Noninvasive Measurement of Central Vascular Pressures With Arterial Tonometry: Clinical Revival of the Pulse Pressure Waveform?
2010; Elsevier BV; Volume: 85; Issue: 5 Linguagem: Inglês
10.4065/mcp.2009.0336
ISSN1942-5546
AutoresMatthew R. Nelson, Jan Stepánek, Michael J. Cevette, Michael Covalciuc, R. Todd Hurst, A. Jamil Tajik,
Tópico(s)Hemodynamic Monitoring and Therapy
ResumoThe arterial pulse has historically been an essential source of information in the clinical assessment of health. With current sphygmomanometric and oscillometric devices, only the peak and trough of the peripheral arterial pulse waveform are clinically used. Several limitations exist with peripheral blood pressure. First, central aortic pressure is a better predictor of cardiovascular outcome than peripheral pressure. Second, peripherally obtained blood pressure does not accurately reflect central pressure because of pressure amplification. Lastly, antihypertensive medications have differing effects on central pressures despite similar reductions in brachial blood pressure. Applanation tonometry can overcome the limitations of peripheral pressure by determining the shape of the aortic waveform from the radial artery. Waveform analysis not only indicates central systolic and diastolic pressure but also determines the influence of pulse wave reflection on the central pressure waveform. It can serve as a useful adjunct to brachial blood pressure measurements in initiating and monitoring hypertensive treatment, in observing the hemodynamic effects of atherosclerotic risk factors, and in predicting cardiovascular outcomes and events. Radial artery applanation tonometry is a noninvasive, reproducible, and affordable technology that can be used in conjunction with peripherally obtained blood pressure to guide patient management. Keywords for the PubMed search were applanation tonometry, radial artery, central pressure, cardiovascular risk, blood pressure, and arterial pulse. Articles published from January 1, 1995, to July 1, 2009, were included in the review if they measured central pressure using radial artery applanation tonometry. The arterial pulse has historically been an essential source of information in the clinical assessment of health. With current sphygmomanometric and oscillometric devices, only the peak and trough of the peripheral arterial pulse waveform are clinically used. Several limitations exist with peripheral blood pressure. First, central aortic pressure is a better predictor of cardiovascular outcome than peripheral pressure. Second, peripherally obtained blood pressure does not accurately reflect central pressure because of pressure amplification. Lastly, antihypertensive medications have differing effects on central pressures despite similar reductions in brachial blood pressure. Applanation tonometry can overcome the limitations of peripheral pressure by determining the shape of the aortic waveform from the radial artery. Waveform analysis not only indicates central systolic and diastolic pressure but also determines the influence of pulse wave reflection on the central pressure waveform. It can serve as a useful adjunct to brachial blood pressure measurements in initiating and monitoring hypertensive treatment, in observing the hemodynamic effects of atherosclerotic risk factors, and in predicting cardiovascular outcomes and events. Radial artery applanation tonometry is a noninvasive, reproducible, and affordable technology that can be used in conjunction with peripherally obtained blood pressure to guide patient management. Keywords for the PubMed search were applanation tonometry, radial artery, central pressure, cardiovascular risk, blood pressure, and arterial pulse. Articles published from January 1, 1995, to July 1, 2009, were included in the review if they measured central pressure using radial artery applanation tonometry. Applanation tonometry (AT) is a noninvasive, reproducible, and accurate representation of the aortic pressure waveform.1O'Rourke MF Seward JB Central arterial pressure and arterial pressure pulse: new views entering the second century after Korotkov.Mayo Clin Proc. 2006; 81: 1057-1068Abstract Full Text Full Text PDF PubMed Scopus (65) Google Scholar Measurement of the aortic waveform can provide clinically useful information beyond brachial-measured blood pressure. A trove of information can be gleaned from the shape, amplitude, and duration of the waveform that provides insights into the diagnosis and management of many disease states, including hypertension, coronary artery disease (CAD), obstructive sleep apnea (OSA), diabetes, and diastolic dysfunction (DD). This review aims to provide the clinician with an understanding of the central pressure waveform and its application to patient management. PubMed was searched for all articles referencing radial artery AT from January 1, 1995, to July 1, 2009. The following keywords were used in the search: applanation tonometry, radial artery, central pressure, cardiovascular risk, blood pressure, and arterial pulse. Articles were included in the report if they used AT from the radial and not the carotid artery in their analysis. The physical examination of the human arterial pulse by healers and medical professionals has historically been important in assessing health. Descriptions from Egypt in the Edwin Smith Papyrus dating to 1600 bc contain references to the examination of the pulse.2Breasted JH The Edwin Smith Surgical Papyrus. Vol 1. University of Chicago Press, Chicago, IL1930: 105Google Scholar In 6th century bc Chinese medicine, the palpation of the pulse was the only part of the physical examination that a male physician could perform on a female patient, provided that he was separated from her by a bamboo curtain.3Acierno L The History of Cardiology. 1 ed. Taylor and Francis, 1994: 758Google Scholar Modern recording of the pulse waveform became possible through the invention of the sphygmograph by Etienne Jules Marey in 1860 (Figure 1).4Snellen HA E.J. Marey and Cardiology: Physiologist and Pioneer of Technology (1830-1904). Kooyker Scientific Publications, Rotterdam, The Netherlands1980Google Scholar The introduction of cardiac catheterization by Werner Forssman in 1929 further added valuable data to the correlation between central vascular pressures and the peripheral pulse waveform. Cournand and Ranges successfully placed catheters in the right atrium in living humans, paving the way for physiologic exploration of the cardiopulmonary system.5Cournand A Ranges A Catheterization of the right auricle in man.Proc Soc Exp Biol Med. 1941; 46: 462-466Crossref Scopus (147) Google Scholar Earl H. Wood and Edwin J. Kroeker laid the foundation for the concept of the vascular tree responding to the pressure wave from each heart beat in a classic frequency amplitude response curve.6Kroeker EJ Wood EH Beat-to-beat alterations in relationship of simultaneously recorded central and peripheral arterial pressure pulses during Valsalva maneuver and prolonged expiration in man.J Appl Physiol. 1956; 8: 483-494PubMed Google Scholar They also observed that amplification of blood pressure from the aorta to the periphery occurs as a result of an increase in systolic pressure and that the reflection of the cardiac pressure impulse at the level of the peripheral vasculature shapes the peripheral and central pulse waveforms.7Kroeker EJ Wood EH Comparison of simultaneously recorded central and peripheral arterial pressure pulses during rest, exercise and tilted position in man.Circ Res. 1955; 3: 623-632Crossref PubMed Scopus (298) Google Scholar With the advent of sphygmomanometry after Scipione Riva-Rocci in the late 19th century, physicians focused only on the pressure waveform peak (systole) and trough (diastole) and ignored the rest of the arterial pressure waveform. Several limitations exist with peripheral blood pressures obtained with either a sphygmomanometer or an oscillometric device. First, central pressures seem to be a more accurate predictor of cardiovascular events than peripheral pressures.8Roman MJ Devereux RB Kizer JR et al.Central pressure more strongly relates to vascular disease and outcome than does brachial pressure: the Strong Heart Study.Hypertension. 2007; 50: 197-203Crossref PubMed Scopus (986) Google Scholar, 9London GM Blacher J Pannier B Guerin AP Marchais SJ Safar ME Arterial wave reflections and survival in end-stage renal failure.Hypertension. 2001; 38: 434-438Crossref PubMed Scopus (727) Google Scholar, 10Safar ME Blacher J Pannier B et al.Central pulse pressure and mortality in end-stage renal disease.Hypertension. 2002; 39: 735-738Crossref PubMed Scopus (685) Google Scholar Second, despite similar reductions in peripheral blood pressure, cardiovascular outcomes may differ between different classes of antihypertensive medications, and this difference could be due to their variable effects on central pressure.11Williams B Lacy PS Thom SM et al.Differential impact of blood pressure-lowering drugs on central aortic pressure and clinical outcomes: principal results of the Conduit Artery Function Evaluation (CAFE) study.Circulation. 2006; 113: 1213-1225Crossref PubMed Scopus (2051) Google Scholar, 12Dahlof B Devereux RB Kjeldsen SE et al.Cardiovascular morbidity and mortality in the Losartan Intervention For Endpoint reduction in hypertension study (LIFE): a randomised trial against atenolol.Lancet. 2002; 359: 995-1003Abstract Full Text Full Text PDF PubMed Scopus (4786) Google Scholar, 13London GM Asmar RG O'Rourke MF Safar ME Mechanism(s) of selective systolic blood pressure reduction after a low-dose combination of perindopril/indapamide in hypertensive subjects: comparison with atenolol.J Am Coll Cardiol. 2004; 43: 92-99Abstract Full Text Full Text PDF PubMed Scopus (297) Google Scholar, 14O'Rourke MF Nichols WW Effect of ramipril on cardiovascular events in high-risk patients [letter].N Engl J Med. 2000; 343: 64-65Crossref PubMed Scopus (11) Google Scholar Finally, peripheral systolic pressures, primarily measured from the brachial artery, do not represent pressure as recorded in the aorta and central arteries because of peripheral amplification.15Sharman JE Stowasser M Fassett RG Marwick TH Franklin SS Central blood pressure measurement may improve risk stratification.J Hum Hypertens. 2008; 22: 838-844Crossref PubMed Scopus (72) Google Scholar, 16McEniery CM Yasmin McDonnell B et al.Central pressure: variability and impact of cardiovascular risk factors: the Anglo-Cardiff Collaborative Trial II.Hypertension. 2008; 51: 1476-1482Crossref PubMed Scopus (340) Google Scholar For example, several reports in large populations have demonstrated a 60% to 70% overlap in central pressures between groups classified by current hypertension guidelines.15Sharman JE Stowasser M Fassett RG Marwick TH Franklin SS Central blood pressure measurement may improve risk stratification.J Hum Hypertens. 2008; 22: 838-844Crossref PubMed Scopus (72) Google Scholar, 16McEniery CM Yasmin McDonnell B et al.Central pressure: variability and impact of cardiovascular risk factors: the Anglo-Cardiff Collaborative Trial II.Hypertension. 2008; 51: 1476-1482Crossref PubMed Scopus (340) Google Scholar This overlap can be explained by the observation that brachial–central pressure differences vary by 1 to 33 mm Hg.15Sharman JE Stowasser M Fassett RG Marwick TH Franklin SS Central blood pressure measurement may improve risk stratification.J Hum Hypertens. 2008; 22: 838-844Crossref PubMed Scopus (72) Google Scholar, 17Nakamura M Sato K Nagano M Estimation of aortic systolic blood pressure in community-based screening: the relationship between clinical characteristics and peripheral to central blood pressure differences.J Hum Hypertens. 2005; 19: 251-253PubMed Google Scholar Another example of peripheral amplification is spurious systolic hypertension of youth, in which extreme peripheral amplification leads to an elevated isolated systolic pressure despite normal central pressures.18O'Rourke MF Vlachopoulos C Graham RM Spurious systolic hypertension in youth.Vasc Med. 2000; 5: 141-145PubMed Google Scholar The limitations of peripheral blood pressure measurements may be overcome with AT. Tonometry of the radial artery provides an accurate, reproducible, noninvasive assessment of the central pulse pressure (PP) waveform. Tonometry means "measuring of pressure," whereas applanation means "to flatten." Radial artery AT is performed by placing a hand-held tonometer (strain gauge pressure sensor) over the radial artery and applying mild pressure to partially flatten the artery (Figure 2). The radial artery pressure is then transmitted from the vessel to the sensor (strain gauge) and is recorded digitally. A mathematical formula using a fast Fourier transformation has resulted in a Food and Drug Administration–approved algorithm that permits derivation and calculation of central pressure indices from a peripheral brachial blood pressure and concomitant recording of a PP wave with radial tonometry (Figure 3).19Chen CH Nevo E Fetics B et al.Estimation of central aortic pressure waveform by mathematical transformation of radial tonometry pressure: validation of generalized transfer function.Circulation. 1997; 95: 1827-1836Crossref PubMed Scopus (1103) Google Scholar Transfer functions are fairly accurate in predicting central pressures.19Chen CH Nevo E Fetics B et al.Estimation of central aortic pressure waveform by mathematical transformation of radial tonometry pressure: validation of generalized transfer function.Circulation. 1997; 95: 1827-1836Crossref PubMed Scopus (1103) Google Scholar, 20Karamanoglu M O'Rourke MF Avolio AP Kelly RP An analysis of the relationship between central aortic and peripheral upper limb pressure waves in man.Eur Heart J. 1993; 14: 160-167Crossref PubMed Scopus (746) Google Scholar, 21Pauca AL O'Rourke MF Kon ND Prospective evaluation of a method for estimating ascending aortic pressure from the radial artery pressure waveform.Hypertension. 2001; 38: 932-937Crossref PubMed Scopus (971) Google Scholar Measurements of central pressures with AT are easily reproducible even in the hands of novices.22Crilly M Coch C Clark H Bruce M Williams D Repeatability of the measurement of augmentation index in the clinical assessment of arterial stiffness using radial applanation tonometry.Scand J Clin Lab Invest. 2007; 67: 413-422Crossref PubMed Scopus (21) Google Scholar, 23Crilly M Coch C Bruce M Clark H Williams D Repeatability of central aortic blood pressures measured non-invasively using radial artery applanation tonometry and peripheral pulse wave analysis.Blood Press. 2007; 16: 262-269Crossref PubMed Scopus (23) Google Scholar Radial artery AT, as opposed to carotid artery evaluation, is more comfortable for the patient and is easier to use in the clinical setting.24Adji A Hirata K O'Rourke MF Clinical use of indices determined non-invasively from the radial and carotid pressure waveforms.Blood Press Monit. 2006; 11: 215-221Crossref PubMed Scopus (34) Google ScholarFIGURE 3Radial artery applanation tonometry recording of a 41-yr-old man. The upper long panel shows the radial pressure waveform above the derived central pressure waveform. The bottom left panel demonstrates a magnified radial arterial waveform. Systolic and diastolic pressures are 117/85 mm Hg. The bottom right panel provides a magnified derived central pressure waveform. Central pressure is 105/85 mm Hg.View Large Image Figure ViewerDownload (PPT) Understanding AT requires comprehension of pressure waveform physiology. The pressure wave contour in any artery is the result of the summation of the forward transmission of the cardiac pressure impulse and a backward reflection generated by the peripheral vascular system at the interface between large arteries and resistance vessels (arteries and arterioles). The reflected wave has high velocities and is reflected back to the central arteries during the same ejection cycle of the heart. Pressure recorded anywhere in the arterial system is thus the sum of the forward wave and the reflected wave and is dependent on 3 factors: the amplitude and duration of ventricular ejection, the amplitude of the reflected wave, and the velocity of the reflected wave from the periphery. These 3 key parameters are influenced by several important factors. Central systolic blood pressure (SBP) increases with age. Before age 50 years the increase in central SBP is primarily due to greater wave reflection amplitude; however, after age 50 years pulse wave velocity (PWV) increases, leading to augmentation of central SBP.25McEniery CM Yasmin Hall IR Qasem A Wilkinson IB Cockcroft JR Normal vascular aging: differential effects on wave reflection and aortic pulse wave velocity: the Anglo-Cardiff Collaborative Trial (ACCT).J Am Coll Cardiol. 2005; 46: 1753-1760Abstract Full Text Full Text PDF PubMed Scopus (1026) Google Scholar A slower heart rate (HR) leads to a longer ejection time (ET), increasing the likelihood that the reflected wave will return earlier during the cardiac cycle, thereby augmenting systole. Conversely, an elevated HR has a faster ejection period, and the reflected wave returns later in the cardiac cycle.26Spodick DH Kumar S Left ventricular ejection period. Measurement by atraumatic techniques: results in normal young men and comparison of methods of calculation.Am Heart J. 1968; 76: 70-73Abstract Full Text PDF PubMed Scopus (34) Google Scholar Small stature leads to an earlier return of the reflected wave because points of reflection in the vascular tree are closer to the aorta. With increased height, the wave reflection sites are farther from the aorta, and the reflected wave returns at a later point in the cardiac cycle.27Yasmin Brown MJ Similarities and differences between augmentation index and pulse wave velocity in the assessment of arterial stiffness.QJM. 1999; 92: 595-600Crossref PubMed Scopus (179) Google Scholar, 28Wilkinson IB Mohammad NH Tyrrell S et al.Heart rate dependency of pulse pressure amplification and arterial stiffness.Am J Hypertens. 2002; 15: 24-30Crossref PubMed Scopus (276) Google Scholar Lower diastolic pressure, reflecting lower systemic vascular resistance, reduces the magnitude of wave reflection. Women have more augmentation of central pressure via the reflected wave than men; however, men have a faster PWV.27Yasmin Brown MJ Similarities and differences between augmentation index and pulse wave velocity in the assessment of arterial stiffness.QJM. 1999; 92: 595-600Crossref PubMed Scopus (179) Google Scholar Although not part of the routine measurement of radial AT, the concept of PWV should be familiar to all clinicians. Pulse wave velocity is described by the Moens-Korteweg equation derived in the 1920s that relates PWV to vessel distensibility: c0 = √Eh/2Rρ, where c0 is the wave speed, E is Young modulus in the circumferential direction, h is wall thickness, R is vessel radius, and ρ is the density of fluid. Aortic PWV is usually measured between the carotid and femoral artery. Normal values in the typical middle-aged adult are 4 m/s in the ascending aorta, 5 m/s in the abdominal aorta and carotids, 7 m/s in the brachial artery, and 8 m/s in the iliac arteries.29Zambanini A Cunningham SL Parker KH Khir AW McG Thom SA Hughes AD Wave-energy patterns in carotid, brachial, and radial arteries: a noninvasive approach using wave-intensity analysis.Am J Physiol Heart Circ Physiol. 2005; 289: H270-H276Crossref PubMed Scopus (120) Google Scholar Factors that cause less distensibility ("stiffness") of the vessel lead to a faster PWV. Advancing age also leads to a faster PWV.25McEniery CM Yasmin Hall IR Qasem A Wilkinson IB Cockcroft JR Normal vascular aging: differential effects on wave reflection and aortic pulse wave velocity: the Anglo-Cardiff Collaborative Trial (ACCT).J Am Coll Cardiol. 2005; 46: 1753-1760Abstract Full Text Full Text PDF PubMed Scopus (1026) Google Scholar Atherosclerotic risk factors lead to vascular remodeling, creating arterial "stiffness" within the aorta and other large arteries.30Weber T Auer J O'Rourke MF et al.Arterial stiffness, wave reflections, and the risk of coronary artery disease.Circulation. 2004; 109: 184-189Crossref PubMed Scopus (885) Google Scholar Pulse wave velocity increases proportionally to the number of cardiovascular risk factors present.31Lehmann ED Hopkins KD Rawesh A et al.Relation between number of cardiovascular risk factors/events and noninvasive Doppler ultrasound assessments of aortic compliance.Hypertension. 1998; 32: 565-569Crossref PubMed Scopus (146) Google Scholar It is associated with fitness level,32Vaitkevicius PV Fleg JL Engel JH et al.Effects of age and aerobic capacity on arterial stiffness in healthy adults.Circulation. 1993; 88: 1456-1462Crossref PubMed Scopus (835) Google Scholar cardiovascular events,33Boutouyrie P Tropeano AI Asmar R et al.Aortic stiffness is an independent predictor of primary coronary events in hypertensive patients: a longitudinal study.Hypertension. 2002; 39: 10-15Crossref PubMed Scopus (1487) Google Scholar and mortality in patient populations with end-stage renal disease,9London GM Blacher J Pannier B Guerin AP Marchais SJ Safar ME Arterial wave reflections and survival in end-stage renal failure.Hypertension. 2001; 38: 434-438Crossref PubMed Scopus (727) Google Scholar diabetes,34Cruickshank K Riste L Anderson SG Wright JS Dunn G Gosling RG Aortic pulse-wave velocity and its relationship to mortality in diabetes and glucose intolerance: an integrated index of vascular function?.Circulation. 2002; 106: 2085-2090Crossref PubMed Scopus (1292) Google Scholar and metabolic syndrome,35Kim YK Impact of the metabolic syndrome and its components on pulse wave velocity.Korean J Intern Med. 2006; 21: 109-115Crossref PubMed Scopus (27) Google Scholar as well as in healthy elderly adults.36Sutton-Tyrrell K Najjar SS Boudreau RM et al.Elevated aortic pulse wave velocity, a marker of arterial stiffness, predicts cardiovascular events in well-functioning older adults.Circulation. 2005; 111: 3384-3390Crossref PubMed Scopus (973) Google Scholar Wave reflection is an integral part of the central pulse waveform. The interface between the larger arteries and resistance vessels will instantaneously reflect the incoming cardiac pressure pulse wave. A pressure wave returning during the systolic ejection period due to an increased PWV, a more proximal site of wave reflection, or prolonged ET will likely augment systole (Figure 4). Systolic augmentationleads to increased cardiac loading and over time may lead to left ventricular (LV) hypertrophy, systolic or diastolic heart failure, left atrial strain and enlargement, and atrial fibrillation as well as atrial fibrillation–associated thromboembolic disease. Absence of diastolic augmentation could potentially aggravate myocardial ischemia. Conversely, decreased PWV, more distal reflecting sites, and a shorter ET may result in a reflected wave that augments the diastolic component of the central pressure waveform. The arrival of this reflected wave in diastole augments coronary arterial blood flow and decreases LV systolic workload. Hypertension management should focus on treatments that decrease the amplitude of the returning wave, slow the velocity of wave reflection, and/or increase the distance between the aorta and sites of reflection. Derivation of the central pressure waveform by AT allows the measurement of central pressures. Central SBP, diastolic blood pressure, and PP can easily be determined by measuring the peak and trough of the central pressure waveform. Augmentation of the central pressure can be quantified as the amount of pressure added to the systolic pressure peak based on the reflected wave. This pressure is referred to as augmentation pressure (AP) (Figure 5). The ratio of the AP to the central PP (systolic-diastolic pressure) is referred to as the augmentation index (Aix) and is expressed as a percentage. This measurement represents the percentage of central PP that is constituted by the AP. For ease of comparison for different HRs, the Aix is often reported normalized to an HR of 75 beats/min. Ejection time can also be calculated by defining the distance from the onset of the pulse wave to the dicrotic notch on the descending side of the waveform. Time to reflection (Tr) is defined as the time between the onset of the pulse waveform and the onset of the reflected systolic central waveform. The current limitation with measuring central pressures via radial artery AT is that neither the age-, sex-, and ethnicity-specific reference ranges nor the specific central pressure treatment targets have been well defined. Central pressure measurements by radial artery AT are rarely described according to age and sex in healthy populations (Table 1) or between hypertensive and nonhypertensive populations (Table 2).Table 1Central Pressure Measurements, Stratified by Age and Sex in Normotensive PopulationsReferenceNo. of participantsAge (y)CSP (mm Hg)CPP (mm Hg)PP Amp (mm Hg)AP (mm Hg)Aix (%)Tr (ms)Healthy females McEniery et al,25McEniery CM Yasmin Hall IR Qasem A Wilkinson IB Cockcroft JR Normal vascular aging: differential effects on wave reflection and aortic pulse wave velocity: the Anglo-Cardiff Collaborative Trial (ACCT).J Am Coll Cardiol. 2005; 46: 1753-1760Abstract Full Text Full Text PDF PubMed Scopus (1026) Google Scholar 2005133 5528±2 McEniery et al, 200550960–69118±1043±81.21±0.1015±534±9131±14 McEniery et al, 200529070–79119±956±81.19±0.1016±535±9129±12 O'Rourke & Adji,40O'Rourke MF Adji A Basis for the use of central blood pressure measurement in office clinical practice.J Am Soc Hypertens. 2008; 2: 28-38Abstract Full Text Full Text PDF PubMed Scopus (26) Google Scholar 200854871±13132±2250±1620±1132±11 McEniery et al, 20053880–90120±1149±121.18±0.1118±737±10125±12Healthy males McEniery et al, 2005172<20103±829±51.72±0.11−1±3−2±8150±17 McEniery et al, 200517820–29105±820±61.7±0.141±42±11154±21 Van Trijp et al, 200622428±1.03.2±11 McEniery et al, 200518330–39109±931±61.50±0.184±512±13151±21 Yasmin & Brown, 19994140±8113±138.6±13 McEniery et al, 200525840–49113±934±61.39±0.157±419±10148±16 McEniery et al, 200542950–59115±935±71.33±0.169±524±10143±15 Kampus et al,38Kampus P Muda P Kals J et al.The relationship between inflammation and arterial stiffness in patients with essential hypertension.Int J Cardiol. 2006; 112: 46-51Abstract Full Text Full Text PDF PubMed Scopus (40) Google Scholar 20063552±811±14152±11 McEniery et al, 200543060–69117±939±71.26±0.1311±528±9141±12 O'Rourke & Adji, 200895769±13124±1953±1713±924±12 McEniery et al, 200528070–79118±942±71.24±0.1213±530±9136±12 McEniery et al, 20053980–90120±845±91.25±0.1414±530±10133±16Data are provided as mean ± SD, unless otherwise indicated. Blank cells indicate that the study did not report the given value. Aix = augmentation index; AP = augmentation pressure; CPP = central pulse pressure; CSP = central systolic pressure; PP amp = pulse pressure amplifcation; T = time to refection. Open table in a new tab TABLE 2Central Pressure Measurements in Hypertensive vs Nonhypertensive PopulationsaData are provided as mean ± SD, unless otherwise indicated. Blank cells indicate that the study did not report the given value. Aix = augmentation index; [email protected] = Aix normalized at 75 heart beats/min; AP = augmentation pressure; CPP = central pulse pressure; CSP = central systolic pressure; HTN = hypertension; PP amp = pulse pressure amplifcation; Tr = time to refection.ReferemcePopulationNo. of participantsAge (y)CSP (mm Hg)CPP (mm Hg)PP amp (mm Hg)AP (mm Hg)Aix (%)@Aix 75 (%)Tr (ms)Mahmud & Feely,41Mahmud A Feely J Aldosterone-to-renin ratio, arterial stiffness, and the response to aldosterone antagonism in essential hypertension.Am J Hypertens. 2005; 18: 50-55Crossref PubMed Scopus (93) Google Scholar 2005HTN7847±12140±2047.5±14Kampus et al,38Kampus P Muda P Kals J et al.The relationship between inflammation and arterial stiffness in patients with essential hypertension.Int J Cardiol. 2006; 112: 46-51Abstract Full Text Full Text PDF PubMed Scopus (40) Google Scholar 2006Men, HTN3554±720±12bIndicates signifcant differences between groups.143±11bIndicates signifcant differences between groups.Men, no HTN3552±811±14152±11Women, HTN750±629±8bIndicates signifcant differences between groups.129±7bIndicates signifcant differences between groups.Women, no HTN748±617±10144±9Strauch et al,42Strauch B Petrak O Wichterle D Zelinka T Holaj R Widimsky Jr, J Increased arterial wall stiffness in primary aldosteronism in comparison with essential hypertension.Am J Hypertens. 2006; 19: 909-914Crossref PubMed Scopus
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