What are alternative treatments for glaucoma if timolol (beta blocker) is causing bradycardia (abnormally slow heart rate)?

Alternative Glaucoma Treatments When Timolol Causes Bradycardia

Discontinue timolol immediately and switch to a prostaglandin analog (latanoprost, bimatoprost, or travoprost) as first-line alternative therapy, as these agents are equally or more effective than timolol for reducing intraocular pressure without systemic cardiac effects. 1

Immediate Management of Timolol-Induced Bradycardia

• Stop the timolol eye drops immediately upon recognition of symptomatic bradycardia, as case series demonstrate that heart rate normalizes (returns to 60-100 bpm) after discontinuation 2
• Timolol is systemically absorbed (~80% of the ophthalmic dose enters systemic circulation, bypassing first-pass metabolism), causing beta-adrenergic blockade comparable to oral administration 3
• The FDA label explicitly warns that timolol can precipitate cardiac failure and bradycardia, particularly in patients with pre-existing cardiac conditions 4

First-Line Alternative: Prostaglandin Analogs

Prostaglandin analogs (bimatoprost, latanoprost, travoprost) should be the immediate replacement therapy as they:

• Demonstrate equivalent or superior IOP reduction compared to timolol 0.5% 1
• Lack systemic cardiovascular effects since they work via local prostaglandin receptors in the eye 1
• Require once-daily dosing (typically at bedtime) 1
• Are well-tolerated with primarily local ocular side effects (iris pigmentation changes, eyelash growth) 1

Second-Line Alternatives

If prostaglandin analogs are contraindicated or ineffective, consider:

• Alpha-2 agonists (brimonidine): Reduce aqueous humor production without beta-blockade effects, though may cause fatigue and dry mouth through central alpha-2 effects 1
• Carbonic anhydrase inhibitors (dorzolamide, brinzolamide): Topical formulations reduce IOP without cardiac effects, though less effective than prostaglandins or timolol 1
• Rho kinase inhibitors (netarsudil): Newer agents that increase aqueous outflow without systemic cardiovascular effects 1

Critical Patient-Specific Considerations

Identify high-risk patients before bradycardia develops:

• Patients with CYP2D6 poor metabolizer status have 2-3 fold higher plasma timolol levels and are at substantially increased risk for bradycardia 5, 3
• Concomitant use of CYP2D6 inhibitors (paroxetine, fluoxetine) or other beta-blockers dramatically increases bradycardia risk 3
• Pre-existing conduction disorders (sick sinus syndrome, second- or third-degree AV block) are absolute contraindications to timolol 4
• The FDA label specifically contraindicates timolol in patients with bradycardia <50 bpm 4

Monitoring After Switching Therapy

• Verify IOP control 2-4 weeks after switching to alternative agent, as prostaglandin analogs may take several weeks to reach maximal effect 1
• Document resolution of bradycardia symptoms (dizziness, syncope, fatigue) after timolol discontinuation 2
• Consider ECG if bradycardia was severe or symptomatic to rule out persistent conduction abnormalities 3

Common Pitfalls to Avoid

• Do not continue timolol at reduced frequency or concentration - even 0.1% gel formulations cause significant systemic absorption and bradycardia, particularly during exercise 5
• Do not substitute with other topical beta-blockers (betaxolol, levobunolol, carteolol) as all carry similar cardiac risks 4
• Do not use non-dihydropyridine calcium channel blockers as alternatives, as these also cause bradycardia and AV block 6
• Avoid combination products containing timolol (e.g., timolol/dorzolamide, timolol/brimonidine) as the beta-blocker component remains problematic 3