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Updated: Jul 11, 2026

Measurement of Myocardial Lactate Production for Diagnosis of Coronary Microvascular Spasm
Published on: September 17, 2021
Comparison of frequency of coronary spasm in Korean patients with versus without myocardial bridging
Jin Won Kim1, Chang Gyu Park, Soon Yong Suh
1Cardiovascular Center, Korea University, Guro Hospital, Seoul, Republic of Korea.
Insights
Myocardial bridging, a heart condition, can cause endothelial dysfunction, increasing the risk of coronary artery spasm. This study confirms this link, highlighting the importance of understanding this relationship for patient care.
Area of Science:
- Cardiovascular Medicine
- Clinical Cardiology
- Vascular Biology
Background:
- Myocardial bridging can cause mechanical stress on the coronary endothelium.
- This stress may lead to endothelial dysfunction and increased risk of coronary spasm.
Purpose of the Study:
- To test if myocardial bridging induces endothelial dysfunction.
- To determine if myocardial bridging increases the risk of coronary spasm.
- To investigate the response to medication in patients with myocardial bridging and coronary spasm.
Main Methods:
- Spasm provocation testing using incremental acetylcholine infusion in the left coronary artery.
- Comparison between 81 patients with myocardial bridging and 195 control patients.
- Angiographic confirmation of myocardial bridging and absence of atherosclerotic lesions in controls.
Main Results:
- Coronary spasm was significantly more frequent in patients with myocardial bridging (62/81) compared to controls (31/195).
- Focal coronary spasm was predominantly observed within the bridging segments.
- Endothelial dysfunction in the bridging segment was identified as the likely cause.
Conclusions:
- Myocardial bridging is associated with a higher risk of coronary spasm.
- Endothelial dysfunction within the myocardial bridging segment contributes to coronary spasm.
- Findings emphasize the direct impact of myocardial bridging on coronary artery function.
Abstract:
The longstanding compression-relaxation effects of myocardial bridging may produce endothelial dysfunction by direct stress on the endothelium. We tested the hypothesis that myocardial bridging induces endothelial dysfunction and subsequently increases the risk of coronary spasm and investigated the symptomatic response to medication in patients with documented myocardial bridging and coronary spasm. In 81 patients with myocardial bridging (44 men; mean age 57.2 years) and 195 control patients without bridging and atherosclerotic lesions confirmed by angiography (97 men; mean age 58.4 years), spasm provocation testing was done by incremental acetylcholine infusion into the left coronary artery. Spasm was documented in 62 of 81 patients with bridging and in 31 of 195 controls (p <0.001). A focal spasm was limited to the bridging segments compared with controls (p <0.001). In conclusion, the results of this study showed that myocardial bridging increased the risk of coronary spasm by endothelial dysfunction in the bridging segment.
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