Pulse Pressure Amplification and Risk of Cardiovascular Disease

Nijdam, Marie-Elise; Plantinga, Yvonne; Hulsen, Hans T.; Bos, Willem Jan W.; Grobbee, Diederick E.; Schouw, Yvonne T. van der; Bots, Michiel L.

doi:10.1038/ajh.2007.89

Cited by 40 publications

(26 citation statements)

References 26 publications

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“…This amplification is determined by a combination of factors including left ventricular contractility, heart rate, arterial stiffness, arterial caliber, arterial path length, timing and/or magnitude of wave reflections, and arteriolar tone/vascular resistance (Avolio et al 2009). Reduced pulse pressure amplification occurs with aging (O'Rourke et al 1968) and disease (hypertension, diabetes, hypercholesterolemia, coronary artery disease) and is associated with traditional cardiovascular risk factors (McEniery et al 2008;Vergnaud et al 2008) and overall vascular burden (Nijdam et al 2008). Moreover, reduced pulse pressure amplification is associated with target organ damage (Nijdam et al 2008;Temmar et al 2010) and independently predicts future cardiovascular mortality (Benetos et al 2010;Safar et al 2002).…”

Section: Discussionmentioning

confidence: 95%

“…Reduced pulse pressure amplification occurs with aging (O'Rourke et al 1968) and disease (hypertension, diabetes, hypercholesterolemia, coronary artery disease) and is associated with traditional cardiovascular risk factors (McEniery et al 2008;Vergnaud et al 2008) and overall vascular burden (Nijdam et al 2008). Moreover, reduced pulse pressure amplification is associated with target organ damage (Nijdam et al 2008;Temmar et al 2010) and independently predicts future cardiovascular mortality (Benetos et al 2010;Safar et al 2002). Thus, pulse pressure amplification has been proposed as a potential mechanical biomarker of cardiovascular risk and global arterial function (Benetos et al 2010).…”

Section: Discussionmentioning

confidence: 99%

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Peripheral augmentation index as a biomarker of vascular aging: an invasive hemodynamics approach

et al. 2011

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We compared two measures of vascular function obtained from digital volume waveforms with measures of target organ damage and novel invasive measures of vascular function as they relate to vascular aging. Aortic pulse pressure amplification, pulsatility, form factor and extent of coronary atherosclerosis (modified Gensini score) were obtained invasively in 59 patients undergoing left heart catheterization. Digital volume waveforms were captured via peripheral arterial tone (PAT) and used to derive augmentation index (AIx) and the pulse wave amplitude-reactive hyperemia index (PWA-RHI). AIx was associated with age (r = 0.50, p < 0.05) and aortic pulsatility (r = 0.45, p < 0.05) and inversely associated with estimated glomerular filtration rate (-0.29, p < 0.05) aortic pulse pressure amplification (r = -0.28, p < 0.05) and aortic form factor (r = -0.38, p < 0.05). AIx was slightly higher in patients with left ventricular hypertrophy (LVH) versus those without left ventricular hypertrophy (30 vs. 14%, p = 0.058). There was no association between AIx and Gensini score. PWA-RHI was not associated with age, estimated glomerular filtration rate or invasive vascular parameters and did not differ in patients with versus without LVH (p = ns). PWA-RHI was inversely associated with Gensini score (r = -0.32, p < 0.05). AIx derived from PAT is correlated with age-associated changes in vascular function and target organ damage but not coronary atherosclerotic burden. PWA-RHI is associated with coronary atherosclerotic burden but is not associated with target organ damage or other measures of vascular aging assessed in this study. Each parameter provides distinct insight into systemic vascular aging and target organ damage.

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Section: Discussionmentioning

confidence: 95%

Section: Discussionmentioning

confidence: 99%

Peripheral augmentation index as a biomarker of vascular aging: an invasive hemodynamics approach

et al. 2011

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“…This might have significant prognostic implications. 5,42 The immunosuppressed group had higher cholesterol and glucose levels, with one possible explanation being the use of continuous corticosteroid treatment. Hypercholesterolemia and diabetes are both associated with increased arterial stiffness, 43,44 and these associations may have also contributed to further clouding any potential association between lower arterial stiffness and immunosuppressant use, as indeed would have been the adverse vascular effects of corticosteroids.…”

Section: Discussionmentioning

confidence: 99%

Does immunosuppressant medication lower blood pressure and arterial stiffness in patients with chronic kidney disease? An observational study

et al. 2010

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Chronic kidney disease is a proinflammatory state associated with increased arterial stiffness. We hypothesized that chronic kidney disease patients on long-term immunosuppression would have lower arterial stiffness and require treatment with less antihypertensive medication compared with non-immunosuppressed patients. A total of 254 patients (97 on immunosuppression) with chronic kidney disease were recruited from specialist renal clinics. Brachial blood pressure, central aortic pressure and waveform and pulse wave velocity were measured. Age, peripheral blood pressure and pulse wave velocity increased with worsening renal function but were not different between immunosuppressed and non-immunosuppressed patients. Central systolic (Po0.001) and pulse pressure (P¼0.003) and the number of antihypertensive medications (Po0.001) increased with worsening renal function and were higher in non-immunosuppressed patients (P¼0.02, P¼0.004 and Po0.001, respectively). Age, mean arterial pressure, number of antihypertensive medications and a diagnosis of diabetes were found to be independent predictors of pulse wave velocity (R 2 ¼0.375; Po0.001). In a subgroup of 30 patient pairs without diabetes mellitus and cardiovascular disease and with a proven renal diagnosis, carefully matched for age, gender, renal function and systolic pressure, the prescribed antihypertensive medication remained lower in the immunosuppressed patients compared with nonimmunosuppressed patients (P¼0.04). Pulse wave velocity was lower in the immunosuppressed group (7.5 ± 1.8 vs. 8.8±1.9 m s -1 ; P¼0.02). This study suggests that immunosuppression might be a method of reducing blood pressure and arterial stiffness in patients with chronic kidney disease.

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“…Increased SMC tone (contraction) increases wave refl ection amplitude and reduces PP amplifi cation, while decreased tone (relaxation) has the opposite effect. Reduced PP amplifi cation occurs with aging [ 3 , 86 , 117 , 127 ], obesity, and arterial disease (hypertension, diabetes, hypercholesterolemia, coronary artery disease, renal disease) and is associated with traditional cardiovascular risk factors [ 128 , 129 ] and overall vascular burden [ 130 ]. Moreover, PP amplifi cation is associated with overt target organ damage and regression of target organ damage with therapy (i.e., LVH regression with antihypertensive therapy and exercise conditioning) [ 131 ], and it independently predicts future cardiovascular mortality [ 132 , 133 ].…”

Section: Pressure Differences Within the Arterial Tree And Pulse Presmentioning

confidence: 99%

Overview of the Normal Structure and Function of the Macrocirculation and Microcirculation

2015

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Pulse Pressure Amplification and Risk of Cardiovascular Disease

Abstract: Our study shows that a higher PPA reflects a lower vascular risk in men between 40 and 80 years of age, as shown by a better cardiovascular risk profile, a reduced PWV, common CIMT, and a lower Framingham risk of coronary heart disease.

Cited by 40 publications

References 26 publications

Peripheral augmentation index as a biomarker of vascular aging: an invasive hemodynamics approach

Peripheral augmentation index as a biomarker of vascular aging: an invasive hemodynamics approach

Does immunosuppressant medication lower blood pressure and arterial stiffness in patients with chronic kidney disease? An observational study

Overview of the Normal Structure and Function of the Macrocirculation and Microcirculation

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