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Abstract #18356 Published in IGR 3-3
Exacerbation of angina associated with latanoprost
Mitra M; Chang B; James TBritish Medical Journal (Clinical Research Edition) 2001; 323: 783
Latanoprost is a prostaglandin F2α analogue used to treat open-angle glaucoma. Ocular side-effects include conjunctival hyperemia, iris pigmentation, anterior uveitis, and cystoid macular edema in patients who have had surgery for cataract. The authors report a patient developing an exacerbation of angina while receiving treatment with latanoprost for glaucoma. A 73-year-old man was referred with pseudoexfoliative glaucoma. He had peripheral vascular disease and ischemic heart disease. His symptoms were well controlled with glyceryl trinitrate, amlodipine, and clopidogrel. He was prescribed latanoprost 0.005% eye drops once daily. Four weeks later, he noticed the onset of angina within 45 minutes to one hour of instillation of the drop. He increased his dose of glyceryl trinitrate to alleviate the pain. Assuming that latanoprost was exacerbating his angina, he stopped taking the drops. This ameliorated his angina. Over the next ten days he rechallenged himself three times with latanoprost, and each time he experienced angina within an hour of taking the drug. Latanoprost was therefore discontinued. His glaucoma is now controlled by dorzolamide eye drops, and his angina is now stable. The authors know of no published report of exacerbation of angina by latanoprost. The Latanoprost Study Group reported no adverse systemic side-effects, and reports to the Medicines Control Agency are rare. The authors postulate two possible ways that latanoprost may cause angina. Prostaglandin F2α is a known vasoconstrictor and the systemic absorption of latanoprost applied topically can induce vasoconstriction in the coronary vessels, causing angina, especially in patients with unstable angina. Several prostaglandins, including prostaglandin F2α, have been shown to induce hypertrophy of cardiac myocytes in an animal model by the expression of c-fos, atrial natriuretic factor, and a skeletal actin. Ventricular hypertrophy can lead to abnormally increased oxygen demand, thereby causing myocardial ischemia and angina in an already compromised heart. Although there is no quantitative proof of the angina in the form of an ST segment ischemia on electrocardiography, this patient experienced worsening angina on rechallenge on three separate occasions. The authors have reported this incident to the Medicines Control Agency and the manufacturer.
Dr M. Mitra, Royal Halifax Infirmary, Halifax HX1 2YP, UK
Classification:
11.4 Prostaglandins (Part of: 11 Medical treatment)
