Bridging the Gap in a Rare Cause of Angina
Sumanth Khadke1, Jovana Vidovic2, Vinod Patel3
1Our Lady of Fatima University, Fatima College of Medicine Manila, Philippines.
Insights
Myocardial bridging, where coronary arteries run within the heart muscle, can cause ischemia during tachycardia. Deeper bridges with specific physiological measures require treatment.
Area of Science:
- Cardiology
- Vascular Biology
- Biomedical Engineering
Background:
- Myocardial bridging involves coronary arteries running intramurally, potentially causing dynamic obstruction and myocardial ischemia during tachycardia.
- Associated conditions include acute coronary syndrome, arrhythmia, and sudden cardiac death.
- Atherosclerosis can develop within myocardial bridges due to altered hemodynamics like low shear stress and flow recirculation.
Purpose of the Study:
- To review the pathophysiology and clinical implications of myocardial bridging.
- To discuss the role of hemodynamic factors in atherosclerosis development within myocardial bridges.
- To outline current diagnostic and treatment strategies for myocardial bridging.
Main Methods:
- Literature review of studies on myocardial bridging, coronary artery disease, and hemodynamics.
- Analysis of factors contributing to atherosclerosis in bridged segments.
- Examination of diagnostic criteria and treatment guidelines.
Main Results:
- Myocardial bridging can lead to ischemia by compromising coronary filling time, especially during tachycardia.
- Altered flow patterns within bridges promote atherosclerotic plaque formation.
- Distinguishing physiological compression from pathological stenosis is crucial for management.
Conclusions:
- Myocardial bridging is a significant condition with diverse clinical manifestations.
- Hemodynamic principles are key to understanding atherosclerosis in these anomalies.
- Treatment decisions are guided by symptom severity and objective physiological measurements, with surgery reserved for severe cases.
Abstract:
Myocardial bridging occurs when coronary arteries run intramurally. Episodes of tachycardia can cause a dynamic obstruction that extends into diastole, compromising coronary filling time, and subsequently leading to ischaemia. Myocardial ischaemia, acute coronary syndrome, coronary spasm, myocardial stunning, arrhythmia, takotsubo cardiomyopathy, and sudden cardiac death have all been reported with bridging. Atherosclerotic plaques develop proximally in the bridge due to low shear stress and high oscillatory wall-flow. Factors affecting atherosclerotic build-up include disrupted flow patterns (particularly flow recirculation, which exacerbates LDL internalisation), cell adhesion and monocyte adhesion to the endothelium. Endothelial health depends on arterial flow patterns, given that the vessel reacts differently to various flow types, as confirmed in 3D simulations. Medication is the first-line therapy, while surgical de-roofing and coronary bypass are reserved for severe stenosis. Distinguishing physiological arterial compression from pathological stenosis is essential. Deeper bridges correlating with recurrent angina with an instantaneous wave-free ratio ≤0.89 or fractional flow reserve ≤0.80 are treated.
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