Dual Case Report: Symptomatic Myocardial Bridging Managed with Calcium Channel Blockers

Background: Myocardial bridging (MB) is a congenital coronary artery anomaly in which a segment of an epicardial coronary artery, most commonly the left anterior descending (LAD) artery, courses intramyocardially, and undergoes systolic compression. Although historically regarded as a benign anatomical variant, myocardial bridging has increasingly been recognized as a potential cause of myocardial ischemia, exertional chest pain, and other cardiac symptoms, particularly in patients without obstructive coronary artery disease. Awareness of this condition is important, as its diagnosis and management differ from those of atherosclerotic coronary disease. Case presentation: We report 2 cases of symptomatic myocardial bridging involving the mid-segment of the LAD artery. The first case involved a 35-year-old male with a 2-month history of exertional chest pain and no cardiovascular risk factors. Initial evaluation, including electrocardiography, cardiac biomarkers, and transthoracic echocardiography, was unremarkable. Coronary angiography demonstrated a myocardial bridge in the mid-LAD with systolic compression and normal diastolic filling, without evidence of obstructive coronary artery disease. The patient was treated with diltiazem, resulting in complete symptom resolution at 1-month follow-up. The second case involved a 48-year-old male with a history of smoking and well-controlled hypertension who presented with exertional chest pain radiating to the left arm, accompanied by palpitations. Laboratory investigations, electrocardiography, and echocardiography were normal. Coronary angiography again revealed myocardial bridging of the mid-LAD without obstructive lesions. Treatment with diltiazem led to complete symptom resolution, and the patient remained clinically stable at 2-month follow-up. Discussion: These cases highlight the clinical significance of myocardial bridging as a cause of angina-like symptoms in patients with non-obstructive coronary arteries. The pathophysiology is multifactorial and includes dynamic systolic compression, delayed diastolic relaxation, endothelial dysfunction, and increased susceptibility to ischemia during tachycardia. Medical therapy aimed at reducing heart rate and myocardial contractility, particularly with non-dihydropyridine calcium channel blockers, remains the cornerstone of management. Conclusion: Myocardial bridging should be considered in the differential diagnosis of chest pain in patients with normal coronary arteries. Early recognition and appropriate medical therapy can result in effective symptom control and may prevent unnecessary invasive interventions.