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Updated: Aug 26, 2026

Measurement of Myocardial Lactate Production for Diagnosis of Coronary Microvascular Spasm
Published on: September 17, 2021
Coronary vasospasm and the regulation of coronary blood flow
Srilakshmi Konidala1, David D Gutterman
1Department of Medicine, Cardiovascular Center, General Clinical Research Center, Milwaukee, WI 53226, USA.
Insights
Endothelial dysfunction shifts coronary artery response from vasodilation to constriction, causing coronary vasospasm. This review explores mechanisms, predisposing factors, and new therapies for this condition.
Area of Science:
- Cardiovascular Physiology
- Endothelial Function
- Vascular Biology
Background:
- Epicardial arteries normally contribute little to coronary vascular resistance.
- Endothelial dysfunction can reverse vasodilator responses to vasoconstriction.
- Coronary vasospasm arises from this shift, leading to transient arterial obstruction.
Purpose of the Study:
- To review mechanisms of coronary circulation in health.
- To examine pathophysiologic changes in coronary vasospasm.
- To discuss predisposing conditions and novel therapies.
Main Methods:
- Literature review of current understanding.
- Analysis of pathophysiologic mechanisms.
- Exploration of genetic and other predisposing factors.
Main Results:
- Endothelial dysfunction triggers vasoconstriction in response to stimuli like acetylcholine and serotonin.
- Coronary vasospasm involves focal, transient epicardial artery obstruction.
- The condition is linked to myocardial ischemia and characteristic echocardiographic changes.
Conclusions:
- Coronary vasospasm results from a loss of endothelial vasodilator influence and unopposed vasoconstriction.
- Understanding these mechanisms is key to developing targeted therapies.
- Genetic factors and contractile dysfunction are important considerations.
Abstract:
Under physiologic conditions, epicardial arteries contribute minimally to coronary vascular resistance. However, in the presence of endothelial dysfunction, stimuli that normally produce vasodilation may instead cause constriction. Examples include neural release of acetylcholine or norepinephrine, platelet activation and production of serotonin and thrombin, and release of local factors such as bradykinin. This shift from a primary endothelial-mediated vasodilator influence to one of endothelial dysfunction and unchecked vasoconstriction is precisely the milieu in which coronary vasospasm is observed. This condition, which typically occurs during periods of relatively sedentary activity, is associated with focal and transient obstruction of an epicardial arterial segment resulting in characteristic echocardiographic changes and symptoms of myocardial ischemia. This review highlights the current understanding of mechanisms regulating the coronary circulation during health and examines the pathophysiologic changes that occur with coronary spasm. Genetic and other predisposing conditions are addressed, as well as novel therapies based on recent mechanistic insights of the coronary contractile dysfunction associated with coronary spasm.
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