Abstract

Decreased heart-rate-variability (HRV) indicates increased sympathetic nervous system (SNS) activity and modulation with a shift in the sympatho-vagal balance towards SNS predominance. Increased SNS activity may precede volume-loading hypertension, contribute to increases in cardiac troponin T (cTnT), endothelial dysfunction and small vessel disease. Therefore, we investigated the retinal vasculature, HRV during flicker-light-induced-provocation (FLIP) and systemic cTnT, a marker of cardiac stress, to provide further evidence in support of the brain-retina-heart link. Cross-sectional observations were obtained from a bi-ethnic cohort (N = 264), aged 23-68 years. Fasting serum samples for cTnT were obtained. Retinal vascular calibres were quantified from mydriatic eye fundus images and dynamic retinal vessel calibre responses were determined during FLIP. Time-and frequency domain parameters of HRV were calculated during FLIP for each participant. Africans had wider venules and attenuated time domain parameters during FLIP. In Africans, inverse associations emerged between arteriolar dilation and both cTnT and root-mean squared of the standard deviations of successive RR-intervals (rMSSD) (p = 0.030), and between arteriolar constriction and both low-frequency expressed in normalised units (LFnu) (p = 0.003) and high-frequency expressed in normalised units (p = 0.021). Wider venules inversely associated with standard deviation of the NN intervals (SDNN) as well as LFnu (p = 0.009) in Africans. An opposite profile was observed in Caucasians with both time-and frequency domain parameters of HRV in relation to retinal vessel structure and function. FLIP elicited increased SNS activity and modulation in this bi-ethnic cohort. In Africans, decreased HRV during FLIP accompanied arteriolar and venular responses and elevated systemic levels of cTnT, implying that the SNS exerted a significant effect on the smooth muscle tone of the retinal vasculature. Disrupted retinal autoregulation may imply general autonomic nervous system dysfunction; exemplifying central control by the brain on all systemic regulatory functions, across different vascular beds.

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