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Decoding long COVID-associated cardiovascular dysfunction: Mechanisms, models, and new approach methodologies.

Dilip Thomas1, Phillip C Yang1, Joseph C Wu1

  • 1Stanford Cardiovascular Institute, Stanford University School of Medicine; Stanford, CA 94305, USA; Division of Cardiovascular Medicine, Department of Medicine; Stanford University School of Medicine; Stanford, CA 94305, USA.

Journal of Molecular and Cellular Cardiology
|October 2, 2025
PubMed
Summary
This summary is machine-generated.

Long COVID, or post-acute sequelae of SARS-CoV-2 infection (PASC), significantly impacts the cardiovascular system. Research explores immune dysregulation, viral persistence, and novel preclinical models to understand and treat these long-term heart conditions.

Keywords:
Cardiovascular dysfunctionEndothelial injuryLong COVIDPrecision medicineiPSC-derived cardiac models

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Area of Science:

  • Cardiology
  • Infectious Diseases
  • Immunology

Background:

  • COVID-19 (SARS-CoV-2) infection causes long-term cardiovascular sequelae, known as Long COVID or post-acute sequelae of SARS-CoV-2 infection (PASC).
  • Persistent symptoms like fatigue, dyspnea, and palpitations indicate multi-organ system involvement, particularly the heart.

Purpose of the Study:

  • To review the current understanding of cardiovascular complications in Long COVID.
  • To highlight mechanistic insights from clinical and preclinical studies.
  • To outline future directions for diagnostics and therapeutics.

Main Methods:

  • Synthesis of clinical data from epidemiological studies on COVID-19 survivors.
  • Analysis of mechanistic studies investigating viral, immune, and coagulation pathways.
  • Review of advanced preclinical platforms like iPSC-based organoids and organ-on-a-chip systems.

Main Results:

  • Cardiovascular complications in Long COVID are driven by immune dysregulation, endothelial dysfunction, viral persistence, and coagulopathy.
  • Direct viral infection, autoantibodies, and cytokine injury contribute to myocardial inflammation, fibrosis, and arrhythmias.
  • Epidemiological studies confirm increased risks of pericarditis, cardiomyopathy, dysrhythmias, and heart failure post-COVID-19.

Conclusions:

  • Advanced preclinical models integrated with AI analytics are crucial for dissecting Long COVID pathophysiology.
  • These models facilitate biomarker discovery, risk stratification, and precision therapeutic development for cardiovascular Long COVID.
  • Further research is needed to innovate diagnostic and therapeutic strategies for Long COVID cardiovascular sequelae.