Impact of hypertension on choroidal thickness in central serous chorioretinopathy

Abstract

 

Purpose

 

To study the association between blood pressure (BP) and choroidal thickness (ChT) in central serous chorioretinopathy (CSCR).

 

Methods

 

Consecutive treatment naïve CSCR patients and healthy controls were prospectively recruited. Examinations included resting blood pressure (BP), intraocular pressure (IOP) and enhanced depth optical coherence tomography (EDI OCT). Patients with CSCR were sub-divided into 2 groups: 1) normotensive if BP<140/90 mmHg without medication and 2) hypertensive if on anti-hypertensive medication or if systolic BP ≥140 mmHg and/or diastolic BP of ≥90 mmHg without anti-hypertensive medication. The mean macular choroidal thickness (MChT) was calculated by averaging ChT of the 9 Early Treatment Diabetic Retinopathy Study (ETDRS) subfields. The ocular perfusion pressure (OPP) was calculated as 2/3 × (MAP-IOP) (MAP: mean arterial BP; BP_diast+1/3(BP_syst-BP_diast)). A univariate analysis with Bonferroni correction was used to compare ChTs between groups.

 

Results

 

42 CSCR patients (age 47±12 years) and 25 healthy controls (age 42±7 years) were recruited between September 2013 and October 2014. 52.4% CSCR patients had hypertension at presentation. The mean MChT (95% confidence interval) of healthy controls, normotensive and hypertensive CSCRs was 334 (296-371) µm, 408 (366-450) µm and 464 (421-507) µm, respectively. The MChT and ChT of all ETDRS subfields of hypertensive CSCR were thicker compared to healthy controls (p<0.001).The MChT and ChT of 7 out of 9 ETDRS subfields of normotensive CSCR were significantly thicker than those of controls (p<0.05) except for inner and outer nasal subfields. There was no statistically significant difference in MChT or ETDRS ChT between normotensive and hypertensive CSCR patients (p>0.05). In hypertensive CSCR, there was a statistically significant correlation between the OPP and ChTs for outer temporal and inner superior ETDRS subfields (p<0.05), but not in the normotensive CSCR or healthy controls.

 

Conclusions

 

The role of hypertension and its effect on choroid vasculature in CSCR has not been previously explored. Majority of CSCR patients in our study had hypertension and ChT was thickest in this group. This indicates that hypertension is an under-recognised risk factor in the pathogenesis of CSCR. The choroidal vascular bed of hypertensive CSCR may be more vulnerable to systemic changes than that of the normotensive CSCR.