Key result
Zofenopril significantly reduced oxidative stress and adhesion molecules (P<0.05) and increased flow-mediated dilation (P<0.001) in mildly hypertensive patients compared to ramipril and atenolol.
Why the study?
Does zofenopril improve endothelial function and reduce oxidative stress compared to ramipril or atenolol in essential mildly hypertensive patients?
RCT (n=90)
randomized
Does zofenopril improve endothelial function and reduce oxidative stress compared to ramipril or atenolol in essential mildly hypertensive patients?
p-value: p=<0.001
Zofenopril, a sulfhydryl-containing ACE inhibitor, improves endothelial function and reduces oxidative stress in mildly hypertensive patients beyond its blood pressure-lowering effects.
May favor zofenopril selection for endothelial benefits in mild hypertension; extends pleiotropic data on sulfhydryl ACEIs beyond BP reduction.
BACKGROUND: Oxidative inactivation of nitric oxide (NO) is regarded as an important cause of reduced endothelium-dependent vasodilation in essential hypertension. Because zofenopril, an angiotensin-converting enzyme (ACE) inhibitor with a sulfhydryl (SH) group, has demonstrated antioxidant properties and to reduce adhesion molecule expression in vitro, in this study we evaluated the effect of this drug in comparison with the carboxylic ACE inhibitor ramipril and the beta-adrenoreceptor blocker atenolol on (1) circulating adhesion molecules and some oxidative stress parameters and (2) endothelium-dependent vasodilation in essential mildly hypertensive patients. METHODS: A total of 45 healthy subjects and 45 matched hypertensive patients participated in the study. Hypertensive patients were randomly treated with zofenopril (15 to 30 mg/d), ramipril (2.5 to 5 mg/d), and atenolol (50 to 100 mg/d). At baseline and after an 8-week therapy we evaluated blood pressure (BP) values, plasma and LDL hydroperoxides, plasma 8-isoprostanes, circulating levels of oxidized-(ox)LDL and of adhesion molecules (intercellular cell adhesion molecule-1 [ICAM-1], and vascular cell adhesion molecule-1 [VCAM-1], and E-selectin). Furthermore, all patients underwent ultrasound detection of brachial artery reactivity and endothelium-dependent dilation (flow-mediated dilation, FMD) was evaluated. RESULTS: All the treatments determined similar significant (P < .001) reduction of both systolic and diastolic BP values. Plasma (P < .01) and LDL hydroperoxides (P < .01), plasma 8-isoprostanes (P < .05), circulating oxLDL (P < .05), and adhesion molecules (P < .05) were significantly reduced only in patients receiving zofenopril. Similarly FMD was significantly increased (P < .001) in the zofenopril-treated group. CONCLUSIONS: Our results suggest that in mildly hypertensive patients without organ damage zofenopril, beyond its BP-lowering effects and through its sustained antioxidant activity, offers important advantages in reducing endothelial activation.
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Pasini et al. (2007) conducted an RCT in Essential mild hypertension (n=90). Zofenopril vs. Ramipril (2.5 to 5 mg/d) and atenolol (50 to 100 mg/d) was evaluated on Circulating adhesion molecules, oxidative stress parameters, and endothelium-dependent vasodilation (FMD) (p=<0.001). Zofenopril significantly reduced oxidative stress and adhesion molecules (P<0.05) and increased flow-mediated dilation (P<0.001) in mildly hypertensive patients compared to ramipril and atenolol.