Inflammation and Immune Response in Angina and Heart Failure
Chronic low-grade inflammation has emerged as a central driver of both angina and heart failure. Beyond classical ischemic mechanisms, inflammatory mediators contribute to endothelial dysfunction, microvascular instability, and myocardial injury. Cytokines such as TNF-α, IL-6, and CRP have been implicated in adverse remodeling, while immune cell infiltration accelerates fibrosis and impairs contractility. Evidence also suggests that persistent immune activation worsens plaque instability, linking inflammation to both acute coronary syndromes and progression to heart failure.
Recent trials targeting inflammation—such as IL-1β blockade in CANTOS—demonstrate the potential of anti-inflammatory strategies in reducing cardiovascular risk. Ongoing research is evaluating immune-modulatory drugs, including colchicine, JAK-STAT inhibitors, and novel biologics, for their cardioprotective potential. This track will explore how fine-tuning immune responses may prevent angina progression, improve outcomes in established heart failure, and integrate with standard therapies. The session will also emphasize biomarkers of inflammation for patient stratification and discuss translational challenges in balancing immunosuppression with the risk of infection.
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