Obesity-related hypertension is commonly characterized by increased sympathetic nerve activity and is therefore acknowledged as a predominantly neurogenic form of hypertension. The sustained sympatho-excitation not only contributes to the rise in blood pressure but also elicits a vicious cycle which facilitates further weight gain and progression of associated co-morbidities. While weight loss and exercise remain at the forefront of therapy for obesity and obesity-related hypertension, the difficulties in achieving and maintaining long-term weight loss with lifestyle measures and the variable blood pressure response to weight loss often necessitate prescription of antihypertensive drug therapy. Remarkably, there are no specific recommendations for pharmacologic treatment for obese patients with arterial hypertension in any of the current guidelines and general principles of antihypertensive treatment are applied. The use of β-blockers and diuretics is commonly discouraged as first- or second-line therapy due to their unfavorable metabolic effects. This review explores evolving therapeutic strategies which based on their interference with pathophysiologic mechanism relevant in the context of obesity may guide optimized treatment of obesity-related hypertension.
Microvascular disease and rarefaction are key pathological hallmarks of hypertension. The retina uniquely allows direct, non-invasive investigation of the microvasculature. Recently developed optical coherence tomography angiography now allows investigation of the fine retinal capillaries, which may provide a superior marker of overall vascular damage. This was a prospective cross-sectional study to collect retinal capillary density data on 300 normal eyes from 150 hypertensive adults, and to investigate possible associations with other organ damage markers. The average age of participants was 54 years and there was a greater proportion of males (85; 57%) than females. Multivariate, confounder adjusted linear regression showed that retinal capillary rarefaction in the parafovea was associated with increased pulse wave velocity (β = − 0.4, P = 0.04), log-albumin/creatinine ratio (β = − 0.71, P = 0.003), and with reduced estimated glomerular filtration rate (β = 0.04, P = 0.02). Comparable significant associations were also found for whole-image vascular-density, for foveal vascular-density significant associations were found with pulse wave velocity and estimated glomerular filtration rate only. Our results indicate that retinal capillary rarefaction is associated with arterial stiffness and impaired kidney function. Retinal capillary rarefaction may represent a useful and simple test to assess the integrated burden of hypertension on the microvasculature irrespective of current blood pressure levels.
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