Invited Symposium: Glaucoma: Diagnosis and Therapy
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Introduction
0,25 % Betaxolol ophthalmic suspension is a potentially vasodilating selective betablocker (3) that may change the velocity of small orbital vessels if its effect were the same of 0,50 % ophthalmic solution as reported by A.Harris et al.(2) who found decreased resistivity index of medial short posterior ciliary artery in patients with normal tension glaucoma, and by K.Emi and Y.Uji (1,5) who found short and longterm increased velocity of central retinal artery and posterior ciliary artery after 0,5% Betaxolol topical administration . The aim of the study was to evaluate blood flow velocity of ophthalmic artery (OA), central retinal artery (CRA), medial short ciliary artery (mSPCA), heart rate, arterial pressure and intraocular pressure (IOP) at baseline and two weeks after 0,25% Betaxolol suspension.
Materials and Methods
We selected fourteen patients with minor glaucomatous visual field defects or ocular hypertension but no systemic disease, and twelve healthy volunteers.The age of these subjects ranged between 42 and 59 (average 52) and between 41 and 56 (average 51) years respectively in patients and controls. After adeguate washout measurements of peak systolic velocity (PSV) and resistivity index (RI) of OA, CRA and mSPCA were performed by means of a GE LOGIQ 500 color doppler unit equipped with a 6.5 MHZ transducer in both patients and controls; intraocular pressure, blood pressure and heart rate were also recorded. Both patients and controls were fully re-evaluated two weeks after 0,25% Betaxolol suspension twice a day.
Results
No significant inter or intragroup difference was found between PSV and RI in the three examined orbital vessels before and after Betaxolol treatment both in patients and controls:
Mean ± SD in PSV (and RI) of OA were 31,6 ± 7,1 (0,72 ± 0,07) and 31.9± 8,8 (0,72 ± 0,07) cm/sec before treatment and 30.6 ± 6.5 (0,71 ±0,06) and 34,2 ± 9,8 (0,71 ± 0,07) cm/sec after treatment in patients and controls respectively.
Mean ± SD in PSV (and RI) of CRA were 10,4 ± 2,4 (0,69 ± 0,08) and 10,8 ± 0,9 ( 0,7 ± 0,05 ) cm/sec before treatment and 11 ± 2,6 ( 0,68 ± 0,10 ) and 10,8 ± 2,5 ( 0,7 ± 0,06 ) cm/sec after treatment in patients and controls respectively.
Mean ± SD in PSV (and RI) of mSPCA were 10,8 ± 2,9 (0,66 ±0,08) and 11 ± 2,4 (0,68 ±0,07) cm/sec before treatment and 10,7 ± 2,9 (0,67 ± 0,09) and 10,4 ± 2,8 ( 0,70 ± 0,06) cm/sec after treatment in patients and controls respectively.
IOP significantly decreased (p smaller than 0.01) in glaucoma patients only; systolic and diastolic arterial pressure and heart rate did not significantly change in the two groups before and after
Betaxolol treatment:
Mean ±SD in IOP were 21.5 ±2.6 and 17 ±3.5 before treatment, and 16.8 ±3 and 16.5 ± 4 mmHg after treatment in patients and controls respectively.
Mean ± SD in systolic (and diastolic) blood pressure were 128± 10.9 (85.4 ± 9.1) and 130.5 ±15.7 (80 ± 11.1) mmHg before treatment , and 140 ±14.4 ( 84.4 ± 10.1) and 139 ±11 (78 ± 6.6) mmHg after treatment in patients and controls respectively.
Mean ±SD heart rate were 78.2 ± 7.5 and 73.5 ± 6.7 before treatment , and 81 ±10.3 and 73.8 ± 8.5 after treatment in patients and controls respectively.
Discussion and Conclusion
The strict patient selection with special concern on relatively young age, absence of cardiovascular disease or advanced POAG may account for the similar peak systolic velocity (PSV) and resistive index (RI) measurements of blood flow in orbital vessels compared with controls; so we cannot confirm the hemodynamic changes found by other researchers (1,2,5) after 0.5% Betaxolol.
The absence of significant variation in blood flow velocity of orbital vessels ( and probably flow, but we cannot measure the diameter of the vessels ! ) , in arterial pressure and, interestingly, in heart rate of both glaucoma patients and controls after 0.25% Betaxolol indicates negligible or undetectable systemic absorption of the topical slowly released IOP lowering drug.
However a longer follow-up of a larger series of patients seems necessary in order to ascertain the substantial lack of cardiovascular effects of 0.25% Betaxolol suspension; on the other hand it is worthwhile to note that also Nicolela and al. (4) were unable to detect significative change in PSV and RI of CDI examined orbital vessels (OA,CRA,SPCA) after either 0.5% Timolol or 0.05% Latanoprost in patients with open angle glaucoma or ocular hypertension.
References
1. K. Emi , Nakai Y, Ito Y, Nishi A, Uij Y. The change of blood flow velocity in the orbital arteries in glaucomas after the instillation of 0,5 % Betaxolol. AAO 1995, Atlanta, Georgia, Abstract # 211.
2. A. Harris, G.L.Spaeth, R.C. Sergott, L.J. Katz, L.B. Cantor, B.J. Martin. Retrobulbar Arterial Hemodynamic Effects of Betaxolol and Timolol in normal- tension glaucoma. Am J Ophthalmol 1995;120:168-175.
3. R.K. Hester, Z. Chen, E.J. Becker, M. McLaughlin, L. De Santis. The direct vascular relaxing action of Betaxolol, Carteolol and Timoptol in porcine long ciliary artery. Surv. Ophthalmol. 1994, 38: 125-133.
4. MT Nicolela, AR Buckley, BE Walman, SM Drance. A compatative study of the effects of timolol and latanoprost on blood flow velocity of the retrobulbar vessels. Am J Ophthalmol 1996; 122: 784-789
5. Y. Uij. Effects of betablockers on blood velocities in the orbital arteries in chronic open angle glaucoma. In vascular risk factors and neuroprotection in glaucoma- Update 1996. S.M. Drance ed. 1997 Kugler Publ. Amsterdam pp 241-248.
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