Increased Aortic Stiffness: An Unfavorable Cardiorenal Connection

Mitchell, Gary F.

doi:10.1161/01.hyp.0000114581.77705.29

Cited by 68 publications

(63 citation statements)

References 12 publications

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“…Moreover, the aortic pulse pressure has been shown to correlate with proteinuria and serum creatinine more closely than the peripheral (femoral) pulse pressure in patients with coronary risk (Temmar et al 2010). All these data indicate an etiological role of increased central pressure pulsation in renal microvascular damage ("pressure" hypothesis) (Mitchell 2004;Safar 2004). Fig.…”

Section: Central Hemodynamics and Kidneymentioning

confidence: 76%

Central Hemodynamics and Target Organ Damage in Hypertension

Hashimoto

2014

Tohoku J. Exp. Med.

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Recent advances in technology have enabled the noninvasive evaluation of pulsatile hemodynamics in the central aorta; namely, central pressure and flow measurements. The central blood pressure represents the true load imposed on the heart, kidney and brain, and the central blood flow influences the local flow into these vital organs. An elevation of the central blood pressure has a direct, adverse impact on the target organ and, thus, the cardiovascular prognosis in patients with hypertension. A decrease in the central blood flow can cause organ dysfunction and failure. The central pressure and flow dynamics were conventionally regarded as unidirectional from the heart to the periphery. However, current evidence suggests that it should be recognized as a bidirectional interplay between the central and peripheral arteries. Specifically, the pressure pulse wave is not only transmitted forward to the periphery but also reflected backward to the central aorta. The flow pulse wave is also composed of the forward and reverse components. Aortic stiffening and arteriolar remodeling due to hypertension not only augment the central pressure by increasing the wave reflection but also may alter the central bidirectional flow, inducing hemodynamic damage/dysfunction in susceptible organs. Therefore, central hemodynamic monitoring has the potential to provide a diagnostic and therapeutic basis for preventing systemic target organ damage and for offering personalized therapy suitable for the arterial properties in each patient with hypertension. This brief review will summarize hypothetical mechanisms for the association between the central hemodynamics and hypertensive organ damage in the heart, kidney and brain.

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Section: Central Hemodynamics and Kidneymentioning

confidence: 76%

Central Hemodynamics and Target Organ Damage in Hypertension

Hashimoto

2014

Tohoku J. Exp. Med.

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“…A fall in AIx with salbutamol is related to nitric oxide release and a decrease in arterial stiffness. Data from reference 118 levels of pressure in a variety of microvascular beds including the brain and kidney (37). Studies previous to this have shown a stronger relationship between the AIx and age (38).…”

Section: Relationship Of Arterial Stiffness To Risk Factors and Theirmentioning

confidence: 93%

Arterial stiffness or endothelial dysfunction as a surrogate marker of vascular risk

Anderson

2006

Canadian Journal of Cardiology

154

113

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T he understanding of the pathophysiology of atherosclerosis and its vascular complications has increased dramatically over the past decade. Numerous measurable biomarkers play a role in the atherosclerosis process, and are associated with clinically important vascular events. Not only has their evaluation advanced our knowledge of the atherosclerotic process but it has also accelerated a search for new diagnostic tools to aid in risk stratification. Putative factors include soluble biomarkers and imaging assessments of vascular structure and function. The endothelium plays a key role in vascular homeostasis through the release of a variety of paracrine factors that interact with platelets, inflammatory cells and the vessel wall. The endothelium's central location allows it to sense and respond to a variety of perturbations. Endothelial dysfunction is an early marker of disease. Risk factors can also affect mechanical properties such as arterial stiffness, which is now recognized as a major contributor to systolic hypertension in elderly people. Methods of assessing endothelial function and arterial stiffness are available for clinical research and recent evidence suggests that these measures may provide important prognostic information. ATTRIBUTES OF A SURROGATE BIOMARKEREpidemiological studies, such as Framingham, have allowed longitudinal assessment of cardiovascular events and the development of simple scoring tables for risk calculation (1,2). These factors involved include blood pressure, lipid profile, smoking status and age. More recently, many factors thought to be associated with the atherosclerotic process have been studied. Some of these have been shown to correlate with clinical outcomes and have been deemed biomarkers (3,4). However, association does not necessarily imply causation and, due to a variety of limitations, most of these markers will not be useful for the clinical evaluation of risk or drug therapy (5). To become clinically important, a biomarker must fulfill the criteria for a surrogate marker. A surrogate substitutes for clinically important end points with respect to how an individual feels, functions or survives. Classic examples include blood pressure and low density lipoprotein cholesterol. These are targets of treatment. A surrogate should meet the following criteria:• Adds independent information above currently used criteria;• Is reliably and reproducibly measured;• Accounts for a significant proportion of disease risk;• Provides good predictive value;• Is reasonably associated with the underlying pathophysiology;• If it is to be used in risk prevention, is present before the clinical appearance of the outcome; and• Is available and practical for widespread application (5-8). ADVANCES IN VASCULAR BIOLOGY

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“…The excess cardiovascular risk is contributed to traditional risk factors and nontraditional risk factors including arterial stiffening (1,2). Increased arterial stiffness may be responsible for cardiovascular burden in the CKD population (3,4). Previous studies have reported the association between decreased estimated GFR (eGFR) and increased arterial stiffness (5)(6)(7).…”

Section: Introductionmentioning

confidence: 99%

Brachial-Ankle Pulse Wave Velocity and Rate of Renal Function Decline and Mortality in Chronic Kidney Disease

Chen

Chang²,

Liu³

et al. 2011

Clinical Journal of the American Society of Nephrology

106

104

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SummaryBackground and objectives Increased arterial stiffness was reported to be associated with decreased estimated GFR (eGFR). Previous studies suggested that arterial stiffness might play a role in renal function progression in patients with chronic kidney disease (CKD). The aim of this study was to investigate whether there was an independent association between brachial-ankle pulse wave velocity (baPWV), a marker of arterial stiffness, and renal function progression in CKD patients.Design, setting, participants, & measurements This longitudinal study enrolled 145 patients with CKD stages 3 to 5. The baPWV was measured by using an ABI-form device. The change in renal function was estimated by eGFR slope. The study endpoints were defined as commencement of dialysis or death.Results After a stepwise multivariate analysis, the eGFR slope was positively associated with baseline eGFR and negatively associated with hypertension and baPWV (␤ ϭ Ϫ0.165, P ϭ 0.033). Seventeen patients entering dialysis, and eight deaths were recorded. Multivariate forward Cox regression analysis identified that higher baPWV (hazard ratio, 1.001; P ϭ 0.001), lower baseline eGFR, and higher serum phosphate level were independently associated with progression to commencement of dialysis or death. ConclusionsOur results show an independent association between baPWV and renal function decline and progression to commencement of dialysis or death in patients with CKD. Screening CKD patients by means of baPWV may help identify a high-risk group of rapid renal function decline and progression to commencing dialysis or death.

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Increased Aortic Stiffness: An Unfavorable Cardiorenal Connection

Cited by 68 publications

References 12 publications

Central Hemodynamics and Target Organ Damage in Hypertension

Central Hemodynamics and Target Organ Damage in Hypertension

Arterial stiffness or endothelial dysfunction as a surrogate marker of vascular risk

Brachial-Ankle Pulse Wave Velocity and Rate of Renal Function Decline and Mortality in Chronic Kidney Disease

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