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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
PubMed

Insights

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.

Keywords:
Rho-kinasechronic inflammationcoronary artery vasospasmendothelial dysfunctionmicrovascular dysfunctionperivascular adipose tissuevascular smooth muscle cells

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