Pathological Mechanisms and Research Progress of Multilevel Intervention Therapy for Coronary He

13 Apr 20264 min read0 viewsJournal Feed

GIST (Key Takeaways)

Coronary heart disease (CHD) is a chronic cardiovascular disease with coronary atherosclerosis as the main pathological basis. Its occurrence and progression are not a simple process of lipid deposition, but a systemic pathological process jointly driven by metabolic disorders, chronic low-grade inflammation, and immune imbalance.
Recent studies have shown that endothelial dysfunction is a key event in the early occurrence of CHD. Abnormal lipid metabolism, immune cell infiltration, and continuous activation of inflammatory signals together promote plaque formation, maturation, and destabilization.
Especially under the regulation of the metabolism-inflammation-immunity network, a positive feedback loop is formed between immune cell metabolic reprogramming, macrophage polarization, inflammasome activation, and oxidative stress response, which accelerates the progression of atherosclerosis and increases the risk of acute coronary events. Traditional therapeutic strategies centered on lipid-lowering, antiplatelet therapy, and revascularization can reduce the incidence of short-term events, but there are still limitations in long-term risk control and fundamental reversal of the disease.

Clinical Editorial

Pathophysiology and conceptual framing: the systemic nature of CHD

The interplay of metabolic disturbances, chronic low-grade inflammation, and immune imbalance shapes disease onset and progression.

CHD is characterized by coronary atherosclerosis as its central pathological substrate, but its development arises from an integrated, systemic process rather than lipid accumulation alone.

Mechanistic drivers and early events

This loop involves metabolic reprogramming in immune cells, macrophage polarization, inflammasome activity, and oxidative stress responses, all of which can hasten atherogenesis and heighten acute coronary risk.

Endothelial dysfunction is highlighted as a critical early event in CHD.
Abnormal lipid handling, immune cell infiltration, and persistent inflammatory signaling collectively contribute to plaque formation, growth, and eventual destabilization.
A metabolism–inflammation–immunity network is proposed to sustain a positive feedback cycle.

Therapeutic landscape and limitations

Conventional management emphasizes lipid lowering, antiplatelet therapy, and revascularization.
While these approaches can mitigate short-term event rates, they show limitations for long-term risk reduction and for reversing underlying disease processes.

Synthesis and research directions: a multilevel intervention perspective

The article consolidates current knowledge on CHD pathophysiology, metabolic and immune regulation, plaque stability, and risk determinants from a systems view.
It emphasizes the potential utility of multilevel, systematic intervention strategies for precise prevention and therapy, aiming to inform translational research and personalized treatment approaches.

Open questions and limitations

The report notes limitations in translating mechanistic insights into sustained disease reversal and long-term outcomes, and it underscores the need for further study to validate multilevel strategies over conventional modalities.