Key result
After 8 weeks of treatment in hypertensive patients, neither ramipril nor telmisartan significantly changed the Reactive Hyperemia Index (p=0.256 between groups).
Why the study?
Does ramipril improve endothelial function compared to telmisartan in hypertensive patients?
RCT (n=20)
Web-based randomization program
No
Does ramipril improve endothelial function compared to telmisartan in hypertensive patients?
In hypertensive patients, 8 weeks of treatment with ramipril or telmisartan similarly reduced blood pressure without significantly changing overall endothelial function, though pulse pressure reduction correlated with endothelial improvement only with ramipril.
Answers are grounded in this paper and cite their sources.
Neither ramipril nor telmisartan improves endothelial function by RHI after 8 weeks; challenges short-term vascular benefit assumptions beyond BP reduction.
Endothelium has a function to regulate vascular tone by releasing mediators either vasodilating or vasoconstricting blood vessels. Endothelial dysfunction can be measured conveniently by Reactive Hyperemia Index (RHI) with a peripheral arterial tonometry. Angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin II (AT II) receptor blockers (ARBs) are considered to have beneficial effects on endothelium through inhibition of AT II. This study was performed to compare the effect of ACEIs or ARBs on endothelial function estimated by RHI in hypertensive patients. Twenty consecutive patients with hypertension (57.9 ± 11.3 years, 60% men) were assigned to receive treatment with ramipril or telmisartan for eight weeks (n = 10 per group). Blood pressure (BP) and RHI were measured at baseline and after eight weeks treatment. The two groups were similar in terms of demographic and laboratory characteristics. But baseline systolic BP and pulse pressure (PP) were higher in telmisartan group than ramipril group (systolic BP, 159 ± 6.83 vs 150 ± 7.49, p = 0.028; PP, 75.0 ± 14.0 vs 60.3 ± 12.4, p = 0.034). In both groups, systolic and diastolic BP decreased significantly after eight weeks treatment (p < 0.05 for each). Although PP reduced in both group (ramipril group, 60.3 ± 12.4 mm Hg to 50.4 ± 7.60 mm Hg; telmisartan group, 75.0 ± 14.0 mm Hg to 57.4 ± 15.1 mm Hg), change was statistically remarkable only in telmisartan group. During eight weeks, there was no significant changes of RHI in both groups. There was a positive relationship between decrease of PP after 8 weeks and the improvement of endothelial function only in ramipril group, but not in telmisartan group (ramipril group, r = 0.671, p = 0.034; telmisartan group, r = −0.487, p = 0.153). Despite PP reduction effect favoring endothelial function, it’s not correlated with RHI improvement with telmisartan. These findings suggest telmisartan itself may negatively influence endothelium dependent vasodilatation different from ramipril.
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Ki et al. (2017) conducted an RCT in Essential hypertension (n=20). Ramipril vs. Telmisartan 40 mg once a day was evaluated on Reactive Hyperemia Index (RHI) at 8 weeks (p=0.256). After 8 weeks of treatment in hypertensive patients, neither ramipril nor telmisartan significantly changed the Reactive Hyperemia Index (p=0.256 between groups).
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