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ABSTRACT: Background Triiodothyronine (T3) has many effects on the heart and marked changes in cardiac function and structure occur in patients with (subclinical) thyroid disease. We investigated whether between-subject variation in thyroid hormone levels within the euthyroid range is also associated with heart rate and echocardiographic heart function and structure. Methods Subjects were selected from the Asklepios study (n=2524), a population-representative random sample between 35 and 55 yrs, free from overt cardiovascular disease at baseline. Analyses were restricted to 2078 subjects (1013 women and 1065 men), not using antihypertensive or thyroid medication nor having anti-TPO levels above clinical cut-off or TSH levels outside the reference range. All subjects were phenotyped in-depth and underwent comprehensive echocardiography, including diastolic evaluation. Thyroid function parameters were determined by automated electrochemiluminescence. Results Heart rate was robustly positively associated with (quartiles of) (F)T3, both in subjects with TSH levels within reference (0.27-4.2 µU/l) as in narrow TSH-range (0.5-2.5 µU/l) (p≤0.0001). (F)T3 was negatively associated with LV (left ventricular) end-diastolic volume but positively with relative wall thickness. TT3 was associated with enhanced ventricular contraction (as assessed by tissue Doppler imaging). FT4, FT3 and TT3 were positively associated with late ventricular filling, and TT3 was associated with early ventricular filling. Conclusion We have demonstrated a strong positive association between thyroid hormone levels within the euthyroid range and heart rate, and more subtle effects on cardiac function and structure. More specifically, we suggest smaller LV cavity size (with increased relative wall thickness), an enhanced atrial and ventricular contraction and LV relaxation with higher circulating thyroid hormones. These results illustrate that variation of thyroid hormone levels even within the reference range exerts effects on the heart.
Thyroid: official journal of the American Thyroid Association 01/2013; · 2.60 Impact Factor
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ABSTRACT: Experimental studies implicate late systolic load as a determinant of impaired left-ventricular relaxation. We aimed to assess the relationship between the myocardial loading sequence and left-ventricular contraction and relaxation. Time-resolved central pressure and time-resolved left-ventricular geometry were measured with carotid tonometry and speckle-tracking echocardiography, respectively, for computation of time-resolved ejection-phase myocardial wall stress (EP-MWS) among 1214 middle-aged adults without manifest cardiovascular disease from the general population. Early diastolic annular velocity and systolic annular velocities were measured with tissue Doppler imaging, and segment-averaged longitudinal strain was measured with speckle-tracking echocardiography. After adjustment for age, sex, and potential confounders, late EP-MWS was negatively associated with early diastolic mitral annular velocity (standardized β=-0.25; P<0.0001) and mitral inflow propagation velocity (standardized β=-0.13; P=0.02). In contrast, early EP-MWS was positively associated with early diastolic mitral annular velocity (standardized β=0.18; P<0.0001) and mitral inflow propagation velocity (standardized β=0.22; P<0.0001). A higher late EP-MWS predicted a lower systolic mitral annular velocity (standardized β=-0.31; P<0.0001) and lesser myocardial longitudinal strain (standardized β=0.32; P<0.0001), whereas a higher early EP-MWS was associated with a higher systolic mitral annular velocity (standardized β=0.16; P=0.002) and greater longitudinal strain (standardized β=-0.24; P=0.002). The loading sequence remained independently associated with early diastolic mitral annular velocity after adjustment for systolic mitral annular velocity or systolic longitudinal strain. In the context of available experimental data, our findings support the role of the myocardial loading sequence as a determinant of left-ventricular systolic and diastolic function. A loading sequence characterized by prominent late systolic wall stress was associated with lower longitudinal systolic function and diastolic relaxation.
Hypertension 01/2013; · 6.21 Impact Factor
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Heart (British Cardiac Society) 01/2013; 99(1):55-64. · 4.22 Impact Factor
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Caroline M Van Daele,
Tim De Meyer,
Marc L De Buyzere, Thierry C Gillebert,
Simon L I J Denil,
Sofie Bekaert,
Julio A Chirinos,
Patrick Segers,
Guy G De Backer,
Dirk De Bacquer,
Ernst R Rietzschel,
On Behalf Of The Asklepios Investigators
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ABSTRACT: Whereas the importance of family history (FH) is widely recognized in cardiovascular risk assessment, its full potential could be underutilized, when applied with its current simple guidelines-based definition (cFH): presence of premature cardiovascular disease (CVD) in a first-degree relative. We tested the added value of a new, extended family history definition (eFH), also taking into account later onset of disease, second-degree relatives and number of affected relatives, on profiling cardiovascular risk and atherosclerotic burden in the general population.
longitudinal population study.
random, representative population sample from Erpe-Mere and Nieuwerkerken (Belgium, primary care).
2524 male/female volunteers, aged 35-55 years, free from overt CVD.
Subjects were extensively phenotyped including presence of atherosclerosis (ultrasound) and a newly developed FH questionnaire (4 generations).
Compared to cFH, eFH was superior in predicting an adverse risk profile (glycemic state, elevated blood pressure, lipid abnormalities, presence of metabolic syndrome components) and presence of atherosclerosis (all age & sex-adjusted p<0.05). Unlike cFH, eFH remained a significant predictor of subclinical atherosclerosis after adjusting for confounders. Most relations with eFH were not graded but showed clear informational breakpoints, with absence of CVD (including late onset) in any first-degree relative being a negative predictor of atherosclerosis, and a particularly interesting phenotype for further study.
A novel, extended FH definition is superior to the conventional definition in profiling cardiovascular risk and atherosclerotic burden in the general population. There remain clear opportunities to refine and increase the performance and informational content of this simple, readily-available inexpensive tool.
PLoS ONE 01/2013; 8(5):e63185. · 4.09 Impact Factor
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Tim De Meyer,
Caroline M Van Daele,
Marc L De Buyzere,
Simon L I J Denil,
Dirk De Bacquer,
Patrick Segers,
Luc Cooman,
Guy G De Backer, Thierry C Gillebert,
Sofie Bekaert,
Ernst R Rietzschel
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ABSTRACT: OBJECTIVE: Shorter telomere length is associated with the occurrence of cardiovascular events, but the question of causality is complicated by the intertwined effects of inheritance, aging, and lifestyle factors on both telomere length and cardiovascular disease (CVD). Some studies indicated that healthy offspring of coronary artery disease patients exhibited shorter telomeres than subjects without a family history. Importantly, this result would imply that inheritance of shorter telomeres is a primary abnormality associated with an increased risk of CVD, the so-called Telomere Hypothesis of CVD. Therefore, we aimed at further validating the latter results in the large, population-representative Asklepios Study.Methods and results-Peripheral blood leukocyte telomere length was measured using telomere restriction fragment analysis in the young to middle-aged (≈35-55 years old) Asklepios study population, free from overt CVD, and could be successfully combined with data from the Asklepios Family History Database for 2136 subjects. No shorter telomere length could be found in healthy subjects with a family history of CVD compared with those without. CONCLUSIONS: These findings cast serious doubt on the hypothesis that telomere length is shorter in families with an increased risk of CVD and do not support the Telomere Hypothesis of CVD.
Arteriosclerosis Thrombosis and Vascular Biology 10/2012; · 6.37 Impact Factor
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JACC. Cardiovascular imaging 09/2012; 5(9):871-3. · 14.29 Impact Factor
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Hypertension 07/2012; 60(1):64-70. · 6.21 Impact Factor
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ABSTRACT: Myocardial and arterial load are time-varying phenomena. Despite their importance in myocardial function, the arterial properties that determine time-resolved myocardial wall stress are unknown. We aimed to assess arterial properties as determinants of time-resolved myocardial stress among 1214 men and women enrolled in the Asklepios Study. Time-resolved central pressure, flow, and left ventricular geometry were measured with carotid tonometry, Doppler, and speckle-tracking echocardiography, respectively, for computation of arterial load and ejection-phase time-varying myocardial wall stress. For any given end-diastolic left ventricular geometry and cardiac output, peak myocardial stress correlated directly with systemic vascular resistance (standardized β=1.12; P<0.0001) and aortic characteristic impedance (standardized β=0.17; P<0.0001). The ejection-phase stress-time integral correlated with systemic vascular resistance (standardized β=1.06; P<0.0001), lower total arterial compliance (standardized β=-0.13; P=0.0008), and earlier return of wave reflections (standardized β=-0.10; P<0.0001) but not with reflection magnitude, whereas end-systolic wall stress correlated with systemic vascular resistance (standardized β=1.06; P<0.0001) and reflection magnitude (standardized β=0.12; P<0.0001). After adjustment for age, all of the measured arterial properties, end-diastolic left ventricular geometry, and cardiac output, women demonstrated greater peak (534 versus 507 kdyne/cm(2); P<0.0001), end-systolic (335 versus 320 kdyne/cm(2); P<0.0001), and ejection-phase stress-time integral (157 versus 142 kdyne · s · cm(-2); P<0.0001). In conclusion, different arterial properties have selective effects on time-resolved ejection-phase myocardial wall stress, which are not apparent from single-time point measurements. Women demonstrate less efficient myocardial-arterial coupling, with higher wall stress development for any given left ventricular geometry, arterial properties, and flow output. These observations may relate to the differential susceptibility of women to heart failure.
Hypertension 06/2012; 60(1):64-70. · 6.21 Impact Factor
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ABSTRACT: In animal experiments, elevating systolic pressures induces diastolic dysfunction and may contribute to congestion, a finding not yet translated to humans. Coronary surgery patients (63 ± 8 years) were studied with left ventricular (LV) pressure (n = 17) or pressure-volume (n = 3) catheters, immediately before cardiopulmonary bypass. Single-beat graded pressure elevations were induced by clamping the ascending aorta. Protocol was repeated after volume loading (n = 7). Consecutive patients with a wide range of systolic function were included. Peak isovolumetric LV pressure (LVP(iso)) ranged from 113 to 261 mmHg. With preserved systolic function, LVP elevations neither delayed relaxation nor increased filling pressures. With decreasing systolic function, diastolic tolerance to afterload progressively disappeared: relaxation slowed and filling pressures increased (diastolic dysfunction). In severely depressed systolic function, filling pressures increased even with minor LVP elevations, suggesting baseline load-dependent elevation of diastolic pressures. The magnitude of filling pressure elevation induced in isovolumetric heartbeats was closely and inversely related to systolic performance, evaluated by LVP(iso) (r = -0.96), and directly related to changes in the time constant of relaxation τ (r = 0.95). The maximum tolerated systolic LVP (without diastolic dysfunction) was similarly correlated with LVP(iso) (r = 0.99). Volume loading itself accelerated relaxation, but augmented afterload-induced upward shift of filling pressures (7.9 ± 3.7 vs. 3.0 ± 1.5; P < 0.01). The normal human response to even markedly increased systolic pressures is no slowing of relaxation and preservation of normal filling pressures. When cardiac function deteriorates, the LV becomes less tolerant, responding with slowed relaxation and increased filling pressures. This increase is exacerbated by volume loading.
Archiv für Kreislaufforschung 03/2012; 107(2):251. · 7.35 Impact Factor
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Evelien Hermeling,
Sebastian J Vermeersch,
Ernst R Rietzschel,
Marc L de Buyzere, Thierry C Gillebert,
Roel J van de Laar,
Isabel Ferreira,
Arnold P Hoeks,
Luc M van Bortel,
Robert S Reneman,
Patrick Segers,
Koen D Reesink
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ABSTRACT: The current standard for arterial stiffness assessment, aortic pulse wave velocity (aPWV), is measured at diastolic pressure. Arterial stiffness, however, is pressure dependent. At the carotid artery level, the degree of this dependency can be quantified as the difference (ΔPWV) between systolic and diastolic (cPWVd) carotid pulse wave velocity. Biomechanically, a greater ΔPWV implies greater increases in left ventricular afterload with physical activity. Therefore, we hypothesized, that ΔPWV is more strongly associated with left ventricular mass index (LVMI) than aPWV and cPWVd.
In 1776 healthy individuals from the Asklepios cohort (age 35-55 years), ΔPWV was obtained from combined carotid artery ultrasound and tonometry recordings. Multiple linear regression analysis was performed to investigate the associations of ΔPWV, cPWVd and aPWV with LVMI, adjusting for age, sex, mean blood pressure (MBP), central pulse pressure, and other possible confounders.
ΔPWV was 2.4 ± 1.2 m/s (mean ± SD), ranging from 0.8 m/s, indicating almost constant arterial stiffness over the cardiac cycle, to 4.4 m/s, reflecting substantial pressure dependency. ΔPWV was significantly associated with LVMI (β of 2.46 g/m per m/s, P < 0.001), even after full adjustment (β of 0.56 g/m per m/s, P = 0.03). cPWVd and aPWV had clear crude associations with LVMI (P < 0.001), but lost significance after adjustment (β of -0.48 and -0.33 g/m per m/s, with P = 0.11 and 0.2, respectively).
The change in arterial stiffness over the cardiac cycle, rather than diastolic stiffness, is independently associated with LVMI in healthy middle-aged individuals. Therefore, the pressure dependency of arterial stiffness should be considered in cardiovascular risk assessment.
Journal of hypertension 12/2011; 30(2):396-402. · 4.02 Impact Factor
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Gary F Mitchell,
Germaine C Verwoert,
Kirill V Tarasov,
Aaron Isaacs,
Albert V Smith,
Yasmin,
Ernst R Rietzschel,
Toshiko Tanaka,
Yongmei Liu,
Afshin Parsa, [......],
John R Cockcroft,
Vilmundur Gudnason,
Guy G De Backer,
Luigi Ferrucci,
Tamara B Harris,
Alan R Shuldiner,
Cornelia M van Duijn,
Daniel Levy,
Edward G Lakatta,
Jacqueline C M Witteman
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ABSTRACT: Carotid-femoral pulse wave velocity (CFPWV) is a heritable measure of aortic stiffness that is strongly associated with increased risk for major cardiovascular disease events.
We conducted a meta-analysis of genome-wide association data in 9 community-based European ancestry cohorts consisting of 20 634 participants. Results were replicated in 2 additional European ancestry cohorts involving 5306 participants. Based on a preliminary analysis of 6 cohorts, we identified a locus on chromosome 14 in the 3'-BCL11B gene desert that is associated with CFPWV (rs7152623, minor allele frequency=0.42, β=-0.075±0.012 SD/allele, P=2.8×10(-10); replication β=-0.086±0.020 SD/allele, P=1.4×10(-6)). Combined results for rs7152623 from 11 cohorts gave β=-0.076±0.010 SD/allele, P=3.1×10(-15). The association persisted when adjusted for mean arterial pressure (β=-0.060±0.009 SD/allele, P=1.0×10(-11)). Results were consistent in younger (<55 years, 6 cohorts, n=13 914, β=-0.081±0.014 SD/allele, P=2.3×10(-9)) and older (9 cohorts, n=12 026, β=-0.061±0.014 SD/allele, P=9.4×10(-6)) participants. In separate meta-analyses, the locus was associated with increased risk for coronary artery disease (hazard ratio=1.05; confidence interval=1.02-1.08; P=0.0013) and heart failure (hazard ratio=1.10, CI=1.03-1.16, P=0.004).
Common genetic variation in a locus in the BCL11B gene desert that is thought to harbor 1 or more gene enhancers is associated with higher CFPWV and increased risk for cardiovascular disease. Elucidation of the role this novel locus plays in aortic stiffness may facilitate development of therapeutic interventions that limit aortic stiffening and related cardiovascular disease events.
Circulation Cardiovascular Genetics 11/2011; 5(1):81-90. · 6.11 Impact Factor
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Laura Ernande,
Cyrille Bergerot,
Ernst R Rietzschel,
Marc L De Buyzere,
Hélène Thibault,
Pierre Gautier Pignonblanc,
Pierre Croisille,
Michel Ovize,
Laure Groisne,
Philippe Moulin, Thierry C Gillebert,
Geneviève Derumeaux
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ABSTRACT: Diastolic dysfunction is considered the first marker of diabetic cardiomyopathy. However, preclinical systolic alteration was also recently described by strain, but its association with diastolic dysfunction has never been investigated.
One hundred fourteen patients with type 2 diabetes mellitus (DM) with controlled blood pressure and without overt heart disease were prospectively enrolled and compared with 88 age-matched controls. All subjects underwent comprehensive echocardiography, including diastolic evaluation according to current recommendations and speckle-tracking imaging. The prevalence of diastolic dysfunction, the determinants of diastolic parameters, and the association between preclinical systolic and diastolic dysfunctions were studied.
Diastolic parameters were altered in patients compared with controls, with lower E/A ratios, longer mitral deceleration and isovolumic relaxation times, and higher E/e' ratio. Diastolic dysfunction occurred in 47% of patients with DM (33% and 14% with grade I and II diastolic dysfunction, respectively) and systolic alteration (longitudinal strain ≥ -18%) in 32% of patients. Whereas longitudinal systolic strain was independently associated with DM and gender, diastolic parameters were influenced by many factors, including age, rate-pressure product, history of hypertension, and body mass index. Systolic alteration occurred in 28% of patients with DM with normal diastolic function and in 35% with diastolic dysfunction.
Diastolic dysfunction diagnosed according to current recommendations is frequent in patients with DM but is also influenced by other factors. Systolic strain alteration may exist despite normal diastolic function, indicating that diastolic dysfunction should not be considered the first marker of a preclinical form of diabetic cardiomyopathy.
Journal of the American Society of Echocardiography: official publication of the American Society of Echocardiography 09/2011; 24(11):1268-1275.e1. · 2.98 Impact Factor
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Journal of the American Society of Echocardiography: official publication of the American Society of Echocardiography 08/2011; 24(8):932-3. · 2.98 Impact Factor
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Hypertension 03/2011; 57(3):e9-10. · 6.21 Impact Factor
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Circulation 11/2010; 122(21(supplement)):A16854. · 14.74 Impact Factor
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CIRCULATION. 11/2010; 122(supplement):A16854.
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Laura Ernande,
Ernst R Rietzschel,
Cyrille Bergerot,
Marc L De Buyzere,
Frédéric Schnell,
Laure Groisne,
Michel Ovize,
Pierre Croisille,
Philippe Moulin, Thierry C Gillebert,
Geneviève Derumeaux
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ABSTRACT: Diabetic cardiomyopathy has been characterized by an early impairment of left ventricular (LV) longitudinal function as opposed to preserved LV radial function.
Conventional echocardiography and longitudinal (ε(L)) and radial (ε(R)) systolic strain assessed by speckle-tracking imaging were obtained in 114 type 2 diabetic patients and 88 age-matched controls.
LV ejection fraction was similar in diabetic patients and controls. The presence of subclinical LV systolic dysfunction in diabetic patients was demonstrated by lower values of midwall fractional shortening (18% ± 3% vs 20% ± 3%, P = .006), ε(L) (-19% ± 3% vs -22% ± 2%, P < .001), and ε(R) (50% ± 16% vs 56% ± 12%, P = .003) compared with controls. On multivariate analysis, factors predicting strain values were diabetes (P = .001) and gender (P = .001) for ε(L) and diabetes (P = .003) for ε(R).
Diabetic patients without overt heart disease display subclinical alteration of both radial and longitudinal LV systolic function even after adjustment for blood pressure, age, and body mass index.
Journal of the American Society of Echocardiography: official publication of the American Society of Echocardiography 10/2010; 23(12):1266-72. · 2.98 Impact Factor
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ABSTRACT: The need for left ventricular mass (LVM) normalization to body size is well recognized. Currently used allometric exponents to normalize LVM may not account for the confounding effect of sex. Because sex is a strong determinant of body size and LVM, we hypothesized that these are subject to potential bias. We analyzed data from 7528 subjects enrolled in the Asklepios Study (n=2524) and the Multiethnic Study of Atherosclerosis (limited access data set; n=5,004) to assess metric relationships between LVM and body size, generate normative data for indexed LVM, and compare the ability of normalization methods to predict cardiovascular events. The allometric exponent that adequately described the LVM-body height relationship was 1.7 in both studies and significantly different from both the unity and 2.7, whereas the LVM-body surface area relationship was approximately linear. LVM/height(2.7) consistently demonstrated important residual relationships with body height and systematically misclassified subjects regarding the presence of LVH. LVH defined by LVM/height(1.7) was more sensitive than LVM/body surface area to identify obesity-related LVH and was most consistently associated with cardiovascular events and all-cause death. In contrast to current assumptions, LVM/height(2.7) is not an adequate method to normalize LVM for body size. We provide more appropriate normalization methods, normative data by 2D echocardiography and gradient-echo cardiac MRI, and cutoffs for defining LVH, along with prognostic validation data.
Hypertension 07/2010; 56(1):91-8. · 6.21 Impact Factor
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Dries Mahieu,
Jan Kips,
Ernst R Rietzschel,
Marc L De Buyzere,
Francis Verbeke, Thierry C Gillebert,
Guy G De Backer,
Dirk De Bacquer,
Pascal Verdonck,
Luc M Van Bortel,
Patrick Segers,
on behalf of the Asklepios investigators
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ABSTRACT: Objectives: Noninvasive estimation of central blood pressure (BP) from radial artery pressure waveforms is increasingly applied. We investigated the impact of radial artery waveform calibration on central BP assessment and calculated pressure amplification, with focus on the one-third rule used to estimate mean arterial BP (MAP).
Methods: Pressure waveforms were noninvasively measured at the radial and carotid arteries in 1873 individuals (age 45.8±6.1 years). Radial and carotid artery waveforms were calibrated using brachial artery DBP and SBP, MAP estimated with the one-third rule and MAP estimated as brachial DBP along with 40% of brachial artery pulse pressure.
Results: Central SBP obtained via a transfer function was 123.5 ± 15.7, 117.8 ± 14.2 and 126.0 ± 15.4 mmHg (mean ± SD) following above-mentioned three calibration schemes, respectively. Using the same calibration schemes, carotid artery SBP was 131.4 ± 15.2, 118.4 ± 14.4 and 126.8 ± 15.7 mmHg, respectively. Central-to-brachial amplification was 13.0 ± 3.6 mmHg using second method as compared with 4.6 ± 3.8 mmHg with third method. Brachial-to-radial amplification was actually negative (−6.3 ± 4.5 mmHg) using second method, whereas 3.4 ± 5.5 mmHg was found with third method.
Conclusion: Both carotid artery SBP and central SBP obtained via a transfer function are highly sensitive to the calibration of the respective carotid artery and radial artery pressure waveforms. Our data suggest that the one-third rule to calculate MAP from brachial cuff BP should be avoided, especially when used to calibrate radial artery pressure waveforms for subsequent application of a pressure transfer function. Until more precise estimation methods become available, it is advisable to use 40% of brachial pulse pressure instead of 33% to assess MAP.
Journal of Hypertension 01/2010; 28(2):300–305. · 4.02 Impact Factor
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CIRCULATION. 01/2010; 122(supplement):A16854.
