Details

Autor(en) / Beteiligte

• Bellido, Claudio A.
• Iavícoli, Oscar R.
• Piñeiro, Daniel J.
• Rusak, Eduardo J.
• Sanz, Alejandro P.
• Vazquez, Sonia T.
• Pittaluga, Enrique L.
• Lerman, Jorge

Titel

P-262: Continuous improvement of arterial compliance beyond blood pressure decrease after three years of antihypertensive treatment

Ist Teil von

• American journal of hypertension, 2004-05, Vol.17 (S1), p.128A-128A

Ort / Verlag

Oxford: Oxford University Press

Erscheinungsjahr

2004

Quelle

Oxford Journals 2020 Medicine

Beschreibungen/Notizen

• Pulse wave velocity (PWV) is a reliable marker of arterial compliance. Large and elastic arteries' stiffness leads to a faster propagation of pulse wave. Studies concerning the long term effects of antihypertensive treatment on PWV are scarce. The aim of the study was to evaluate long term changes in arterial compliance due to treatment inhibiting the renin-angiotensin-aldosterone system (RAAS), and its relationship with systolic (SBP) and diastolic (DBP) blood pressure decrease. We determined PWV (COMPLIOR®), SBP and DBP, at baseline and throughout 60 months, in 55 previously untreated hypertensive patients (17 men and 38 women, aged 53.3 ± 9.6 years, range 38-73 years at baseline). All patients received either angiotensin converting enzyme inhibitors or angiotensin receptor blocking agents at useful doses to control blood pressure. All patients were followed-up during 60 months. The statistical analysis was performed by means of ANOVA with α=0.05. SBP and DBP decreased during the first year without significant changes thereafter. PWV showed a continuous and significant decrease throughout the follow-up period, but its rate of reduction since the third year was more evident than the decrease of SBP and DBP (p<0.0001 to SBP and p<0.03 to DBP). Anti-hypertensive treatment blocking the RAAS results in decrease of PWV independently of its effect on BP after the third year. This observation could be related with changes in arterial remodeling due to ACE inhibition. (See Figure) Am J Hypertens (2004) 17, 128A–128A; doi: 10.1016/j.amjhyper.2004.03.337