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Cardiovascular sequelae of Long COVID: immune dysregulation inflammation as central drivers

Anhui Liu1,2, Hanbing Chen3,4, Qingxiang Liu5

  • 1Wuxi School of Medicine, Jiangnan University, Wuxi, China.

Frontiers in Immunology
|July 9, 2026
PubMed

Insights

Long COVID-19 cardiovascular issues stem from immune system overactivity and persistent inflammation, leading to heart damage. Targeting these immune responses may offer therapeutic benefits for Long COVID patients.

Area of Science:

  • Immunology
  • Cardiology
  • Infectious Diseases

Background:

  • Long coronavirus disease 2019 (Long COVID-19), a post-acute sequela of SARS-CoV-2 infection, presents diverse systemic symptoms.
  • Cardiovascular manifestations, including myocarditis, arrhythmias, and heart failure, are increasingly recognized as key features of Long COVID-19.

Purpose of the Study:

  • To review current evidence on immune-mediated mechanisms driving cardiovascular sequelae in Long COVID-19.
  • To explore potential therapeutic strategies targeting inflammation and immune dysregulation in Long COVID-19 cardiovascular complications.

Main Methods:

  • Literature review of clinical and experimental studies.
  • Analysis of immune system activation pathways in SARS-CoV-2 infection.
  • Examination of cardiovascular injury markers and mechanisms.

Main Results:

  • Immune dysregulation and persistent inflammation are central to Long COVID-19 cardiovascular injury.
  • Persistent immune activation leads to endothelial injury, thrombo-inflammation, and adverse myocardial remodeling.
  • Specific immune pathways implicated in cardiovascular damage have been identified.

Conclusions:

  • Immune-mediated mechanisms are critical in the pathogenesis of Long COVID-19 cardiovascular complications.
  • Therapeutic strategies should focus on modulating persistent inflammation and immune dysregulation.
  • Further research is needed to develop targeted treatments for Long COVID-19 cardiovascular sequelae.

Keywords:
Long COVIDadaptive immune responsecardiovascular sequelaeimmune dysregulationinnate immune response

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