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Apparent Longitudinal Variation in the Angiographic Expression of Myocardial Bridging: Reduced Dynamic Left Anterior
Naresh Bohara1, Adarsha Mahaseth2, Jianwei Zhou1
1Interventional Cardiology, Yangzhou University Affiliated Northern Jiangsu People's Hospital, Yangzhou, CHN.
Insights
Myocardial bridging (MB) can change in appearance on angiography over time. These changes may reflect imaging variability or functional modulation, not necessarily anatomical changes.
Area of Science:
- Cardiology
- Medical Imaging
- Congenital Heart Disease
Background:
- Myocardial bridging (MB) is a congenital coronary anomaly where a segment of a coronary artery travels within the heart muscle.
- This intramyocardial course can lead to dynamic systolic compression, most commonly affecting the left anterior descending (LAD) artery.
- The angiographic appearance of MB can fluctuate due to various factors, including hemodynamics and imaging techniques.
Abstract:
Myocardial bridging (MB) is a congenital coronary anomaly characterized by an intramyocardial course of an epicardial coronary artery, resulting in dynamic systolic compression, most commonly involving the left anterior descending (LAD) artery. Although the anatomical substrate is generally considered congenital and structurally fixed, the angiographic expression of MB may vary according to hemodynamic conditions, pharmacologic therapy, imaging projection, and coexisting coronary artery disease. We report the case of a 71-year-old woman with hypertension and dyslipidemia who presented in 2020 with recurrent chest discomfort. Coronary angiography demonstrated a proximal-to-mid LAD MB with approximately 50-60% systolic compression and preserved flow, and she was managed conservatively with beta-blocker therapy. Six years later, she re-presented with recurrent chest pain. Repeat coronary angiography showed reduced dynamic systolic compression of the previously bridged LAD segment, which now appeared as an approximately 60% fixed luminal narrowing, along with newly detected dynamic MB in the distal branch of the left circumflex artery. These findings were interpreted as apparent longitudinal variation in angiographic expression rather than confirmed anatomical regression or de novo formation. The patient was managed medically without percutaneous coronary intervention because there was no flow-limiting stenosis, biomarkers were negative, and physiologic confirmation of ischemia was not obtained. This case highlights that serial coronary angiography in MB should be interpreted cautiously, particularly when imaging conditions and physiologic assessment are not standardized. For clinicians, the key implication is that apparent changes in MB over time may reflect functional modulation, imaging variability, and superimposed atherosclerosis rather than true structural evolution.
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