Forearm arterial distensibility in patients with hypertension: Comparative effects of long-term ACE inhibition and β-blocking

Cesaris, R. De; Ranieri, G.; Filitti, V.; Andriani, A; Bonfantino, Massimo Vincenzo

doi:10.1038/clpt.1993.33

Cited by 20 publications

(12 citation statements)

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“…6 The effect of lisinopril on stiffness may extend beyond its antihypertensive effect, suggesting structural changes; the effect persisted for at least four weeks following withdrawal of lisinopril. 46 Trandolopril 47 increased brachial artery compliance and reversed left ventricular hypertrophy and decreased arterial wall stiffness in hypertensive subjects treated for one year. Again, the benefit persisted for one month after discontinuation of treatment.…”

Section: Ace Inhibitorsmentioning

confidence: 99%

Review: Arterial stiffness and the renin-angiotensin-aldosterone system

Mahmud

Feely

2004

J Renin Angiotensin Aldosterone Syst

112

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Arterial stiffness has recently been recognised as an independent risk factor for cardiovascular morbidity and mortality in hypertension. Many of the complications seen with angiotensin II (Ang II) excess or hyperaldosteronism -an increased event rate, left ventricular hypertrophy, endothelial dysfunction and target organ damage -are also associated with arterial stiffness. It is possible that reduced arterial compliance may be one mechanism whereby increased activity of the renin-angiotensin-aldosterone system (RAAS) produces adverse vascular effects. Common pathophysiological processes, altered collagen turnover and increased fibrosis may underlie both arterial stiffness and RAAS-associated vascular damage.While it is recognised that patients with hyperaldosteronism have increased arterial stiffness, the role of the RAAS in modulating arterial compliance in essential hypertension and in normotensive subjects is less clear cut. There is, however, more consistent data which show that drugs that interfere with Ang II or aldosterone, namely angiotensin-converting enzyme (ACE) inhibitors, angiotensin receptor blockers (ARBs) and aldosterone antagonists, all reduce arterial stiffness. In many cases, this is to a greater extent than predicted from the extent of reduction in blood pressure (BP), suggesting a role for RAAS in vascular stiffness in hypertensive subjects. There is also evidence that combined ACE inhibitors (ACE-Is) and ARBs may have an additive effect in reducing stiffness. The reduction in cardiovascular mortality in end-stage renal disease patients treated with ACE-Is was preferentially seen in those who had reduced arterial stiffness. These data suggest that, in addition to regulation of vascular biology and BP, the RAAS is an important determinant of arterial stiffness in health and, more particularly, in disease. IntroductionThe pulse has retained a central role throughout the history of medicine. It was, however, more an art than a science until the 19th century, when sphygmography provided the first graphic recordings of the arterial pressure pulse. Abnormalities in the pulse wave contour were considered indicative of stiff arteries and subsequently used to diagnose hypertension and Bright's disease.About the same time as Tigerstedt and Bergman discovered renin, sphygmography was abandoned in favour of cuff sphygmomanometry. There has been a recent awakening in the field of arterial stiffness follow-

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Section: Ace Inhibitorsmentioning

confidence: 99%

Review: Arterial stiffness and the renin-angiotensin-aldosterone system

Mahmud

Feely

2004

J Renin Angiotensin Aldosterone Syst

112

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“…With nitroglycerin [15] or nifedipine [16], a reduction in stiffness and with atropine an increase in stiffness [17,18] have been reported, but mere blood pressurerelated effects cannot be excluded. ACE inhibitors have been shown to directly influence the elastic properties of peripheral arterial walls to a greater extent than would be expected from their blood pressurelowering effect [19][20][21][22][23][24][25]. The aim of this study was to elucidate whether there might be an effect of an ACE inhibitor on aortic elastic properties.…”

mentioning

confidence: 99%

Influence of antihypertensive therapy with cilazapril and hydrochlorothiazide on the stiffness of the aorta

Breithaupt-Grögler¹,

Leschinger²,

Gg³

et al. 1996

Cardiovasc Drug Ther

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The purpose of this study was to examine the effects of the angiotensin-converting enzyme (ACE) inhibitor cilazapril on the elastic properties of the aorta. A standard diuretic antihypertensive drug, hydrochlorothiazide, served for comparisons. Increased aortic stiffness leads to a reduction of the buffering windkessel function and is a major component in the pathophysiology of systolic hypertension, inducing an increase in left ventricular afterload and arterial pulsatile stress as well as a decrease in the subendocardial blood supply. Stiffness of arteries increases with age and blood pressure, and depends on the functional elastic structures of the aortic wall. ACE inhibitors have been shown to directly influence elastic properties of peripheral arteries. Seventeen patients with mild to moderate essential hypertension (age 45-67 years) were treated for 3 months double-blind randomized with either cilazapril (C) 5 mg daily (n = 9) or hydrochlorothiazide (HCTZ) 25 mg daily (n = 8). Aortic elastic properties were noninvasively assessed by measurement of pulse wave velocity along the aorta at rest and during isometric handgrip stress. Accelerated pulse wave velocity indicates elevated arterial stiffness and vice versa. A pressure standardized index of aortic cross-sectional distensibility (2 m) was calculated from arterial mean pressure and pulse wave velocity. Compared with pretreatment values, both therapies significantly reduced blood pressure and pulse wave velocity at rest (C: 9.4 +/- 0.9 vs. 7.7 +/- 0.7 m/sec; HcTZ: 8.9 +/- 0.3 vs. 7.8 +/- 0.4 m/sec; means +/- SEM p < 0.05). During isometric stress only C showed a significant decrease in pulse wave velocity (C: 11.3 +/- 0.8 vs. 9.1 +/- 0.8 m/sec; HCTZ: 9.9 +/- 0.5 vs. 9.0 +/- 0.5 m/sec; means +/- SEM p < 0.05). The index 2m at rest and during handgrip increased significantly (p < 0.05) after C but not after HCTZ. With cilazapril we obtained steeper slopes for the treatment-induced reductions in blood pressure and pulse wave velocity for both rest and handgrip stress values. Correlation of the data at rest and during stress revealed a direct relationship between blood pressure and pulse wave velocity. HCTZ linearly extended the relation observed before treatment toward lower values of blood pressure and corresponding pulse wave velocity without changing the relation per se. Cilazapril, in contrast, moved the relation between these variables and decelerated the pulse wave velocities to a greater extent than would have been expected from the corresponding blood pressure reduction (delta approximately 1 m/sec). These results in patients with mild to moderate essential hypertension support the idea that ACE inhibitors, in addition to reducing blood pressure, may exert an additional hemodynamic effect in improving the elastic properties of the aorta.

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“…2). An increase in distensibility during ACE inhibition was further confirmed by others [49,[93][94][95][96][97], Recently, Girerd et al [98] studied a large group of elderly patients with isolated systolic hypertension which were randomized in a double-blind parallel study to receive either perindopril (2-8 mg) or hydrochlorothia zide + amiloride (hydrochlorothiazide 12.5-50 mg) dur ing 9 months. If SBP remained above 160 mm Hg after 5 months, atenolol or chlorthalidone was added.…”

Section: Clinical Studiesmentioning

confidence: 94%

Resistance and Conduit Arteries following Converting Enzyme Inhibition in Hypertension

Safar

Bortel²,

Struijker‐Boudier³

1997

J Vasc Res

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Alterations in the structure of resistance and conduit arteries are a characteristic hallmark in hypertension. Studies carried out in hypertensive rats and in humans suggest that angiotensin I-converting enzyme inhibition has an effect on arterial structure of resistance arteries. In hypertensive rats the reduction of the media to lumen ratio is dose-dependent and significantly different from the effects of other antihypertensive agents at doses causing an equal degree of blood pressure reduction. In large conduit arteries, hypertrophy of the vessels is reversed by converting enzyme inhibition both in hypertensive rats (studies on central arteries) and in human (studies on peripheral arteries) hypertension. The reduction of hypertrophy is associated with a decrease in arterial stiffness, partly independent of blood pressure reduction. These findings suggest that regression of structural vascular changes may contribute to both the decrease in the arteriolar resistance and the improvement in the buffering function of large arteries. The decrease in arteriolar resistance and the improvement of large artery compliance may participate in blood pressure reduction and an improvement in pulse pressure amplification produced by converting enzyme inhibition.

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Forearm arterial distensibility in patients with hypertension: Comparative effects of long-term ACE inhibition and β-blocking

Cited by 20 publications

References 0 publications

Review: Arterial stiffness and the renin-angiotensin-aldosterone system

Review: Arterial stiffness and the renin-angiotensin-aldosterone system

Influence of antihypertensive therapy with cilazapril and hydrochlorothiazide on the stiffness of the aorta

Resistance and Conduit Arteries following Converting Enzyme Inhibition in Hypertension

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