Narrative review: immunometabolic mechanisms of coronary microvascular dysfunction in chronic coronary syndromes
This narrative review proposes a systems-level framework in which coronary microvascular dysfunction in chronic coronary syndromes is viewed as an immunometabolic vascular network disorder, with reduced coronary flow reserve as an integrative functional endpoint. [1]
Automatic summary · not editorially reviewed
The key findings
The review states that coronary microvascular dysfunction is a major determinant of myocardial ischemia, heart failure progression and adverse cardiovascular outcomes, even without obstructive coronary artery disease. [1]
According to the review, mitochondrial stress including NAD decline and redox injury promote endothelial senescence and increase susceptibility to regulated cell death. [1]
The authors propose a framework in which reduced coronary flow reserve is the integrative functional endpoint and a robust predictor of major cardiovascular events. [1]
The source at a glance
- Study type / format
- Narrative review (abstract only)
- Population / context
- People with chronic coronary syndromes and coronary microvascular dysfunction, as discussed in a narrative review.
- Summary based on
- Study abstract
- Original publication
- June 23, 2026
Coronary microvascular dysfunction beyond epicardial stenosis
The review describes chronic coronary syndromes as complex immunometabolic vascular disorders. Coronary microvascular dysfunction is presented as a heterogeneous condition with functional and structural endotypes and as a major determinant of myocardial ischemia, heart failure progression and adverse cardiovascular outcomes, even without obstructive coronary artery disease.
Supporting source [1]
Proposed network of mitochondrial stress and endothelial senescence
According to the review, metabolic shifts toward glycolysis, mitochondrial dysfunction, redox imbalance and dysregulated lipid metabolism sustain inflammatory activation in the coronary microenvironment. Convergent mitochondrial stress, including NAD decline, and redox injury are said to promote endothelial senescence and increase susceptibility to regulated cell death, limiting vasodilatory reserve and predisposing to microvascular rarefaction. Pyroptosis and ferroptosis-like lipid peroxidation are described as further worsening endothelial barrier disruption.
Supporting source [1]
Reduced coronary flow reserve as proposed integrative endpoint
The authors propose a systems-level framework in which coronary microvascular dysfunction is conceptualized as an immunometabolic vascular network disorder. Reduced coronary flow reserve, often termed myocardial flow reserve in PET studies, is presented as the integrative functional endpoint of these interacting molecular perturbations and as a robust predictor of major cardiovascular events.
Supporting source [1]
How to interpret this
This is a narrative review; the abstract reports no study design, sample, follow-up or effect sizes, and the full text was not reviewed. The systems-level framework is proposed, not validated. Associations described are not established causes, and the molecular mechanisms are not shown to extend human lifespan.
Based on the study abstract; the full paper, tables and supplementary data were not reviewed.
Source & supporting passages
Lucki M, Lucka E, Mitkowski P, Lesiak M. · europepmc.org · June 23, 2026