ETD

• adaptive optics
• hypertensive retinopathy
• microcirculation
• wall-lume ratio

Hypertension and obesity represent the most prevalent cardiometabolic phenotype, with microcirculation as common target. Retinal microcirculation is a privileged window into systemic microvascular health, offering a promising, low-cost and non-invasive approach for the in vivo evaluation of microvascular damage characterizing this cardiometabolic phenotype.
The aim is to investigate the retinal microvascular structure and function using a non-invasive, direct imaging approach to detect early alterations in patients with arterial hypertension and obesity.
We consecutively enrolled 184 patients referred to the Centre for Arterial Hypertension at Pisa University Hospital. All patients underwent assessment of retinal arteriolar morphology using adaptive optics imaging (RTX-1, Imagine Eyes, Orsay, France). Of these, 134 met the eligibility criteria for microvascular structure analysis.
Additionally, we assessed the inflammatory biomarkers and we investigated the impact of antihypertensive therapy on BP-related microvascular decline.
The wall-to-lumen ratio (WLR) was associated with age, and the steepness of the curve was higher in the cardiometabolic phenotype than in the healthy phenotype. Furthermore, patients with hypertension and obesity had a steeper curve than patients with hypertension alone (1.7 times steeper), even when matched for other clinical variables. Inflammatory biomarkers such as the neutrophil-to-lymphocyte ratio showed a positive association with microvascular impairment (p<0.05). Interestingly, ACE-inhibitor therapy alone was able to modify the effect of blood pressure (BP) and age on microvascular decline: in patients administered ACE-inhibitors, the relationship between age, BP, and microvascular impairment was substantially reduced or eliminated.
So, retinal microvascular imaging represents a highly informative, non-invasive method for assessing the health status of the systemic microcirculation in cardiometabolic patients and our results strengthen the notion that the combination of hemodynamic and metabolic stress impairs microvascular homeostasis to a greater extent than either factor alone.