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Pathophysiological Mechanisms of Myocardial Bridging-Related Angina and Ischemia with Implications for Therapeutic
Srdjan Aleksandric1,2, Barry Uretsky3,4, Ana Djordjevic-Dikic1,2
1Cardiology Clinic, University Clinical Center of Serbia, Koste Todorovica 8, 11000 Belgrade, Serbia.
Insights
Myocardial bridging (MB), a congenital coronary anomaly, can cause angina and ischemia through various mechanisms. Comprehensive coronary physiology testing is crucial for accurate diagnosis and treatment in patients with this condition.
Area of Science:
- Cardiology
- Cardiovascular Research
- Medical Science
Background:
- Myocardial bridging (MB) is a congenital coronary anomaly involving systolic compression of intramyocardial arteries.
- This condition can lead to reduced diastolic lumen diameter and impaired arterial relaxation.
Purpose of the Study:
- To review the pathophysiological and cellular mechanisms underlying MB-related angina and myocardial ischemia.
- To discuss future perspectives in assessing MB severity and its impact on coronary physiology.
Main Methods:
- Literature review of existing evidence on myocardial bridging and its associated mechanisms.
- Analysis of pathophysiological pathways including delayed diastolic relaxation, impaired vasodilation, septal steal, and atherosclerosis.
- Discussion of the role of coronary microcirculation and angina with or without obstructive coronary arteries (ANOCA/INOCA).
Main Results:
- MB can cause angina and ischemia via delayed diastolic relaxation, endothelial dysfunction, septal steal, and accelerated atherosclerosis.
- Isolated MB or coexisting coronary microvascular dysfunction can manifest as angina or ischemia.
- Differentiating MB as the cause of symptoms can be challenging, especially in ANOCA/INOCA patients.
Conclusions:
- Comprehensive coronary physiology testing is recommended for patients with MB to identify the cause of angina/ischemia.
- Understanding the complex interplay of MB and coronary physiology is essential for optimal therapeutic strategies.
- Further research into functional assessment of MB severity is needed.
Abstract:
Myocardial bridging (MB) is a congenital coronary anomaly characterized by systolic compression of the intramyocardial arterial segment and delayed early diastolic artery relaxation, resulting in reduced vessel luminal diameter in diastole. Current evidence suggests that MB, particularly in the left anterior descending artery, may cause anginal symptoms and/or myocardial ischemia through several different pathophysiological and cellular mechanisms acting independently or synergistically: (1) delayed early diastolic relaxation of intramyocardial arterial segment; (2) impaired endothelial-dependent vasodilation with vessel smooth muscle cell hyperactivity in the coronary artery with MB, especially within the bridged segment; (3) focal (septal) ischemia due to "septal steal" phenomenon; and (4) development and progression of an atherosclerotic lesion in the coronary artery segment proximal to MB. Patients with isolated-MB may also experience anginal pain and/or myocardial ischemia due to concomitant structural and/or functional abnormalities of the coronary microcirculation. Both MB and coronary microvascular dysfunction refer to a subgroup of patients with angina and/or ischemia with non-obstructive coronary arteries (ANOCA/INOCA). Therefore, it may be challenging to determine whether MB is causing anginal pain and/or ischemia, particularly since both phenomena have also been reported without MB's existence. Therefore, comprehensive coronary physiology testing should be encouraged in patients with this coronary anomaly to identify the underlying cause of anginal pain and/or myocardial ischemia, enabling optimal therapeutic strategies in these patients. This review is focused on different pathophysiological and cellular mechanisms of MB-related angina and/or ischemia and future perspectives in the functional assessment of MB severity, bearing in mind the complexity of coronary physiology in the presence of this anomaly.
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