Favourable effects on arterial wave reflection and pulse pressure amplification of adding angiotensin II receptor blockade in resistant hypertension

Mahmud, Azra; Feely, J.

doi:10.1038/sj.jhh.1001053

Cited by 69 publications

(44 citation statements)

References 27 publications

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“…The normal amplification of SBP from central to peripheral arteries, which is reduced in hypertension, 30 representing a combination of changes in vessel compliance and structure, was partially reversed. This increase in the amplification ratio, which has been previously demonstrated with ARBs, 31 would suggest that treatment with candesartan may decrease large artery stiffness and that the decrease in AIx is not solely due to changes in wave reflection. MFVR after ischaemia, as measured by venous occlusion plethysmography, was also significantly reduced.…”

Section: Discussionmentioning

confidence: 80%

Effects of candesartan on cardiac and arterial structure and function in hypertensive subjects

Spratt

Webb

Shiels

et al. 2001

J Renin Angiotensin Aldosterone Syst

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ObjectivesTo study the effect of candesartan cilexetil on left ventricular mass index (LVMI), left ventricular systolic and diastolic function, arterial structure and function and blood pressure (BP) in hypertensive patients. Design and methodsPatients (n=35), aged >20 years, with hypertension and average baseline LVMI of 89 g/m 2 were treated for 24 weeks with candesartan, 16 mg o.d., following a fourweek placebo run-in period. If diastolic BP remained above 95 mmHg, hydrochlorothiazide, 12.5 mg o.d., was added. Left ventricular structure and function were assessed using transthoracic echocardiography. Arterial function and structure were assessed using pulse wave analysis to calculate augmentation index (AIx) and forearm plethysmography to calculate minimum vascular resistance. BP was measured in the office and by 24-hour ambulatory BP monitoring (ABPM). ResultsThe mean reduction in LVMI was 4.4 g/m 2 (p=0.022). Left ventricular systolic function was not significantly altered from baseline, but diastolic function significantly improved: the mean change in diastolic time was 54 ms (p=0.037), in peak velocity filling 6.3 cm/s (p=0.023); E:A ratio improved by 0.08 (p=0.049). The mean reduction in forearm vascular resistance was 15 units at rest (p=0.001) and 1.3 units after limb ischaemia (p=0.006). AIx decreased significantly, with a mean reduction of 9% (p<0.001). Central BP also significantly reduced (systolic blood pressure/ diastolic blood pressure 31/20 mmHg; p<0.001). BP was significantly reduced, both in the office (22/16 mmHg; p<0.001) and by 24-hour ABPM (18/12 mmHg; p<0.001). ConclusionsTreatment with candesartan, 16 mg o.d., with or without hydrochlorothiazide, for 24 weeks, significantly reduced left ventricular mass and arterial hypertrophy in patients with hypertension. In parallel, there were significant improvements in left ventricular diastolic function and arterial function. IntroductionThe cardiac effects of hypertension are evident both in structure, where left ventricular hypertrophy (LVH) is a powerful independent marker of mortality, 1,2 and in function, where systolic and predominately diastolic abnormalities

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Section: Discussionmentioning

confidence: 80%

Effects of candesartan on cardiac and arterial structure and function in hypertensive subjects

Spratt

Webb

Shiels

et al. 2001

J Renin Angiotensin Aldosterone Syst

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“…1,2 Angiotensin-converting enzyme inhibitors (ACEIs), angiotensin receptor blockers (ARBs), and calcium channel blockers (CCBs), which are powerful vasodilators, have been shown to improve wave reflection and central aortic pressure. [3][4][5] By contrast, the ␤-blocker atenolol, prescribed alone 6,7 or in combination with thiazides, 8 is less effective than ACEIs, ARBs, and CCBs for lowering central pressure and wave reflection. It is now well accepted that antihypertensive therapy based on brachial artery recordings may overestimate the effect of ␤-blocking drugs on central aortic systolic BP (SBP) and underestimate those of ACEIs, ARBs, and CCBs.…”

mentioning

confidence: 99%

“…11 In addition, atenolol does not reduce total peripheral resistance and sympathetic drive and fails to induce a long-term remodeling of large 6,7 and small arteries, 12 which is required for the functional and structural improvement of arterial stiffness and resistance and the consequent reduction in augmentation index (AIx) and central aortic BP. 10,13 Although the effects of antihypertensive agents on central BP have been studied in several clinical trials as monothera-pies, [2][3][4][5]11,14,15 very few long-term randomized, controlled clinical trials have studied drug strategies and combination therapies. The REASON Study compared an ACEI/diuretic combination with atenolol as monotherapy but not with atenolol included in a combination.…”

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confidence: 99%

Amlodipine-Valsartan Combination Decreases Central Systolic Blood Pressure More Effectively Than the Amlodipine-Atenolol Combination

et al. 2010

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Abstract-The ␤-blocker atenolol is less effective than angiotensin-receptor blockers and calcium-channel blockers for reducing central blood pressure (BP). The trial was designed to determine whether the advantages of angiotensinreceptor blockers over atenolol remained significant when both were combined with the calcium-channel blocker amlodipine. A prospective, randomized, blinded endpoint (PROBE design) parallel group, multicenter trial including 393 patients with essential hypertension resistant to 4 weeks of 5 mg of amlodipine was set out. Central systolic BP, augmentation index (AIx; either rough or adjusted on heart rate), and carotid-to-femoral pulse wave velocity were measured with applanation tonometry (SphygmoCor) at inclusion and after 8 and 24 weeks of active treatment with an amlodipine-valsartan combination (5/80 mg and then 10/160 mg) or an amlodipine-atenolol combination (5/50 mg and then 10/100 mg

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“…Arterial wave reflections measured by the AIx were significantly reduced. 53 In a four-week crossover study with losartan, compared with hydrochlorthiazide, in patients with essential hypertension,for the same BP reduction,only losartan decreased PWV and aortic AIx and enhanced PP amplification. 54 Similar results have been seen with valsartan.…”

mentioning

confidence: 99%

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

Mahmud

Feely

2004

J Renin Angiotensin Aldosterone Syst

114

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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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Favourable effects on arterial wave reflection and pulse pressure amplification of adding angiotensin II receptor blockade in resistant hypertension

Cited by 69 publications

References 27 publications

Effects of candesartan on cardiac and arterial structure and function in hypertensive subjects

Effects of candesartan on cardiac and arterial structure and function in hypertensive subjects

Amlodipine-Valsartan Combination Decreases Central Systolic Blood Pressure More Effectively Than the Amlodipine-Atenolol Combination

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

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