Pulse wave mechanics revisited: Relevance to therapy of cardiovascular disease with calcium antagonists

O’Rourke, Michael

doi:10.1007/bf01744864

Cited by 3 publications

(2 citation statements)

References 54 publications

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“…Other equivalents, such as aortic input impedance and effective arterial elastance, reflect the pulsatile components of left ventricular afterload [41][42][43]. Aortic stiffness can be assessed most easily by measurement of pulse wave velocity (Cw), with a high Cw indicating increased stiffness and vice versa [14,18,[30][31][32][33][34][35][36][44][45][46][47][48][49][50]. The pulse wave velocity mirrors the average stiffness of the aortic pathway and can provide more information than techniques measuring the aortic diameter at only one defined site [51].…”

Section: Assessment Of Aortic Elastic Propertiesmentioning

confidence: 99%

“…Cardiovasc Drugs Ther 1996;10: [49][50][51][52][53][54][55][56][57] Key Words. aortic stiffness, arterial distensibility, pulse wave velocity, Windkessel function, cilazapril, hydrochlorothiazide Increased stiffness of the aorta and the large elastic arteries leads to a reduction of their buffering windkessel function and is a major component in the pathophysiology of systolic hypertension [1][2][3][4].…”

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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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Section: Assessment Of Aortic Elastic Propertiesmentioning

confidence: 99%

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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Elastic properties and Windkessel function of the human aorta

Belz¹

1995

Cardiovasc Drug Ther

381

264

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An understanding of the role of the aortic elastic properties indicates their relevance at several sites of cardiovascular function. Acting as an elastic buffering chamber behind the heart (the Windkessel function), the aorta and some of the proximal large vessels store about 50% of the left ventricular stroke volume during systole. In diastole, the elastic forces of the aortic wall forward this 50% of the volume to the peripheral circulation, thus creating a nearly continuous peripheral blood flow. This systolic-diastolic interplay represents the Windkessel function, which has an influence not only on the peripheral circulation but also on the heart, resulting in a reduction of left ventricular afterload and improvement in coronary blood flow and left ventricular relaxation. The elastic resistance (or stiffness), which the aorta sets against its systolic distention, increases with aging, with an increase in blood pressure, and with pathological changes such as atherosclerosis. This increased stiffness leads to an increase in systolic blood pressure and a decrease in diastolic blood pressure at any given mean pressure, an increase in systolic blood velocity, an increase in left ventricular afterload, and a decrease in subendocardial blood supply during diastole, and must be considered a major pathophysiological factor, for example, in systolic hypertension. The elastic properties of the aortic Windkessel can be assessed in vivo in humans in several ways, most easily by measuring the pulse wave velocity along the aorta. The higher this velocity, the higher the elastic resistance, that is, the stiffness. Other methods depend on assessment of the ratio between pulse pressure and aortic volume changes (delata P/delta V), which can be assessed noninvasively by ultrasonic or tomographic methods. All assessments of vessel stiffness have to take into account the direct effect of current blood pressure, and thus judgements about influences of interventions rely on an unchanged blood pressure. Alternatively, to derive the "intrinsic" stiffness of the aortic wall one has to correct for the effect of the blood pressure present. Recently reports about pharmacologic influences on the elastic properties of the aorta have emerged in the literature.(ABSTRACT TRUNCATED AT 400 WORDS)

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Switch of immunosuppression from cyclosporine A to everolimus: impact on pulse wave velocity in stable de-novo renal allograft recipients

Seckinger

Sommerer

Hinkel

et al. 2008

Journal of Hypertension

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In renal allograft recipients, the prolonged treatment with CsA was associated with a significant increase of PWV whereas no further deterioration of large vessel compliance was observed in patients that were switched to EVR 6 months post transplantation. The cardiovascular risk profile in stable de-novo renal allograft recipients might therefore be positively impacted by an early switch of the primary immunosuppressive therapy from CsA to EVR.

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Pulse wave mechanics revisited: Relevance to therapy of cardiovascular disease with calcium antagonists

Cited by 3 publications

References 54 publications

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

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

Elastic properties and Windkessel function of the human aorta

Switch of immunosuppression from cyclosporine A to everolimus: impact on pulse wave velocity in stable de-novo renal allograft recipients

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