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      Pulse Wave Reflection Is Amplified in Normotensive Patients with Autosomal-Dominant Polycystic Kidney Disease and Normal Renal Function

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          Background: In young ADPKD patients, we have previously found an impaired endothelium-dependent relaxation in small resistance vessels but a normal flow-mediated dilatation of the brachial artery. The present study investigated arterial stiffness in early ADPKD by pulse-wave analysis (PWA) and measurement of pulse-wave velocity (PWV). Methods: 18 young normotensive ADPKD patients with normal renal function and 18 controls were studied by applanation tonometry with the SphygmoCor® equipment. Parameters included an estimate of aortic blood pressure, augmentation index (AIx), AIx standardized to heart rate 75 (AIx(HR75)) and PWV. Glomerular filtration rate (GFR) was measured by the <sup>51</sup>Cr-EDTA plasma clearance method. Statistical comparisons were made with t tests and multiple linear regression analysis. Results: GFR was the same in the two groups. Brachial diastolic blood pressure was slightly but significantly higher in ADPKD patients than in controls (81 ± 9 vs. 73 ± 9 mm Hg, p < 0.05). No significant difference was present in brachial systolic blood pressure. AIx was significantly higher in ADPKD than in controls: 21.6 ± 11.3 vs. 11.4 ± 11.2%, p < 0.02. AIx(HR75) and estimated aortic systolic and diastolic blood pressure was likewise significantly higher in ADPKD than in controls. Multiple linear regression analysis showed AIx and AIx(HR75) to be independently correlated to group (ADPKD/control), p < 0.02 and p < 0.05, respectively. No difference was found between PWV in the two groups. Conclusion: Reflection of the pulse wave was amplified in young normotensive ADPKD patients, demonstrating early pathology in the arterial system.

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          Most cited references 21

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          Prospective evaluation of a method for estimating ascending aortic pressure from the radial artery pressure waveform.

          Pressure wave reflection in the upper limb causes amplification of the arterial pulse so that radial systolic and pulse pressures are greater than in the ascending aorta. Wave transmission properties in the upper limbs (in contrast to the descending aorta and lower limbs) change little with age, disease, and drug therapy in adult humans. Such consistency has led to use of a generalized transfer function to synthesize the ascending aortic pressure pulse from the radial pulse. Validity of this approach was tested for estimation of aortic systolic, diastolic, pulse, and mean pressures from the radial pressure waveform. Ascending aortic and radial pressure waveforms were recorded simultaneously at cardiac surgery, before initiation of cardiopulmonary bypass, with matched, fluid-filled manometer systems in 62 patients under control conditions and during nitroglycerin infusion. Aortic pressure pulse waves, generated from the radial pulse, showed agreement with the measured aortic pulse waves with respect to systolic, diastolic, pulse, and mean pressures, with mean differences <1 mm Hg. Control differences in Bland-Altman plots for mean+/-SD in mm Hg were systolic, 0.0+/-4.4; diastolic, 0.6+/-1.7; pulse, -0.7+/-4.2; and mean pressure, -0.5+/-2.0. For nitroglycerin infusion, differences respectively were systolic, -0.2+/-4.3; diastolic, 0.6+/-1.7; pulse, -0.8+/-4.1; and mean pressure, -0.4+/-1.8. Differences were within specified limits of the Association for the Advancement of Medical Instrumentation SP10 criteria. In contrast, differences between recorded radial and aortic systolic and pulse pressures were well outside the criteria (respectively, 15.7+/-8.4 and 16.3+/-8.5 for control and 14.5+/-7.3 and 15.1+/-7.3 mm Hg for nitroglycerin). Use of a generalized transfer function to synthesize radial artery pressure waveforms can provide substantially equivalent values of aortic systolic, pulse, mean, and diastolic pressures.
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            The influence of heart rate on augmentation index and central arterial pressure in humans.

            Arterial stiffness is an important determinant of cardiovascular risk. Augmentation index (AIx) is a measure of systemic arterial stiffness derived from the ascending aortic pressure waveform. The aim of the present study was to assess the effect of heart rate on AIx. We elected to use cardiac pacing rather than chronotropic drugs to minimize confounding effects on the systemic circulation and myocardial contractility. Twenty-two subjects (13 male) with a mean age of 63 years and permanent cardiac pacemakers in situ were studied. Pulse wave analysis was used to determine central arterial pressure waveforms, non-invasively, during incremental pacing (from 60 to 110 beats min-1), from which AIx and central blood pressure were calculated. Peripheral blood pressure was recorded non-invasively from the brachial artery. There was a significant, inverse, linear relationship between AIx and heart rate (r = -0.76; P < 0.001). For a 10 beats min-1 increment, AIx fell by around 4 %. Ejection duration and heart rate were also inversely related (r = -0. 51; P < 0.001). Peripheral systolic, diastolic and mean arterial pressure increased significantly during incremental pacing. Although central diastolic pressure increased significantly with pacing, central systolic pressure did not. There was a significant increase in the ratio of peripheral to central pulse pressure (P < 0.001), which was accounted for by the observed change in central pressure augmentation. These results demonstrate an inverse, linear relationship between AIx and heart rate. This is likely to be due to alterations in the timing of the reflected pressure wave, produced by changes in the absolute duration of systole. Consideration of wave reflection and aortic pressure augmentation may explain the lack of rise in central systolic pressure during incremental pacing despite an increase in peripheral pressure.
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              Autosomal dominant polycystic kidney disease.

               Aaron Gabow (1993)

                Author and article information

                Am J Nephrol
                American Journal of Nephrology
                S. Karger AG
                May 2007
                27 March 2007
                : 27
                : 3
                : 240-246
                aDepartments of Nephrology B and Clinical Physiology and Nuclear Medicine, Herlev University Hospital, Herlev, Denmark; bDepartment of Nephrology and Hypertension, Georgetown University, Washington, D.C., USA
                101369 Am J Nephrol 2007;27:240–246
                © 2007 S. Karger AG, Basel

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                Page count
                Figures: 1, Tables: 3, References: 28, Pages: 7
                Original Report: Patient-Oriented, Translational Research


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