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Coronary Artery Vasospasm: Cellular and Molecular Insights
Stefan Juricic1, Milan Dobric2,3, Sinisa Stojkovic1,2
1Clinic of Cardiology, University Clinical Center of Serbia, 11000 Belgrade, Serbia.
Cells
|July 13, 2026
Summary
Coronary artery vasospasm (CAV) is a reversible narrowing of heart arteries causing ischemia. Understanding its complex pathophysiology involving vascular smooth muscle cells and endothelial dysfunction is key to developing new treatments.
Area of Science:
- Cardiology
- Vascular Biology
- Molecular Medicine
Background:
- Coronary artery vasospasm (CAV) causes reduced blood flow and myocardial ischemia, often underdiagnosed.
- CAV presents with chest pain, acute coronary syndrome, arrhythmias, or sudden cardiac death.
- Vasospasm occurs in normal arteries or atherosclerotic lesions.
Purpose of the Study:
- To elucidate the multifactorial pathophysiology of coronary artery vasospasm.
- To identify molecular mechanisms underlying vascular smooth muscle cell hyperreactivity and endothelial dysfunction.
- To highlight potential novel therapeutic targets for refractory CAV.
Main Methods:
- Review of molecular mechanisms of vascular smooth muscle cell contraction and relaxation.
- Analysis of the role of endothelial dysfunction, inflammation, and autonomic dysregulation in CAV.
- Examination of signaling pathways including Rho-kinase (ROCK).
Main Results:
- CAV pathophysiology involves vascular smooth muscle cell (VSMC) hyperreactivity, endothelial dysfunction, inflammation, and autonomic dysregulation.
- Key mechanisms include increased intracellular calcium, Rho-kinase (ROCK) mediated inhibition of myosin light chain phosphatase (MLCP), and reduced nitric oxide bioavailability.
- Chronic inflammation and oxidative stress exacerbate VSMC contraction and endothelial dysfunction.
Conclusions:
- Understanding the molecular basis of CAV is crucial for therapeutic advancements.
- Emerging strategies targeting ROCK, endothelin receptors, and inflammation show promise for managing refractory CAV.
- Further research into these pathways may improve clinical outcomes for patients with CAV.
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