Inflammation Modulation in Cardiovascular Events

Inflammation plays a central role in the initiation, progression and resolution of cardiovascular events, from the formation of atherosclerotic plaques to the healing phase after myocardial infarction. Endothelial injury and lipid deposition trigger an innate immune response, recruiting neutrophils and monocytes that release cytokines and reactive oxygen species. Chronic low-grade inflammation accelerates plaque instability, while an excessive acute response contributes to reperfusion injury and adverse ventricular remodelling. Therapeutic modulation of these processes aims to dampen harmful inflammation without impairing essential repair mechanisms. Strategies under investigation include inhibitors of key cytokines such as interleukin-1β and interleukin-6, blockers of inflammasome activation and repurposed agents with anti-inflammatory properties. Recent advances have begun to define patient subgroups most likely to benefit, guided by biomarkers of residual inflammatory risk, and to explore novel drug-delivery platforms and timing of intervention. The global burden of cardiovascular disease underscores the need for targeted, safe and cost-effective immunomodulatory therapies that complement lipid-lowering and antithrombotic regimens.

Research from Nature Portfolio

Recent studies have demonstrated that blockade of interleukin-1β signalling with a recombinant receptor antagonist accelerates the resolution of leukocytosis in acute myocardial infarction. Treatment led to a pronounced reduction in total white blood cell and neutrophil counts within days of administration, accompanied by a transient increase in eosinophils. These effects persisted during therapy and returned to baseline after discontinuation, suggesting a direct immunomodulatory mechanism. The findings provide mechanistic insight into how cytokine inhibition may translate into improved clinical outcomes by tempering the early inflammatory surge following ST-elevation myocardial infarction.

Inflammation Modulation in Cardiovascular Events publication trend

The graph below shows the total number of articles in inflammation modulation in cardiovascular events across all publications each year (not limited to Nature Index journals).

Technical terms

Interleukin-1β: pro-inflammatory cytokine that orchestrates innate immune responses in vascular injury.

Anakinra: recombinant interleukin-1 receptor antagonist that inhibits IL-1β signalling.

C-reactive protein (CRP): acute-phase protein produced by the liver as a marker of systemic inflammation.

Neutrophil: type of leukocyte central to early inflammatory responses and tissue injury.

Eosinophil: white blood cell involved in modulating inflammatory processes and tissue repair.

NLRP3 inflammasome: intracellular multi-protein complex that activates inflammatory cytokines in response to cellular stress.

References

1. Inflammatory Mediators of Endothelial Dysfunction. Life (2023).
2. Do Interleukin-1 and Interleukin-6 Antagonists Hold Any Place in the Treatment of Atherosclerotic Cardiovascular Disease and Related Co-Morbidities? An Overview of Available Clinical Evidence. Journal of Clinical Medicine (2023).
3. Drug repurposing in cardiovascular inflammation: Successes, failures, and future opportunities. Frontiers in Pharmacology (2022).
4. Anti-Inflammatory Drug Candidates for Prevention and Treatment of Cardiovascular Diseases. Pharmaceuticals (2023).
5. Effect of interleukin-1 blockade with anakinra on leukocyte count in patients with ST-segment elevation acute myocardial infarction. Scientific Reports (2022).
6. Change in Eosinophil Count in Patients with Heart Failure Treated with Anakinra. Cells (2023).
7. Acute-on-chronic inflammation in acute myocardial infarction. Current Opinion in Cardiology (2024).
8. Acute coronary syndrome: how to reduce the residual inflammatory risk?. Russian Journal of Cardiology (2020).