[Immune cell activation in cardiovascular disease: new pathophysiological mechanisms explained]

Area of Science:

• Cardiovascular Medicine
• Immunology
• Hematology

Background:

• Optimal treatment of traditional risk factors does not eliminate atherosclerotic cardiovascular disease (ASCVD) risk, termed residual risk.
• Inflammation plays a key role in ASCVD pathophysiology, as evidenced by the efficacy of anti-inflammatory drugs like colchicine and canakinumab.
• Observational studies link circulating granulocytes and activated monocytes to ASCVD.

Purpose of the Study:

• To discuss novel mechanisms contributing to monocyte and neutrophil activation in atherosclerosis.
• To explore the roles of trained immunity and clonal hematopoiesis in cardiovascular disease.
• To highlight the potential of these mechanisms for improving cardiovascular risk prediction and therapeutic strategies.

Main Methods:

• This perspective reviews recent discoveries regarding trained immunity and clonal hematopoiesis.
• It synthesizes findings from observational studies and clinical trials.
• It discusses the implications of these mechanisms for cardiovascular pathophysiology.

Main Results:

• Two key mechanisms, trained immunity and clonal hematopoiesis, have been identified.
• These mechanisms contribute to monocyte and neutrophil activation in atherosclerosis.
• Understanding these pathways offers new insights into residual cardiovascular risk.

Conclusions:

• Trained immunity and clonal hematopoiesis are emerging concepts in cardiovascular disease.
• These mechanisms may improve cardiovascular risk prediction in the near future.
• They represent potential novel therapeutic targets for preventing and treating cardiovascular diseases.