The Experts below are selected from a list of 36252 Experts worldwide ranked by ideXlab platform
Michel E. Safar - One of the best experts on this subject based on the ideXlab platform.
-
Pulse Pressure amplification, Pressure waveform calibration and clinical applications
Atherosclerosis, 2012Co-Authors: Davide Agnoletti, Y. Zhang, Paolo Salvi, Claudio Borghi, Jirar Topouchian, Michel E. Safar, Jacques BlacherAbstract:Abstract Obtaining Pulse Pressure non-invasively from applanation tonometry requires the calibration of Pressure waveform with brachial systolic and diastolic blood Pressure. In the literature, several calibration methodologies are applied, and clinical studies disagree about the predictive value of central hemodynamic parameters. Our aim was to compare 4 calibration methodologies and assess the usefulness of Pulse Pressure amplification as an index independent of calibration. We investigated 108 subjects with tonometry in carotid, femoral, brachial, radial and dorsalis-pedis arteries; Pulse Pressure amplification between arterial waveforms was calculated. Four methods to calibrate the waveforms were compared: the 1/3 rule, the 40% rule, the integral of radial and brachial waveforms. Pulse Pressure amplification in 5 arterial territories (carotid-femoral, carotid-brachial, carotid-radial and carotid-pedis amplifications; femoral-pedis amplification) was studied. Pulse Pressure was successfully measured non-invasively at the 5 arterial sites. Pulse Pressure was markedly dependent on calibration, with differences up to 18 mmHg between methods. Calculation of Pulse Pressure amplification eliminated effects of calibration method. Furthermore, Pulse Pressure amplifications in the 5 arterial sites presented a distinct pattern of clinical/biological determinants: heart rate and body height were common determinants of carotid to brachial, radial and femoral amplifications; diabetes was related to carotid to brachial amplification and Pulse wave velocity to femoral to pedis amplification. In conclusion, the calibration of Pulse Pressure will influence results of clinical trials, but calculation of Pulse Pressure amplification can avoid this. We also suggest that the alteration of amplification in each arterial territory might be considered as a signal of clinical/subclinical damage.
-
Intraaortic Pulse Pressure Amplification in Subjects at High Coronary Risk
Hypertension, 2010Co-Authors: Mohamed Temmar, Piotr Jankowski, Marcel Peltier, Vincent Mouquet, D. Debicka-dabrowska, Farah Hamida, Kalina Kawecka-jaszcz, Michel E. SafarAbstract:Peripheral (brachial) Pulse Pressure normally exceeds central (aortic) Pulse Pressure but is a less powerful predictor of cardiovascular risk. The difference between the 2 variables, called Pulse Pressure amplification, has never been specifically studied between the proximal and distal aorta in coronary patients. Our goal was to determine aortic Pulse Pressure amplification in subjects at high coronary risk, with emphasis on associated renal and inflammatory factors. Blood Pressure was measured invasively in the ascending aorta, abdominal aorta (at the level of kidneys), and iliac artery in 101 subjects (mean age, 63±11 years; 61 men) undergoing coronary angiography. Independently of age, sex, and the presence of coronary stenosis, the increase of Pulse Pressure between the ascending and terminal aorta was over 10 mm Hg ( P P P
-
Pulse Pressure arterial stiffness and drug treatment of hypertension
Hypertension, 2001Co-Authors: Luc M Van Bortel, Harry A J Struijkerboudier, Michel E. SafarAbstract:Epidemiological studies in the past decade have stressed the importance of Pulse Pressure as an independent risk factor for cardiovascular morbidity and mortality. We briefly review the epidemiological evidence and discuss in more detail the pathophysiological basis for this observation and the therapeutic consequences. We focus on the vascular determinants of increased Pulse Pressure. Both longitudinal and cross-sectional components of the vascular system contribute to the shape of the arterial Pressure wave and, thereby, to Pulse Pressure. The primary longitudinal component is the architecture of the arterial tree, which determines the major reflection sites for the Pressure wave. The cross-sectional architecture of the vascular system consists of a geometric (diameter) and a structural (composition vessel wall) component. Both diameter and composition of the vessel wall vary greatly when going from central to more peripheral arteries. We review the implications for the functional properties of various arterial segments. Finally, we discuss the therapeutic consequences of targeting Pulse Pressure rather than mean blood Pressure with various drug classes. Among the antihypertensive agents, nitrates, NO donors, and drugs that interfere with the renin-angiotensin-aldosterone system may offer useful tools to lower Pulse Pressure, in addition to mean blood Pressure. Future developments may include non-antihypertensive agents that target collagen or other components of the arterial wall matrix. However, large-scale clinical trials will have to confirm the therapeutic value of these agents in the treatment of increased Pulse Pressure and arterial stiffness.
-
non invasive assessment of local arterial Pulse Pressure comparison of applanation tonometry and echo tracking
Journal of Hypertension, 2001Co-Authors: Luc M Van Bortel, Michel E. Safar, Jan A. Staessen, Elisabeth J Balkestein, Janneke J Van Der Heijdenspek, Floris Vanmolkot, Johannes A Kragten, Jan W Vredeveld, Harry Struijker A J Boudier, Arnold P G HoeksAbstract:ObjectivesPulse Pressure is not constant throughout the arterial tree. Use of Pulse Pressure at one arterial site as surrogate for Pulse Pressure at another arterial site may be erroneous. The present study compares three non-invasive techniques to measure local Pulse Pressure: (i) internally calibr
-
Pulse Pressure not mean Pressure determines cardiovascular risk in older hypertensive patients
JAMA Internal Medicine, 2000Co-Authors: Jacques Blacher, Jan A. Staessen, Lutgarde Thijs, Robert Fagard, X Girerd, J Gasowski, Ji G Wang, Michel E. SafarAbstract:Background: Current guidelines for the management of hypertension rest almost completely on the measurement of systolic and diastolic blood Pressure. However, the arterial blood Pressure wave is more correctly described as consisting of a pulsatile (Pulse Pressure) and a steady (mean Pressure) component. Objective: To explore the independent roles of Pulse Pressure and mean Pressure as determinants of cardiovascular prognosis in older hypertensive patients. Methods: This meta-analysis, based on individual patient data, pooled the results of the European Working Party on High Blood Pressure in the Elderly trial (n = 840), the Systolic Hypertension in Europe Trial (n = 4695), and the Systolic Hypertension in China Trial (n = 2394). The relative hazard rates associated with Pulse Pressure and mean Pressure were calculated using Cox regression analysis, with stratification for the 3 trials and with adjustments for sex, age, previous cardiovascular complications, smoking, and treatment group. Results: A 10-mm Hg wider Pulse Pressure increased the risk of major cardiovascular complications; after controlling for mean Pressure and the other covariates, the increase in risk ranged from approximately 13% for all coronary end points (P = .02) to nearly 20% for cardiovascular mortality (P = .001). In a similar analysis, mean Pressure predicted the incidence of cardiovascular complications but only after removal of Pulse Pressure as an explanatory variable from the model. Furthermore, the probability of a major cardiovascular end point increased with higher systolic blood Pressure; at any given level of systolic blood Pressure, it also increased with lower diastolic blood Pressure, suggesting that the wider Pulse Pressure was driving the risk of major complications. Conclusions: In older hypertensive patients, Pulse Pressure not mean Pressure is the major determinant of cardiovascular risk. The implications of these findings for the management of hypertensive patients should be further investigated in randomized controlled outcome trials in which the pulsatile component of blood Pressure is differently affected by antihypertensive drug treatment. Arch Intern Med. 2000;160:1085-1089
Gary F Mitchell - One of the best experts on this subject based on the ideXlab platform.
-
Pulse Pressure and risk of new onset atrial fibrillation
JAMA, 2007Co-Authors: Gary F Mitchell, Ramachandran S. Vasan, Michelle J. Keyes, Helen Parise, Thomas J. Wang, Martin G. Larson, William B. Kannel, Daniel Levy, Ralph B Dagostino, Emelia J. BenjaminAbstract:ContextAtrial fibrillation (AF) is responsible for considerable morbidity and mortality, making identification of modifiable risk factors a priority. Increased Pulse Pressure, a reflection of aortic stiffness, increases cardiac load and may increase AF risk.ObjectiveTo examine relations between Pulse Pressure and incident AF.Design, Setting, and ParticipantsProspective, community-based observational cohort in Framingham, Mass, including 5331 Framingham Heart Study participants aged 35 years and older and initially free from AF (median age, 57 years; 55% women).Main Outcome MeasuresIncident AF.ResultsAF developed in 698 participants (13.1%) a median of 12 years after Pulse Pressure assessment. Cumulative 20-year AF incidence rates were 5.6% for Pulse Pressure of 40 mm Hg or less (25th percentile) and 23.3% for Pulse Pressure greater than 61 mm Hg (75th percentile). In models adjusted for age, sex, baseline and time-dependent change in mean arterial Pressure, and clinical risk factors for AF (body mass index, smoking, valvular disease, diabetes, electrocardiographic left ventricular hypertrophy, hypertension treatment, and prevalent myocardial infarction or heart failure), Pulse Pressure was associated with increased risk for AF (adjusted hazard ratio [HR], 1.26 per 20-mm Hg increment; 95% confidence interval [CI], 1.12-1.43; P<.001). In contrast, mean arterial Pressure was unrelated to incident AF (adjusted HR, 0.96 per 10-mm Hg increment; 95% CI, 0.88-1.05; P = .39). Systolic Pressure was related to AF (HR, 1.14 per 20-mm Hg increment; 95% CI, 1.04-1.25; P = .006); however, if diastolic Pressure was added, model fit improved and the diastolic relation was inverse (adjusted HR, 0.87 per 10-mm Hg increment; 95% CI, 0.78-0.96; P = .01), consistent with a Pulse Pressure effect. Among patients with interpretable echocardiographic images, the association between Pulse Pressure and AF persisted in models that adjusted for baseline left atrial dimension, left ventricular mass, and left ventricular fractional shortening (adjusted HR, 1.23; 95% CI, 1.09-1.39; P = .001).ConclusionPulse Pressure is an important risk factor for incident AF in a community-based sample. Further research is needed to determine whether interventions that reduce Pulse Pressure will limit the growing incidence of AF.
-
Pulse Pressure and risk of new-onset atrial fibrillation.
JAMA, 2007Co-Authors: Gary F Mitchell, Ramachandran S. Vasan, Michelle J. Keyes, Helen Parise, Thomas J. Wang, Martin G. Larson, Ralph B. D'agostino, William B. Kannel, Daniel Levy, Emelia J. BenjaminAbstract:ContextAtrial fibrillation (AF) is responsible for considerable morbidity and mortality, making identification of modifiable risk factors a priority. Increased Pulse Pressure, a reflection of aortic stiffness, increases cardiac load and may increase AF risk.ObjectiveTo examine relations between Pulse Pressure and incident AF.Design, Setting, and ParticipantsProspective, community-based observational cohort in Framingham, Mass, including 5331 Framingham Heart Study participants aged 35 years and older and initially free from AF (median age, 57 years; 55% women).Main Outcome MeasuresIncident AF.ResultsAF developed in 698 participants (13.1%) a median of 12 years after Pulse Pressure assessment. Cumulative 20-year AF incidence rates were 5.6% for Pulse Pressure of 40 mm Hg or less (25th percentile) and 23.3% for Pulse Pressure greater than 61 mm Hg (75th percentile). In models adjusted for age, sex, baseline and time-dependent change in mean arterial Pressure, and clinical risk factors for AF (body mass index, smoking, valvular disease, diabetes, electrocardiographic left ventricular hypertrophy, hypertension treatment, and prevalent myocardial infarction or heart failure), Pulse Pressure was associated with increased risk for AF (adjusted hazard ratio [HR], 1.26 per 20-mm Hg increment; 95% confidence interval [CI], 1.12-1.43; P
-
isolated systolic hypertension prognostic information provided by Pulse Pressure
Hypertension, 1999Co-Authors: Michael J Domanski, Barry R Davis, Marc A Pfeffer, Mark Kastantin, Gary F MitchellAbstract:Abstract —Increased arterial stiffness results in increased characteristic impedance of the aorta and increased Pulse wave velocity, which increases systolic and Pulse Pressures. An association between increased Pulse Pressure and adverse cardiovascular events has been found in normotensive and hypertensive patient populations. Increased Pulse Pressure has also been associated with thickening of the carotid intima and media. However, the relationship between Pulse Pressure and stroke has not previously been evaluated. In this study, we examined the hypothesis that Pulse Pressure is an independent predictor of stroke in elderly patients with systolic hypertension entered in the Systolic Hypertension in the Elderly Program. Differences in baseline characteristics were examined by tertiles of Pulse Pressure. The independent prognostic value of Pulse Pressure and mean arterial Pressure for predicting either stroke or total mortality was assessed with Cox proportional hazards models that included Pulse Pressure, mean arterial Pressure, and other variables that were significant on univariate analysis. This analysis demonstrated an 11% increase in stroke risk and a 16% increase in risk of all-cause mortality for each 10-mm Hg increase in Pulse Pressure. Each 10-mm Hg increase in mean arterial Pressure was independently associated with a 20% increase in the risk of stroke and a 14% increase in the risk of all-cause mortality. These data provide strong evidence of an association of increased conduit vessel stiffness, as indicated by increased Pulse Pressure, with stroke and total mortality, independent of the effects of mean arterial Pressure, in elderly patients with isolated systolic hypertension.
-
Increased Pulse Pressure and Risk of Heart Failure in the Elderly
JAMA, 1999Co-Authors: Claudia U. Chae, Marc A Pfeffer, Gary F Mitchell, Robert J. Glynn, James Taylor, Charles H. HennekensAbstract:ContextArterial stiffness increases with age. Thus, Pulse Pressure, an index of arterial stiffening, may predict congestive heart failure (CHF) in the elderly.ObjectiveTo study prospectively the association between Pulse Pressure and risk of CHF.DesignProspective cohort study.SettingThe community-based East Boston Senior Health Project, East Boston, Mass.PatientsA total of 1621 men and women (mean [SD] age, 77.9 [5.0] years) free of CHF who had blood Pressure measurements taken in 1988-1989 and were followed up for 3.8 years.Main Outcome MeasureIncidence of CHF as ascertained by hospital discharge diagnosis (n=208) and death certificates (n=13).ResultsAfter controlling for age, sex, mean arterial Pressure, history of coronary heart disease, diabetes mellitus, atrial fibrillation, valvular heart disease, and antihypertensive medication use, Pulse Pressure was an independent predictor of CHF. For each 10-mm Hg elevation in Pulse Pressure, there was a 14% increase in risk of CHF (95% confidence interval, 1.05-1.24; P=.003). Those in the highest tertile of Pulse Pressure (>67 mm Hg) had a 55% increased risk of CHF (P=.02) compared with those in the lowest (
-
increased Pulse Pressure and risk of heart failure in the elderly
JAMA, 1999Co-Authors: Claudia U. Chae, Marc A Pfeffer, Gary F Mitchell, Robert J. Glynn, James Taylor, Charles H. HennekensAbstract:ContextArterial stiffness increases with age. Thus, Pulse Pressure, an index of arterial stiffening, may predict congestive heart failure (CHF) in the elderly.ObjectiveTo study prospectively the association between Pulse Pressure and risk of CHF.DesignProspective cohort study.SettingThe community-based East Boston Senior Health Project, East Boston, Mass.PatientsA total of 1621 men and women (mean [SD] age, 77.9 [5.0] years) free of CHF who had blood Pressure measurements taken in 1988-1989 and were followed up for 3.8 years.Main Outcome MeasureIncidence of CHF as ascertained by hospital discharge diagnosis (n=208) and death certificates (n=13).ResultsAfter controlling for age, sex, mean arterial Pressure, history of coronary heart disease, diabetes mellitus, atrial fibrillation, valvular heart disease, and antihypertensive medication use, Pulse Pressure was an independent predictor of CHF. For each 10-mm Hg elevation in Pulse Pressure, there was a 14% increase in risk of CHF (95% confidence interval, 1.05-1.24; P=.003). Those in the highest tertile of Pulse Pressure (>67 mm Hg) had a 55% increased risk of CHF (P=.02) compared with those in the lowest (<54 mm Hg). Pulse Pressure was more predictive than systolic blood Pressure alone and was independent of diastolic blood Pressure.ConclusionPulse Pressure, an easily measurable correlate of pulsatile hemodynamic load, is an independent predictor of risk of CHF in this elderly cohort.
J R Cockcroft - One of the best experts on this subject based on the ideXlab platform.
-
increased central Pulse Pressure and augmentation index in subjects with hypercholesterolemia
Journal of the American College of Cardiology, 2002Co-Authors: Ian B Wilkinson, Ian R Hall, David J Webb, K Prasad, Anne Gwenllian Thomas, Helen Maccallum, Michael P Frenneaux, J R CockcroftAbstract:Abstract Objectives The goal of this study was to investigate the relation between serum cholesterol, arterial stiffness and central blood Pressure. Background Arterial stiffness and Pulse Pressure are important determinants of cardiovascular risk. However, the effect of hypercholesterolemia on arterial stiffness is controversial, and central Pulse Pressure has not been previously investigated. Methods Pressure waveforms were recorded from the radial artery in 68 subjects with hypercholesterolemia and 68 controls, and corresponding central waveforms were generated using Pulse wave analysis. Central Pressure, augmentation index (AIx) (a measure of systemic stiffness) and aortic Pulse wave velocity were determined. Results There was no significant difference in peripheral blood Pressure between the two groups, but central Pulse Pressure was significantly higher in the group with hypercholesterolemia (37 ± 11 mm Hg vs. 33 ± 10 mm Hg [means ± SD]; p = 0.028). Augmentation index was also significantly higher in the patients with hypercholesterolemia group (24.8 ± 11.3% vs. 15.6 ± 12.1%; p Conclusions Patients with hypercholesterolemia have a higher central Pulse Pressure and stiffer blood vessels than matched controls, despite similar peripheral blood Pressures. These hemodynamic changes may contribute to the increased risk of cardiovascular disease associated with hypercholesterolemia, and assessment may improve risk stratification.
-
heart rate dependency of Pulse Pressure amplification and arterial stiffness
American Journal of Hypertension, 2002Co-Authors: Ian B Wilkinson, Nadia Haj Mohammad, Sian Tyrrell, Ian R Hall, David J Webb, Vince Paul, T Levy, J R CockcroftAbstract:Background: Pulse Pressure and aortic Pulse wave velocity, measures of arterial stiffness, are both important determinants of cardiovascular risk. However, assessment of peripheral Pulse Pressure does not always provide a reliable measure of changes in central Pulse Pressure or arterial stiffness. The aim of the present study was to assess the effect of acute changes in heart rate on arterial stiffness and on peripheral and central Pulse Pressure in healthy subjects. Methods: Twenty subjects (age range, 20 to 72 years) were studied at cardiac catheterization. Pulse wave analysis was used to determine central Pressure, augmentation index (AIx), a measure of systemic arterial stiffness, and aortic Pulse wave velocity (PWV) during right atrial pacing (80 to 120 beats/min). Results: Pulse Pressure amplification increased during pacing due to a reduction in central Pressure augmentation. AIx was significantly and inversely related to heart rate (r 0.70, P .001) due to an alteration in the relative timing of the reflected Pressure wave, rather than a reduction in arterial stiffness, as PWV did not change. Conclusions: These data suggest that peripheral Pulse Pressure does not provide an accurate assessment of changes in central hemodynamics in relation to changes in heart rate, and that aortic stiffness is not affected by acute changes in heart rate. Am J Hypertens 2002;15:24 ‐30 © 2002 American Journal of Hypertension, Ltd.
Luc M Van Bortel - One of the best experts on this subject based on the ideXlab platform.
-
noninvasive assessment of local Pulse Pressure importance of brachial to radial Pressure amplification
Hypertension, 2005Co-Authors: Francis Verbeke, Patrick Segers, Steven Heireman, Raymond Vanholder, Pascal Verdonck, Luc M Van BortelAbstract:The advocated SphygmoCor procedure uses a radial-to-aorta transfer function with calibration on brachial instead of radial artery Pressure to assess the central Pulse Pressure. We compared these values with carotid artery Pulse Pressures obtained from a validated calibration method, assuming mean minus diastolic blood Pressure constant throughout the large artery tree. From 44 healthy subjects (21 males; 22 to 68 years) Pressure waves were obtained at the radial, brachial, and carotid artery with applanation tonometry. Using the calibration method, radial and carotid artery Pressures were assessed from brachial artery waves and Pressures. The effect of brachial-to-radial Pulse Pressure amplification, brachial Pulse Pressure, mean Pressure, age, gender, height, body mass index, and smoking on differences between the 2 methods was assessed. Brachial artery Pressure was 118±12/72±10 mm Hg. SphygmoCor central Pulse Pressure was 9.7±4.6 mm Hg lower ( P P P =0.005). After calibration of the radial Pressure wave with radial instead of brachial artery Pressures, the difference between SphygmoCor central Pulse Pressure and carotid Pulse Pressure decreased with 4 mm Hg. The advocated SphygmoCor procedure systematically underestimates the central Pulse Pressure with brachial-to-radial Pulse Pressure amplification as important determinant. Therefore, calibration of radial artery Pressure waves on brachial artery Pressures should be avoided. The underestimation of central aortic Pulse Pressure caused by the radial-to-aorta transfer function itself is much less than previously reported.
-
Pulse Pressure arterial stiffness and drug treatment of hypertension
Hypertension, 2001Co-Authors: Luc M Van Bortel, Harry A J Struijkerboudier, Michel E. SafarAbstract:Epidemiological studies in the past decade have stressed the importance of Pulse Pressure as an independent risk factor for cardiovascular morbidity and mortality. We briefly review the epidemiological evidence and discuss in more detail the pathophysiological basis for this observation and the therapeutic consequences. We focus on the vascular determinants of increased Pulse Pressure. Both longitudinal and cross-sectional components of the vascular system contribute to the shape of the arterial Pressure wave and, thereby, to Pulse Pressure. The primary longitudinal component is the architecture of the arterial tree, which determines the major reflection sites for the Pressure wave. The cross-sectional architecture of the vascular system consists of a geometric (diameter) and a structural (composition vessel wall) component. Both diameter and composition of the vessel wall vary greatly when going from central to more peripheral arteries. We review the implications for the functional properties of various arterial segments. Finally, we discuss the therapeutic consequences of targeting Pulse Pressure rather than mean blood Pressure with various drug classes. Among the antihypertensive agents, nitrates, NO donors, and drugs that interfere with the renin-angiotensin-aldosterone system may offer useful tools to lower Pulse Pressure, in addition to mean blood Pressure. Future developments may include non-antihypertensive agents that target collagen or other components of the arterial wall matrix. However, large-scale clinical trials will have to confirm the therapeutic value of these agents in the treatment of increased Pulse Pressure and arterial stiffness.
-
non invasive assessment of local arterial Pulse Pressure comparison of applanation tonometry and echo tracking
Journal of Hypertension, 2001Co-Authors: Luc M Van Bortel, Michel E. Safar, Jan A. Staessen, Elisabeth J Balkestein, Janneke J Van Der Heijdenspek, Floris Vanmolkot, Johannes A Kragten, Jan W Vredeveld, Harry Struijker A J Boudier, Arnold P G HoeksAbstract:ObjectivesPulse Pressure is not constant throughout the arterial tree. Use of Pulse Pressure at one arterial site as surrogate for Pulse Pressure at another arterial site may be erroneous. The present study compares three non-invasive techniques to measure local Pulse Pressure: (i) internally calibr
Ian B Wilkinson - One of the best experts on this subject based on the ideXlab platform.
-
increased central Pulse Pressure and augmentation index in subjects with hypercholesterolemia
Journal of the American College of Cardiology, 2002Co-Authors: Ian B Wilkinson, Ian R Hall, David J Webb, K Prasad, Anne Gwenllian Thomas, Helen Maccallum, Michael P Frenneaux, J R CockcroftAbstract:Abstract Objectives The goal of this study was to investigate the relation between serum cholesterol, arterial stiffness and central blood Pressure. Background Arterial stiffness and Pulse Pressure are important determinants of cardiovascular risk. However, the effect of hypercholesterolemia on arterial stiffness is controversial, and central Pulse Pressure has not been previously investigated. Methods Pressure waveforms were recorded from the radial artery in 68 subjects with hypercholesterolemia and 68 controls, and corresponding central waveforms were generated using Pulse wave analysis. Central Pressure, augmentation index (AIx) (a measure of systemic stiffness) and aortic Pulse wave velocity were determined. Results There was no significant difference in peripheral blood Pressure between the two groups, but central Pulse Pressure was significantly higher in the group with hypercholesterolemia (37 ± 11 mm Hg vs. 33 ± 10 mm Hg [means ± SD]; p = 0.028). Augmentation index was also significantly higher in the patients with hypercholesterolemia group (24.8 ± 11.3% vs. 15.6 ± 12.1%; p Conclusions Patients with hypercholesterolemia have a higher central Pulse Pressure and stiffer blood vessels than matched controls, despite similar peripheral blood Pressures. These hemodynamic changes may contribute to the increased risk of cardiovascular disease associated with hypercholesterolemia, and assessment may improve risk stratification.
-
heart rate dependency of Pulse Pressure amplification and arterial stiffness
American Journal of Hypertension, 2002Co-Authors: Ian B Wilkinson, Nadia Haj Mohammad, Sian Tyrrell, Ian R Hall, David J Webb, Vince Paul, T Levy, J R CockcroftAbstract:Background: Pulse Pressure and aortic Pulse wave velocity, measures of arterial stiffness, are both important determinants of cardiovascular risk. However, assessment of peripheral Pulse Pressure does not always provide a reliable measure of changes in central Pulse Pressure or arterial stiffness. The aim of the present study was to assess the effect of acute changes in heart rate on arterial stiffness and on peripheral and central Pulse Pressure in healthy subjects. Methods: Twenty subjects (age range, 20 to 72 years) were studied at cardiac catheterization. Pulse wave analysis was used to determine central Pressure, augmentation index (AIx), a measure of systemic arterial stiffness, and aortic Pulse wave velocity (PWV) during right atrial pacing (80 to 120 beats/min). Results: Pulse Pressure amplification increased during pacing due to a reduction in central Pressure augmentation. AIx was significantly and inversely related to heart rate (r 0.70, P .001) due to an alteration in the relative timing of the reflected Pressure wave, rather than a reduction in arterial stiffness, as PWV did not change. Conclusions: These data suggest that peripheral Pulse Pressure does not provide an accurate assessment of changes in central hemodynamics in relation to changes in heart rate, and that aortic stiffness is not affected by acute changes in heart rate. Am J Hypertens 2002;15:24 ‐30 © 2002 American Journal of Hypertension, Ltd.
