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

Abstract

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.

Introduction

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, follows an intramyocardial course beneath overlying myocardial fibers. During systole, this tunneled segment may be compressed, leading to transient luminal narrowing. Although coronary perfusion occurs predominantly during diastole, significant systolic compression—particularly during tachycardia or increased myocardial contractility—can impair coronary blood flow and result in ischemic symptoms.^1-3

For many years, myocardial bridging was considered a benign anatomical variant and was often identified incidentally during coronary angiography or autopsy. However, growing clinical and imaging evidence has demonstrated that MB may be associated with exertional chest pain, myocardial ischemia, arrhythmias, and, rarely, sudden cardiac death, even in the absence of obstructive coronary artery disease. Clinical presentation varies widely, ranging from asymptomatic individuals to patients with angina-like symptoms that may mimic atherosclerotic coronary disease. Advances in diagnostic modalities, particularly coronary angiography and coronary computed tomography angiography, have improved recognition of the anatomical and functional significance of myocardial bridging.^2,4

Management of symptomatic myocardial bridging is primarily medical and focuses on reducing heart rate and myocardial contractility in order to decrease systolic compression and prolong diastolic coronary perfusion. Beta-blockers and non-dihydropyridine calcium channel blockers, such as diltiazem and verapamil, are considered first-line therapies. Nitrates are generally avoided, as they may worsen systolic compression through reflex tachycardia and reduced preload. Invasive interventions are reserved for patients with persistent symptoms despite optimal medical therapy.^3,5,6

Case Presentation 1

A 35-year-old male presented to the emergency department with a 2-month history of intermittent chest pain. The pain was exertional and not associated with shortness of breath, palpitations, syncope, nausea, or diaphoresis. He had no known medical conditions and denied smoking, alcohol consumption, or illicit drug use. Physical examination was unremarkable.

Vital signs on presentation included a heart rate of 90 beats per minute (sinus rhythm), blood pressure of 120/75 mmHg respiratory rate of 18 breaths per minute, and oxygen saturation of 97% on room air. Initial laboratory tests revealed a troponin level of <0.010 ng/mL (reference range: 0.010–0.029 ng/mL) and a B-type natriuretic peptide (BNP) level of 40 pg/mL (normal < 100 pg/mL). Additional laboratory results, including complete blood count (CBC) and thyroid-stimulating hormone (TSH), were within normal limits. A chest X-ray (CXR) showed no acute abnormalities.

An electrocardiogram (ECG) was unremarkable (Figure 1). Repeat cardiac biomarkers and ECG remained within normal limits. A transthoracic echocardiogram (TTE) revealed normal cardiac structure and function, with no evidence of left ventricular hypertrophy or wall motion abnormalities. Due to persistent chest pain, the patient underwent diagnostic coronary angiography, which revealed a myocardial bridge in the mid-segment of the left anterior descending (LAD) artery during systole, with a normal appearance during diastole and no evidence of obstructive coronary artery disease (Figure 2A and B). The right coronary artery (RCA) appeared normal (Figure 3).

Figure 1.

Electrocardiogram (ECG) of case 1 showing no remarkable abnormalities.

Figure 2.

Panel A: Angiographic view shows normal flow in the mid LAD during diastole and panel B shows a myocardial bridge in mid LAD in systole (Orange arrow).

Figure 3.

Coronary angiography of the right coronary artery (RCA) in case 1 demonstrating normal findings.

The patient was started on diltiazem 60 mg twice daily for symptomatic management. At a follow-up visit 1 month later, he reported resolution of symptoms and remained clinically stable.

Case Presentation 2

A 48-year-old male presented with a 1-month history of chest pain radiating to the left arm, associated with palpitations. He had a long history of smoking. He denied dyspnea, syncope, alcohol consumption, or illicit drug use. His medical history was significant for well-controlled hypertension managed with amlodipine 10 mg daily. Physical examination revealed no abnormalities.

Vital signs showed a heart rate of 75 beats per minute (sinus rhythm), blood pressure of 130/80 mmHg, respiratory rate of 12 breaths per minute, and oxygen saturation of 98% on room air.

Initial laboratory investigations, including troponin (<0.010 ng/mL; reference range: 0.010–0.029 ng/mL), B-type natriuretic peptide (43 pg/mL; normal < 100 pg/mL), complete blood count (CBC), and thyroid-stimulating hormone (TSH), were within normal limits. A chest X-ray showed no acute pathology.

An electrocardiogram (ECG) was unremarkable (Figure 4). Atransthoracic echocardiogram (TTE) demonstrated normal cardiac structure and function, with no evidence of left ventricular hypertrophy or wall motion abnormalities.

Figure 4.

Electrocardiogram (ECG) of case 2 showing no remarkable abnormalities.

Given the intermittent chest pain and smoking history, coronary angiography was performed, which demonstrated a myocardial bridge in the mid-segment of the left anterior descending (LAD) artery during systole, with normal appearance during diastole and no evidence of obstructive coronary artery disease (Figure 5A and B). The right coronary artery (RCA) was normal (Figure 6).

Figure 5.

Panel A: Angiographic view shows normal flow in the LAD during diastole (red arrow) and panel B (Another angiographic view shows a myocardial bridge in Mid LAD in systole (yellow arrow).

Figure 6.

Coronary angiography of the right coronary artery (RCA) in case 2 demonstrating normal findings.

The patient was started on diltiazem 60 mg twice daily. At a 2-month follow-up visit, he was asymptomatic and remained clinically stable.

Discussion

Myocardial bridging represents a functional coronary abnormality in which dynamic systolic compression of a tunneled coronary segment may lead to myocardial ischemia under specific hemodynamic conditions. Although often identified incidentally, several physiological and imaging studies have demonstrated that myocardial bridging can result in altered coronary flow patterns, delayed diastolic relaxation, and reduced coronary flow reserve, particularly during tachycardia and increased myocardial demand. These features distinguish myocardial bridging from fixed atherosclerotic coronary stenosis and explain its variable clinical presentation. ⁵

In the present report, both patients presented with exertional chest pain and were found to have myocardial bridging of the mid-segment of the LAD artery, the vessel most commonly associated with symptomatic disease. Prior angiographic and Doppler studies have shown that LAD myocardial bridges are more likely to produce hemodynamically significant systolic compression and abnormal flow patterns compared with bridges in other coronary segments.

Normal cardiac biomarkers and echocardiographic findings in these patients further highlight the diagnostic challenge of myocardial bridging and the importance of careful coronary imaging in patients with persistent symptoms and non-obstructive coronary arteries. ⁷

The pathophysiology of ischemia in myocardial bridging is multifactorial. In addition to systolic compression, endothelial dysfunction, enhanced vasoreactivity, and coronary vasospasm have been implicated in symptom generation. These mechanisms may coexist and are often exacerbated by tachycardia, which shortens diastolic filling time and increases myocardial oxygen demand. Therapeutically, reduction of heart rate and myocardial contractility remains central to symptom control. Clinical studies and practical reviews support the use of beta-blockers and non-dihydropyridine calcium channel blockers as first-line therapy, with invasive approaches reserved for patients with refractory symptoms despite optimal medical management. ⁸

Conclusion

Myocardial bridging is an important and often underrecognized cause of exertional chest pain in patients with angiographically normal coronary arteries. Although frequently considered a benign anatomical variant, it may produce clinically significant ischemic symptoms due to dynamic systolic compression and impaired coronary flow, particularly during increased heart rate and myocardial demand. These cases highlight the importance of considering myocardial bridging in the differential diagnosis of angina-like symptoms when obstructive coronary artery disease is absent. Careful coronary imaging is essential for accurate diagnosis. Medical management with non-dihydropyridine calcium channel blockers can effectively relieve symptoms and improve clinical stability. Early recognition and appropriate treatment may prevent unnecessary invasive interventions and reduce recurrent symptoms. Increased awareness among clinicians is essential to ensure timely diagnosis and optimal management of this condition.

Limitations

This report has several limitations. First, it describes only 2 cases, which limits generalizability and prevents definitive conclusions. Second, invasive physiological assessment such as fractional flow reserve (FFR) or instantaneous wave-free ratio (iFR) was not performed; therefore, the hemodynamic significance of the myocardial bridges was inferred from angiographic findings and clinical presentation. Third, advanced imaging modalities such as coronary computed tomography angiography (CCTA) or intravascular ultrasound were not available to further characterize the anatomical depth and length of the bridged segments. Additionally, formal stress testing was not conducted. Finally, follow-up duration was relatively short and based on symptom resolution rather than objective ischemia assessment.