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KMID : 0882420040670030241
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Korean Journal of Medicine
2004 Volume.67 No. 3 p.241 ~ p.248
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Reversal of arterial stiffness by treatment with the angiotensin receptor antagonist irbesartan in essential hypertension
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Kang Ja-Young
Choi Hyun-Ah
Yoon Hong-Sun
Yu Sung-Hoon
Song Min-Joon
Chang Eu-Gene
Kim Hun-Sung
Shin Hyun-Ho
Park Jeong-Bae
Lee Won-Ro
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Abstract
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Background: Alterations of mechanical properties in the vasculature may contribute to complications of hypertension. Since angiotensin II plays a pivotal role in these vascular abnormalities, we tested the hypothesis that the AT1 angiotensin receptor antagonist irbesartan, in contrast to the beta-blocker atenolol, would correct artery stiffness in essential hypertensive patients.
Methods: Thirty untreated essential hypertensive patients (48 +/- 7 years, range 35-65; 72% male) were randomly assigned in a single-blind fashion to irbesartan or atenolol treatment for 6 months. Fifty one age/sex-matched normotensive subjects were also studied. Systemic arterial stiffness (augmentation index; AI) was measured by the pressure transfer function using radial pulse tonometry.
Results: Both treatments reduced blood pressure (BP) to a comparable degree (irbesartan: 160 +/- 19/105 +/- 13 to 133 +/- 16/92 +/- 10 mmHg, p<0.01; atenolol: 166 +/- 17/113 +/- 9 to 132 +/- 15/90 +/- 8 mmHg, p<0.01). Other hemodynamic parameters of peripheral and central arteries showed similar degree of reduction, except significant reduction of central pulse pressure with irbesartan treatment (42 +/- 20 to 29 +/- 8 mmHg, p=0.01 vs 41 +/- 14 to 34 +/- 12 mmHg of atenolol treatment). After 6-month treatment, systemic arterial stiffness (AI) was significantly reduced from 28 +/- 11 to 21 +/- 11% (p=0.01) after irbesartan but atenolol treatment showed no change (from 29 +/- 8 to 29 +/- 13%). Reversal of arterial stiffness correlated mostly with reduction of central pulse pressure (r=0.63, p<0.01).
Conclusion: The AT1 angiotensin antagonist irbesartan corrected the altered arterial stiffness from patients with essential hypertension by reduction of central pulse pressure, whereas the beta-blocker atenolol had no effect.
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KEYWORD
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Blood pressure, Arterial stiffness, Augmentation, Antihypertensive therapy, Angiotensin II receptor
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