Understanding Myocardial Bridging and the Hemodynamic Changes in coronary arteries.

Dr. Zayed | Published : 12, May 2025.

Introduction: MB is a congenital anatomic anomaly characterized by a variable length of coronary artery beneath a section of myocardium resulting in a Dynamic stenosis (vs static stenosis i.e atherosclerosis) that varies with cardiac cycle, heart rate, and sympathetic tone. It mainly involves Left anterior descending artery than right coronary and LCX. The muscle overlying the artery is termed a Myocardial Bridge (MB), and the intramyocardial segment is referred to as a Tunneled artery.

Coronary angiogram during systole vs diastole in MB

for many years myocardial bridging was thought to be non fatal, the reason being coronary blood flow happens during diastole 85% of the time in an individual and the bridge contracts during systole which hinders the blood in remaining 15% of the time. it was later understood this band of tissue not just obstructs blood during systole but also during early diastole due to delayed relaxation which causes suboptimal blood supply which is crucial for the subendocardial tissue resulting in ischemia due to reduced luminal diameter during early diastole and this phenomenon is called "milking effect".

The depth of the tunneled segment and the length of the artery involved plays an integral role in providing the substrate that eventually leads to ischemic symptoms. The depth of the tunneled artery (1-2 mm superficial, >2 mm deep) is related to the degree of systolic compression and course of the artery. The depth of the MB also has implications for treatment, especially when considering surgical intervention. The length of the tunneled segment is important not only as it relates to the amount of the affected artery, but also to the number of branches affected (septal or apical) by the MB. This is especially clinically relevant when considering LAD MBs that affect diagonal or septal branches.

Hemodynamics of bridging: it is evident that the constriction point under the bridge has freedom from plaque formation which mainly seems to be due to separation of perivascular adipose tissue, improvised lymphatics at the narrow segment by compression due to bridge and Wall shear stress. we also witnessed plaque forming changes immediately proximal to the tunnel segment and the main reason seems to be due to wall shear stress (WSS) is the frictional force that acts tangentially to flow and has been shown to play a role in the development of endothelial dysfunction and atherosclerosis, besides this endothelial dysfunction is the very reason for reduced release of Nitric oxide which results in vasospasm. the narrowed segment under the bridge forms 'Venturi effect' causing a negative pressure which results in reduced blood flow in near vicinity than the distal branches (apical branches).

MB is most commonly an incidental finding because most patients are asymptomatic, a majority of whom are viewed as normal variants. For the minority with symptoms, they may present with symptoms of an acute coronary syndrome (ACS) such as reproducible, stable anginal pain, unstable angina, atrioventricular conduction block, Takotsubo syndrome, and rarely sudden death.

Diagnostic Modalities for MB:

Over time, multiple invasive and noninvasive techniques have been employed to diagnose myocardial bridging (MB). Still, there is no specific gold standard, and variabilities exist in the diagnostic accuracies of each methods. above is the classification and the characteristic signs seen in individual imaging studies.

Non-Invasive Methods: Noninvasive modalities include coronary computed tomographic angiography (CCTA); computed tomography fractional flow reserve (CTFFR); stress transthoracic echocardiography (TTE); stress myocardial perfusion imaging (MPI).

Invasive Methods:  It mainly involves Fractional Flow Reserve FFR, Intravascular ultrasonography - IVUS, Optical coherence tomography - OCT, Instantaneous free wave ratio - IFR, intracoronary DFW.

fusiform Signal in OCT

Management: 

Treating symptomatic myocardial bridging (MB) remains a clinical challenge, largely due to its variable presentation and lack of standardized guidelines. Since no major cardiovascular society has issued specific recommendations for its diagnosis or management, treatment strategies must be individualized. Key considerations include the patient's symptom burden, coronary anatomy, extent of myocardial ischemia, and the presence of comorbid conditions such as coronary artery disease (CAD), hypertrophic cardiomyopathy, valvular heart disease, or other structural cardiomyopathies.

The first-line approach is typically medical management, aimed at reducing myocardial oxygen demand and relieving symptoms. Beta-blockers and non-dihydropyridine calcium channel blockers are often used to minimize heart rate and myocardial contractility, thereby decreasing the degree of systolic compression. Lifestyle modifications and aggressive control of cardiovascular risk factors should also be emphasized, alongside close clinical monitoring.

In patients who remain symptomatic despite optimal medical therapy, revascularization may be considered. Options include percutaneous coronary intervention (PCI) or surgical approaches such as coronary artery bypass grafting (CABG) or myotomy (surgical 'unroofing' of the bridged segment). Pre-procedural planning with coronary computed tomography angiography (CCTA) is essential to delineate the anatomical features of the bridged artery and guide the appropriate interventional strategy.

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