Relação entre excreção de sódio urinário 24 horas e rigidez arterial entre hipertensos controlados e hipertensos resistentes

Abstract

Systemic arterial hypertension is one of the major risk factors for the development of cardiovascular disease and target organ damage that leads to fatal events around the world. Sometimes, hypertension becomes difficult to control in several situations, thus characterizing resistant hypertension, which requires a more intensive therapeutic approach. Its pathophysiological mechanism is associated with changes in the blood pressure regulatory system, exacerbation of renin-angiotensinaldosterone system activity, and increased sensitivity to sodium. The participation of sodium in controlling blood pressure is well established. However, the deleterious effects of high dietary sodium intake on vasculature have been of increasing interest. Objectives: To compare the influence of dietary sodium intake through 24-hour urinary sodium excretion on markers of arterial stiffness in hypertensive subjects with controlled and resistant hypertension. Casuistic and methods: A prospective crosssectional observational study was conducted between two groups of hypertensive patients. Twenty-six patients were randomized and divided into controlled hypertensive patients (n = 63) and resistant hypertensive patients (n = 63). Patients underwent physical and laboratory exams of 24-hour urinary sodium excretion and non-invasive hemodynamic studies using the SphygmoCor® and Mobil-O-Graph® for determination of arterial stiffness and variability of peripheral and central arterial pressure. Results: Clinical characteristics and laboratory tests were similar in both groups. There was no statistically significant difference between the controlled hypertensive and resistant hypertensive groups to the values of urinary sodium excretion 24 hours (Na + Ur24h) 186.60 ± 92.15 versus 179.76 ± 66.91 mEq/L, respectively. Mean values of carotidfemoral pulse wave velocity (carotid-femoral PWV) for the hypertensive controlled group were (10.52 ± 2.47 m/s) and for the resistant hypertensive group were (10.21 ± 2.27 m/s). There was a significant difference between the controlled hypertensive and resistant hypertensive groups evaluated by 24-hour ambulatory blood pressure monitoring (ABPM24h). The resistant hypertensive group had higher cardiac output during sleep and greater vascular resistance in the 24 hour period and during wakefulness than the controlled hypertensive group (p <0.05). Conclusion: Controlled hypertensive and resistant hypertensive groups were similar in relation to the values of arterial stiffness evaluated by PWV and in relation to sodium excretion, but a better adherence to restriction in dietary sodium consumption by the resistant hypertensive group was observed.