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Advances in Pathophysiology and Novel Therapeutic Strategies for Coronary No-Reflow Phenomenon

Hubert Borzuta1, Wiktor Kociemba1, Oliwia Bochenek2

  • 1Chair and Department of Experimental and Clinical Physiology, Laboratory of Centre for Preclinical Research, Medical University of Warsaw, Banacha 1b, 02-097 Warsaw, Poland.

Biomedicines
|July 29, 2025
PubMed

Insights

Coronary no-reflow (CNR) hinders blood flow to heart tissue after treatment for ST-segment elevation myocardial infarction (STEMI). Understanding its causes, including microcirculation damage and PCI effects, is key to developing new therapies beyond current treatments.

Area of Science:

  • Cardiovascular Medicine
  • Interventional Cardiology
  • Pathophysiology

Background:

  • Coronary no-reflow (CNR) is a critical complication following reperfusion therapy for ST-segment elevation myocardial infarction (STEMI).
  • CNR significantly increases mortality and the risk of major adverse cardiac events (MACEs).
  • Damage to the cardiac microcirculation during ischemia-reperfusion underlies the no-reflow phenomenon.

Purpose of the Study:

  • To review the pathophysiology of coronary no-reflow.
  • To discuss contemporary treatment trends and current therapeutic approaches for CNR.
  • To highlight emerging opportunities for novel therapeutic strategies based on improved understanding of CNR pathogenesis.

Main Methods:

  • Literature review of animal and preclinical studies on the no-reflow phenomenon.
  • Analysis of the pathophysiological mechanisms contributing to CNR.
  • Evaluation of current pharmacological therapies and their limitations.

Main Results:

  • Pathophysiological causes of CNR include cardiomyocyte vulnerability, microvascular damage, leukocyte activation, reactive oxygen species (ROS) production, and altered microRNA expression.
  • Percutaneous coronary intervention (PCI) can precipitate CNR through distal atherothrombotic embolization.
  • Current pharmacological treatments are limited to intracoronary vasodilators and antiplatelet agents.

Conclusions:

  • A comprehensive understanding of CNR pathophysiology is essential for advancing treatment strategies.
  • Novel therapeutic targets are emerging from research into microvascular dysfunction and molecular pathways.
  • Further research is needed to translate preclinical findings into effective clinical interventions for CNR.

Keywords:
animal modelscoronary no-reflowischemia/reperfusion injurymicrovascular obstructionmyocardial infarctionpathophysiology

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