Why the study?
Does long-term antihypertensive treatment with renin-angiotensin-aldosterone system inhibitors improve arterial compliance beyond blood pressure reduction in previously untreated hypertensive patients?
Does long-term antihypertensive treatment with renin-angiotensin-aldosterone system inhibitors improve arterial compliance beyond blood pressure reduction in previously untreated hypertensive patients?
Long-term antihypertensive therapy with RAAS inhibitors continuously improves arterial compliance over 5 years, an effect that extends beyond the initial stabilization of blood pressure.
May support RAAS inhibitor benefits on arterial compliance beyond BP reduction; hypothesis-generating and requires RCT confirmation.
Pulse wave velocity is a reliable marker of arterial compliance. Stiffness of large and elastic arteries leads to a faster propagation of pulse wave. The aim of this study was to evaluate changes in arterial distensibility using antihypertensive drugs. This treatment focused on the inhibition of the renin-angiotensin-aldosterone system and the changes produced in blood pressure. Measurements were taken at baseline and throughout 60 months in 66 previously untreated hypertensive patients (22 men and 44 women, aged 54 +/- 9.5 years, range 38-73 years at baseline). All patients received either angiotensin-converting enzyme inhibitors or, in case of adverse effects, angiotensin receptor blockers. To control blood pressure, diuretics, calcium channel blocking agents, or beta blockers were added when appropriate. Statistical analysis was performed by means of ANOVA with alpha = 0.05. Systolic and diastolic blood pressure decreased during the first year without significant changes thereafter. There were no significant changes in pulse pressure. Pulse wave velocity showed a continuous and significant decrease throughout the follow-up period, but its reduction since the third year was more evident than the decrease in systolic and diastolic blood pressure (p < 0.0001 for both). This observation could be related to changes in arterial remodeling probably due to angiotensin-converting enzyme inhibition or renin angiotensin system blockade. Further investigations are needed to establish this relationship.
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Bellido et al. (2006) studied this question.
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