Intravitreal ranibizumab may induce retinal arteriolar vasoconstriction in patients with neovascular age-related macular degeneration.
OBJECTIVE
To study the effect of intravitreal (IVT) ranibizumab (Lucentis; Genentech, Inc, San Francisco, CA) on the retinal arteriolar diameter in patients with neovascular age-related macular degeneration (AMD).


METHODS
Prospective consecutive interventional case series.


METHODS
Eleven eyes of eleven patients with previously untreated neovascular AMD.


METHODS
All eyes had 3 monthly IVT injections of ranibizumab. The diameter of the retinal arterioles was measured in vivo with a retinal vessel analyzer (RVA) before the first IVT injection and then 7 and 30 days after the first, second, and third injections.


METHODS
Primary end points were changes in retinal arteriolar diameter and mean arterial pressure (MAP) after IVT ranibizumab. Secondary end points were changes in best-corrected visual acuity (BCVA), central retinal thickness, and intraocular pressure after IVT ranibizumab, and appearance of adverse events during the follow-up period.


RESULTS
A significant decrease of the retinal arteriolar diameter was observed after each IVT injection of ranibizumab. Thirty days after the first, second, and third injections, there was a mean decrease of 8.1+/-3.2%, 11.5+/-4.4%, and 17.6+/-7.4%, respectively, of the retinal arteriolar diameter compared with baseline values (P<0.01). There was no significant change in MAP during the period of follow-up (P>0.05). Thirty days after the third IVT injection of ranibizumab, mean BCVA improved by 6.5+/-4.9 Early Treatment Diabetic Retinopathy Study (ETDRS) letters, and central retinal thickness decreased by 91+/-122 microm (P = 0.03).


CONCLUSIONS
These results suggest that IVT ranibizumab may induce retinal arteriolar vasoconstriction in patients with neovascular AMD after IVT ranibizumab. Further studies evaluating larger sample sizes are needed to confirm these results and potential adverse effects on the retinal circulation in patients with AMD and retinal vascular diseases.


BACKGROUND
The author(s) have no proprietary or commercial interest in any materials discussed in this article.
Papadopoulou
Domniki N
DN
Vitreo-retinal Unit, Department of Ophthalmology, 22 rue Alcide Jentzer, Geneva, Switzerland.
Mendrinos
Efstratios
E
Mangioris
Georgios
G
Donati
Guy
G
Pournaras
Constantin J
CJ
D000368:Aged; D000369:Aged, 80 and over; D020533:Angiogenesis Inhibitors / Q000008:administration & dosage*; D000911:Antibodies, Monoclonal / Q000008:administration & dosage*; D061067:Antibodies, Monoclonal, Humanized; D001160:Arterioles / Q000503:physiopathology; D020256:Choroidal Neovascularization / Q000188:drug therapy / Q000503:physiopathology*; D005260:Female; D005451:Fluorescein Angiography; D006801:Humans; D007267:Injections; D007429:Intraocular Pressure / Q000502:physiology; D008268:Macular Degeneration / Q000188:drug therapy / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies; D000069579:Ranibizumab; D012160:Retina / Q000473:pathology; D012161:Retinal Artery / Q000503:physiopathology*; D042461:Vascular Endothelial Growth Factor A / Q000037:antagonists & inhibitors; D014661:Vasoconstriction / Q000502:physiology*; D014792:Visual Acuity / Q000502:physiology; D014822:Vitreous Body
D020533:Angiogenesis Inhibitors; D000911:Antibodies, Monoclonal; D061067:Antibodies, Monoclonal, Humanized; D042461:Vascular Endothelial Growth Factor A; D000069579:Ranibizumab