Journal of Clinical and Experimental Ophthalmology
Open Access

Abstract

Are Features of the Metabolic Syndrome Associated with Macular Thickness in Individuals without Diabetes Mellitus?

KM Gooding, AC Shore, H von Lany, R Ling, M Mitra, CI Ball, D Mawson and JE Tooke

Background: Maculopathy is a common feature at diagnosis of type 2 diabetes. However, it is not known whether macular thickening, a potential preclinical sign of macular oedema, occurs in individuals with risk factors for diabetes.
Purposes: To examine whether macular thickness is increased in individuals with features of the metabolic syndrome, namely waist circumference, blood pressure, and fasting levels of triglycerides, HDL-cholesterol and glucose in non-diabetic individuals.
Methods: 50 non-diabetic Caucasian individuals were recruited (25 males, age range: 26-78 years, BMI range: 20-46 kg/m²). Macular thickness, divided into fovea and the inner and outer temporal, nasal, superior and inferior quadrants, was assessed by Optical Coherence Tomography. Additional assessments included: arterial blood pressure, fasting glucose and lipid profile (including triglycerides and HDL-cholesterol), BMI and waist circumference. Features of the metabolic syndrome were collectively entered into a forced regression model to examine their relationship with thickness in the macular subdivisions.
Results: Fovea thickness was within the normal range for all participants. Features of the metabolic syndrome were not collectively associated with macular thickness. However, mean arterial blood pressure (MAP) was independently associated with macular thickness in all regions (standardized beta>0.381, p<0.05) except for the outer nasal quadrant (standardized beta=0.346, p=0.071) and a vascular fovea region (standardized beta=0.105, p=0.591).
Conclusions: MAP, independent of other features of the metabolic syndrome, is associated with thickness in the inner and outer quadrants of the macular. Further research is needed to fully elucidate this relationship. However, potential explanations include altered pressure autoregulation (pressure or metabolic induced) and microvascular rarefaction.