Eosinophil Dynamics in Cardiovascular Disease

Summary

Eosinophils, traditionally associated with allergic responses and parasitic defence, have emerged as active players in cardiovascular pathology. These granulocytes circulate in blood but can rapidly migrate into injured vascular tissue, where they release cytotoxic granule proteins, cytokines and chemokines. In acute myocardial infarction, for instance, an early drop in circulating eosinophil count reflects their recruitment to areas of microvascular obstruction and necrosis, correlating with infarct severity and adverse clinical outcomes. Beyond ischaemia–reperfusion injury, eosinophils modulate thrombus formation in acute coronary syndromes and contribute to arterial wall remodelling through interactions with endothelial cells and smooth muscle. In interventions such as drug-eluting stent implantation, baseline eosinophil levels predict the risk of in-stent restenosis, underscoring their value as biomarkers. Moreover, in acute aortic dissection, admission eosinophil counts are linked to mortality risk and thrombus development in the false lumen. Collectively, these insights position eosinophils as both mechanistic mediators and prognostic indicators in cardiovascular disease, opening avenues for targeted modulation of eosinophil function to improve patient outcomes.

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Eosinophil Dynamics in Cardiovascular Disease publication trend

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

Technical terms

Eosinopenia: A reduction in peripheral blood eosinophil count, often reflecting tissue recruitment or consumption.

Reperfusion: Restoration of blood flow to ischaemic myocardium, which can paradoxically exacerbate injury through inflammation.

Microvascular obstruction: Impairment of small-vessel perfusion within the infarct zone, often associated with worse functional recovery.

In-stent restenosis: The re-narrowing of a stented coronary artery segment due to neointimal proliferation and inflammation.

False lumen: The dissected channel within the aortic wall created during dissection, where thrombus formation can occur.

References

  1. Characterization and implications of the dynamics of eosinophils in blood and in the infarcted myocardium after coronary reperfusion. PLOS ONE (2018).
  2. Eosinophil count is related with coronary thrombus in non ST-elevated acute coronary syndrome. Biomedical Papers (2014).
  3. The Early Predictive Value of Circulating Monocytes and Eosinophils in Coronary DES Restenosis. Frontiers in Cardiovascular Medicine (2022).
  4. The role of peripheral blood eosinophil counts in acute Stanford type A aortic dissection patients. Frontiers in Surgery (2022).

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