Arterial Stiffness in Resistant Hypertension: From Physiology to Medical Practice

Considering that the risks of cardiovascular disease still pose a significant challenge despite preventive and therapeutic efforts, we need new pathophysiological models for a better understanding of risks and treatment based on new concepts. Arterial Stiffness (AS) has been increasingly studied as an independent cardiovascular risk factor. The mechanisms by which AS develops are not yet fully understood. However, it clearly involves not only structural changes but also endothelial functional changes. There are several clinical studies showing that vascular damage is an important risk factor for structural and functional injury of high-flow organs. Carotid-femoral Pulse Wave Velocity (PWV-cf) has been considered the gold standard for the evaluation of AS, with a large body of evidence demonstrating its association with cardiovascular disease, regardless of traditional risk factors. Based on the impact of high PWV-cf on cardiovascular prognosis, achieving a decrease in PWV would possibly reduce cardiovascular events. However, the significance of lowering AS to reduce cardiovascular events under treatment remains to be unequivocally demonstrated. Regarding resistant hypertension, it shares risk factors with AS, including advanced age, endothelial dysfunction, left ventricular hypertrophy, obesity, diabetes, and chronic kidney disease. On the other hand, increased AS in resistant hypertensives presents a two-way interaction, where uncontrolled blood pressure results in progressive vascular damage while vascular stiffness increases blood pressure, making its control more difficult and establishing a vicious circle. In this scenario, the better the understanding of the complex interaction of factors to AS development, the more treatment options should become clinically available.