A role for pericytes in coronary no-reflow
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Updated: Apr 30, 2026
Incorporating Pericytes into an Endothelial Cell Bead Sprouting Assay
Published on: February 16, 2018
Fergus M O'Farrell1, David Attwell1
1Department of Neuroscience, Physiology & Pharmacology, University College London, Gower Street, London WC1E 6BT, UK.
Insights
Cardiac pericytes may cause coronary no-reflow after myocardial infarction by constricting capillaries, similar to stroke. Targeting these cells could improve heart attack recovery.
Area of Science:
- Cardiovascular Biology
- Neuroscience
- Microcirculation Research
Background:
- Coronary no-reflow, a failure of microcirculation reperfusion post-myocardial infarction, increases mortality.
- No-reflow also complicates ischemic stroke treatment.
- Contractile pericytes constricting brain capillaries are a known cause of stroke no-reflow.
Purpose of the Study:
- To investigate if cardiac pericytes contribute to coronary no-reflow after myocardial infarction.
- To explore cardiac pericytes as a potential therapeutic target for improving reperfusion in heart attack patients.
Main Methods:
- This study proposes a hypothesis based on existing literature comparing cardiac and cerebral no-reflow phenomena.
- The research focuses on the proposed mechanism of pericyte constriction in the cardiac microvasculature.
Main Results:
- Cardiac pericytes are the second most abundant cell type in the heart.
- Pericyte-induced microvascular obstruction is hypothesized to occur even after successful coronary artery treatment.
- The mechanism of no-reflow in the heart is proposed to be analogous to that observed in the brain.
Conclusions:
- Cardiac pericytes are implicated as a significant factor in coronary no-reflow.
- Targeting cardiac pericytes presents a novel therapeutic strategy for myocardial infarction.
- Understanding pericyte behavior is crucial for improving outcomes after ischemic events in both the heart and brain.
Abstract:
Despite efforts to restore tissue perfusion after myocardial infarction, coronary no-reflow--a failure to achieve adequate reperfusion of the cardiac microcirculation--is a common complication, which correlates with an increased incidence of death and disability. The treatment of ischaemic stroke is also plagued by no-reflow and, in the brain, a major cause of this phenomenon has been shown to be contractile microvascular pericytes irreversibly constricting capillaries and dying. We propose that cardiac pericytes, which are the second most-common cell type in the heart, impede reperfusion of coronary capillaries in a similar fashion to those in the brain after a stroke. Pericyte constriction might contribute to morbidity in patients by causing microvascular obstruction, even after successful treatment of coronary artery block. The similarity of the no-reflow phenomenon in the brain and in the heart suggests that cardiac pericytes are a novel therapeutic target for coronary no-reflow after myocardial infarction.
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