Abstract
Purpose::
To evaluate the vascular response to CO2 provocation in human myopia.
Methods::
The sample comprised 1 eye randomly selected of 66 healthy volunteers, subdivided into two refractive groups by mean spherical equivalent (MSE): 33 emmetropes with MSE ± 0.50D (mean MSE 0.08 ± 0.41; mean age 40.27 ± 16.13 years, range 18-78) and 33 myopic subjects with MSE -1.00 to -9.30D (mean MSE -4.51 ± 2.56; mean age 36.78± 15.00 years, range 20-73). Groups were matched for age, gender and ethnicity. Ocular perfusion was assessed using CDI for the ophthalmic artery (OA), central retinal artery (CRA) and short posterior ciliary arteries (SPCA), Heidelberg Retinal Flowmeter (HRF) for retinal microcirculation and Ocular Blood Flow Analyser (OBFA) for the pulsatile ocular blood flow (POBF) at each of 2 sessions: baseline (B1, breathing room air) and during isoxic hypercapnia (end tidal pCPO2 increased 15% above B1 with constant O2 supply). Blood pressure (BP), intraocular pressure (IOP), and body mass index (BMI) were also recorded.Two-tailed paired student t-test and repeated measure ANOVA were used to analyse the effect of increased pCPO2 breathing on haemodynamic parameters.
Results::
At baseline no differences in age, BMI, systemic BP, mean arterial pressure (MAP) or ocular perfusion pressure (OPP) were found between myopes and emmetropes. During hypercapnia, emmetropes experienced an increase in OA peak systolic velocity (PSv) and OA resistance index (RI) (p=0.008; p=0.019), while in myopes there was a significant increase in MAP (p=0.023), ocular pulse volume (p=0.038) and POBF (p=0.011)
Conclusions::
These data suggest a defective ocular haemodynamic autoregulation, even in low-moderate degrees of myopia. Furthermore, the basis of these vascular defects may lie in autonomic dysregulation in myopic patients.
Keywords: myopia • blood supply