What is the medication for myocardial bridging?

Medical Management of Myocardial Bridging

Beta-blockers are the first-line medication for symptomatic myocardial bridging, and nitrates are contraindicated as they paradoxically worsen symptoms. 1, 2, 3

First-Line Therapy: Beta-Blockers

Beta-blockers should be initiated in all patients with symptomatic myocardial bridging or evidence of ischemia. 1 The mechanism is straightforward: beta-blockers reduce heart rate and myocardial contractility, which decreases the systolic compression of the bridged coronary segment and prolongs diastole to improve coronary perfusion. 1, 2

Specific Beta-Blocker Selection

• Metoprolol (extended-release metoprolol succinate preferred) is commonly used, with target dosing aimed at achieving a resting heart rate of 55-60 beats per minute. 4

• Carvedilol or bisoprolol are appropriate alternatives, particularly if the patient has concurrent left ventricular dysfunction (LVEF ≤40%), where carvedilol may offer superior outcomes. 4, 5

• Avoid beta-blockers with intrinsic sympathomimetic activity as they are less effective for anti-ischemic purposes. 4

Second-Line Therapy: Non-Dihydropyridine Calcium Channel Blockers

If beta-blockers are contraindicated (e.g., severe bradycardia, heart block, active bronchospasm, hypotension) or symptoms persist despite adequate beta-blockade, non-dihydropyridine calcium channel blockers (diltiazem or verapamil) are the next option. 4, 3

• Diltiazem: 120-360 mg daily (extended-release formulation), titrated based on heart rate and blood pressure response. 6, 7

• Verapamil: Similar dosing strategy, but avoid in patients with heart failure or LVEF <40%. 4, 6

• These agents slow heart rate and reduce myocardial contractility through AV nodal effects and negative inotropy, similar to beta-blockers. 4

Critical Contraindication: Nitrates

Nitrates are absolutely contraindicated in myocardial bridging. 1, 2, 3 This is a critical pitfall to avoid. Nitrates cause vasodilation and increase myocardial contractility reflexively, which paradoxically worsens systolic compression of the bridged segment and exacerbates symptoms. 1, 2

Management Algorithm

1. Confirm diagnosis: Coronary angiography showing characteristic systolic compression ("milking effect") of the vessel during the cardiac cycle. 1, 2

2. Assess for ischemia: Perform stress testing (exercise ECG, dobutamine stress echo, or myocardial perfusion scintigraphy) to document inducible ischemia in symptomatic patients. 1

3. Initiate beta-blocker therapy: Start with metoprolol succinate or carvedilol, titrating to target heart rate of 55-60 bpm. 4, 1

4. If beta-blockers fail or are contraindicated: Add or switch to diltiazem or verapamil. 4, 3

5. Avoid nitrates entirely: Do not prescribe short-acting or long-acting nitrates for chest pain relief. 1, 2

6. Reserve invasive therapy for refractory cases: Surgical myotomy or coronary artery bypass grafting may be considered only when medical therapy fails and symptoms remain severe. 3

Special Considerations

• Asymptomatic patients: No treatment is required for incidentally discovered myocardial bridging without symptoms or ischemia. 1

• Competitive athletes: Asymptomatic athletes can participate in all sports without restriction, but symptomatic athletes should be restricted from high-intensity activities until symptoms resolve and stress testing normalizes. 1

• Hypertrophic cardiomyopathy: Myocardial bridging occurs in 30-50% of these patients, making beta-blocker therapy particularly important. 1

Common Pitfalls

• Misdiagnosing as typical coronary artery disease: Myocardial bridging presents with angina and ECG changes indistinguishable from acute coronary syndrome, but the underlying pathophysiology is entirely different. 8

• Prescribing nitrates: This is the most dangerous error, as nitrates worsen symptoms rather than relieve them. 1, 2

• Stenting the bridged segment: Intracoronary stents have poor long-term outcomes due to stent fracture and restenosis from repetitive systolic compression. 3