Manier, BA

Key Highlights

  • Children with multisystem inflammatory syndrome in children exhibit distinct metabolic disruptions similar to severe adult COVID-19.
  • SARS-CoV-2 infection is linked to accelerated coronary plaque progression.
  • COVID-19 does not increase risk of secondary pneumococcal infections, unlike influenza and RSV.
  • Inflammatory markers in pediatric COVID-19 suggest potential long-term cardiovascular risk.

Metabolic Disruptions in Pediatric MIS-C1

A comprehensive metabolic profiling study of 147 children revealed that both acute COVID-19 and multisystem inflammatory syndrome in children (MIS-C) are associated with distinct and systemic metabolic disturbances. Using nuclear magnetic resonance spectroscopy and liquid chromatography–mass spectrometry, researchers identified significant shifts in lipid classes and inflammatory markers, including elevated triglycerides, altered lipoprotein composition, and increased Apo-B100/Apo-A1 ratios. Children with MIS-C displayed more profound triglyceride elevation and lipoprotein remodeling compared to those with acute COVID-19, despite similar or milder respiratory symptoms. These findings suggest that the inflammatory response triggered by SARS-CoV-2 in children may mimic that of severe adult cases, indicating a shared pathological mechanism and raising concerns about the long-term cardiometabolic impact in pediatric populations.

Further analysis showed a disruption in high-density and low-density lipoproteins, with those with MIS-C demonstrating a higher number of circulating very-low-density lipoprotein particles and enriched triglyceride content. These changes could impair reverse cholesterol transport and increase cardiovascular disease risk. The study also found that many of these metabolic markers overlapped with those seen in adults with severe COVID-19. Given that 40% to 55% of the children studied were overweight or obese, the presence of comorbid metabolic risk factors may further compound potential long-term consequences. The researchers emphasize the need for longitudinal monitoring to better understand persistent metabolic alterations post–SARS-CoV-2 infection in children.

Coronary Plaque Progression After COVID-192

In a study involving 803 patients and 2588 coronary lesions, prior SARS-CoV-2 infection was found to significantly accelerate the progression of coronary atherosclerotic plaque. Compared with uninfected individuals, patients who had recovered from COVID-19 exhibited greater annual increases in total percent atheroma volume (0.90% vs 0.62%) and noncalcified plaque volume (0.78% vs 0.42%). Lesions in these patients were also more likely to develop high-risk plaque features and display elevated pericoronary adipose tissue attenuation, a marker of coronary inflammation. The changes persisted despite similar baseline characteristics, lipid profiles, and risk factors across cohorts.

This progression translated into worse clinical outcomes. The adjusted hazard ratio for target lesion failure—including cardiac death, myocardial infarction, or need for revascularization—was 2.90 among patients with prior SARS-CoV-2 infection. Mediation analysis indicated that a portion of the effect on plaque progression was attributable to coronary inflammation. These results support growing evidence that COVID-19 may act as an accelerant of atherosclerosis via systemic and localized vascular inflammation. The findings suggest the importance of cardiac monitoring in those who have been previously diagnosed with COVID-19 and raise the possibility that coronary CT angiography could help identify patients at heightened risk of cardiovascular events after SARS-CoV-2 infection.

COVID-19 Not Linked to Post-Viral Pneumococcal Infection3

A large-scale retrospective analysis of hospitalized patients within the U.S. Veterans Affairs system has identified differing risks of secondary pneumococcal disease following common viral respiratory infections. The study, which included nearly 189,000 patients tested for respiratory viruses from 2015 to 2025, found that influenza and respiratory syncytial virus (RSV) significantly increased the risk of subsequent Streptococcus pneumoniae infection. Specifically, the odds ratios for pneumococcal disease were 2.39 for influenza and 2.50 for RSV. Conversely, patients with a recent COVID-19 diagnosis had lower odds of secondary pneumococcal infection, with an odds ratio of 0.56.

The analysis also highlighted additional risk factors for pneumococcal infection, including smoking and underlying chronic obstructive pulmonary disease. These findings contrast with the well-documented co-infection risks associated with influenza and RSV and suggest differing immunopathological effects of SARS-CoV-2. While the study does not establish causality, it suggests that COVID-19 may not disrupt mucosal immunity in the same manner as influenza or RSV. The results may inform differential clinical strategies for post-viral monitoring and antibiotic stewardship, particularly in older adult populations and those with chronic lung disease.

References:

  1. Lawler NG, Yonker LM, Lodge S, et al. Children with post COVID-19 multisystem inflammatory syndrome display unique pathophysiological metabolic phenotypes. J Proteome Res. 2025;24(6):1234–1256. doi:10.1021/acs.jproteome.5c00062
  2. Dai N, Tang X, Hu Y, et al. SARS-CoV-2 infection association with atherosclerotic plaque progression at coronary CT angiography and adverse cardiovascular events. Radiology. 2025;306(2):e240876. doi:10.1148/radiol.240876
  3. Powers LA, Chan AK, Wattengel BA, et al. Secondary pneumococcal disease in veterans with viral respiratory infections. Clin Infect Dis. Published online May 31, 2025. doi:10.1093/cid/ciaf285