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Relationship between arterial stiffness, cardiac baroreflex sensitivity and blood pressure variability in normotensive healthy adults

Authors:
  • Corporación De Investiciones Biológicas, Universidad de Antioquia
Artery Research
ISSN (Online): 1876-4401 ISSN (Print): 1872-9312
Journal Home Page: https://www.atlantis-press.com/journals/artres
P4.15: RELATIONSHIP BETWEEN ARTERIAL STIFFNESS,
CARDIAC BAROREFLEX SENSITIVITY AND BLOOD
PRESSURE VARIABILITY IN NORMOTENSIVE HEALTHY
ADULTS
J.E. Ochoa, M.M. Correa, A.M. Valencia, J.G. McEwen, J.A. Gallo, G. Bilo, P. Salvi,
D. Aristizabal, G. Parati
To cite this article: J.E. Ochoa, M.M. Correa, A.M. Valencia, J.G. McEwen, J.A. Gallo, G.
Bilo, P. Salvi, D. Aristizabal, G. Parati (2012) P4.15: RELATIONSHIP BETWEEN ARTERIAL
STIFFNESS, CARDIAC BAROREFLEX SENSITIVITY AND BLOOD PRESSURE VARIABILITY IN
NORMOTENSIVE HEALTHY ADULTS, Artery Research6:4, 187187, DOI:
https://doi.org/10.1016/j.artres.2012.09.163
To link to this article: https://doi.org/10.1016/j.artres.2012.09.163
Published online: 21 December 2019
where the strongest correlate was central systolic BP (rZ0.587; p<0.001).
aPWV was not related to AIx in either group (p>0.05 both).
Conclusions: Haemodynamic determinants of AIx in T2DM patients are
significantly different to healthy people where BP is a dominant factor. In
patients with T2DM, however, a high output, low resistance haemodynamic
environment is associated with AIx.
P4.14
EXERCISE AORTIC RESERVOIR FUNCTION IN PATIENTS WITH TYPE 2
DIABETES IS ASSOCIATED WITH BRAIN ATROPHY
R. E. Climie
1
, V. Srikanth
2
, R. Beare
2
, L. J. Keith
1
, J. E. Davies
3
,
J. E. Sharman
1
1
Menzies Research Institute Tasmania, Hobart, Australia
2
Stroke and Ageing Research Group, Melbourne, Australia
3
International Centre for Circulatory Health, London, United Kingdom
Objectives. Vascular mechanisms underlying brain atrophy and white matter
lesions (WML) in patients with type 2 diabetes (T2DM) are unknown.
Increased exercising blood pressure (BP) is associated with end-organ
damage and could explain these brain abnormalities. This study examined
associations between exercise central haemodynamics and brain structure.
Methods: Forty healthy participants (539 years; 50% male) and 40 T2DM
(629 years; 50% male) were examined at rest and during light exercise.
Resting and exercise central haemodynamics, including systolic BP (SBP), pulse
pressure (PP) augmented pressure (AP), augmentation index (AIx), aortic stiff-
ness and aortic reservoir function (including excess pressure integral [xsP])
were recorded by tonometry. Segmented grey (GM) and white matter (WM)
and WML volumes were derived from magnetic resonance imaging.
Results: T2DM participants had lower WM (pZ0.004) and GM (pZ0.07)
volumes, and significant elevation of all central hemodynamic variables
during exercise (p<0.01 all). At rest, greater central (not brachial) haemo-
dynamics (SBP, AP, AIx and PP) were independently associated with greater
WML volume (bZ0.54, pZ0.031, bZ0.55, pZ0.01; bZ0.46, pZ0.046 and;
bZ0.48, pZ0.01, respectively) in controls (not T2DM). During exercise,
increased xsP was independently associated with reduced WM (bZ-0.54,
pZ0.006) and GM (bZ-0.63, pZ0.013) volumes only in T2DM independent
of age, sex, heart rate, and 24-hour ambulatory SBP.
Conclusions: In T2DM, aortic reservoir function and transmission of excess
pressure during exercise is associated with brain atrophy. These findings
suggest that vascular mechanisms underlying structural brain changes may
differ between healthy individuals and those with T2DM.
P4.15
RELATIONSHIP BETWEEN ARTERIAL STIFFNESS, CARDIAC BAROREFLEX
SENSITIVITY AND BLOOD PRESSURE VARIABILITY IN NORMOTENSIVE
HEALTHY ADULTS
J. E. Ochoa
1,3
, M. M. Correa
2
, A. M. Valencia
2
, J. G. McEwen
2
,
J. A. Gallo
2
, G. Bilo
3
, P. Salvi
3
, D. Aristizabal
2
, G. Parati
1,3
1
Department of Clinical Medicine and Prevention, University of Milano-
Bicocca, Milan, Italy
2
Corporacio
´n para Investigaciones Biologicas, Clinical and Research Center,
SICOR, Medellin, Colombia
3
Department of Cardiology, S. Luca Hospital, Istituto Auxologico Italiano,
Milan, Italy
An increased arterial stiffness (AS) has been proposed as a likely mechanism
for a reduced cardiac baroreflex sensitivity (BRS) and the associated
increases in 24h blood pressure (BP) variability (BPV). Aim of the present
study was to explore this issue in a group of 90 normotensive, non-obese,
healthy adults (mean age 4810 yrs, 50% F).
Methods: BRS was assessed by computer analysis of 10 min beat-to-beat BP
and ECG recordings obtained in resting supine. The linear regression slope of
spontaneous concomitant increases or decreases in systolic BP and RR
interval were calculated, averaged and expressed as total slope of BRS
(ms/mmHg). Simultaneous recordings of pulse waveform were obtained by
means of a validated oscillometric device for ABPM (Mobil-O-Graph NG,
IEM, Stolberg, Germany) with inbuilt transfer-function like method, and
pulse wave velocity (PWV, m/s) calculated. BPV was assessed for systolic
and diastolic BP as 24h standard deviation (SD), weighted 24h SD (wSD),
daytime and night-time SD from 24h ABPM.
Results: In multiple linear regression analysis AS (assessed through PWV),
had the strongest effect on BRS variation (beta:-0.50, p<0.0001), followed
by HR and male sex. No significant effect was observed for age or MAP on
BRS (See table). A similar independent analysis, showed a significant inverse
relationship between BRS and daytime systolic BP SD (beta:-0,23; pZ0.036)
Conclusion: Our findings suggest that in normotensive, otherwise healthy
adults, decreased BRS and, indirectly, the associated increased day-time
systolic BPV might be largely explained by an increased AS, independently
of age and BP levels.
P4.16
INSULIN RESISTANCE IS ASSOCIATED WITH INCREASED LARGE ARTERY
STIFFNESS IN NORMOTENSIVE HEALTHY ADULTS
J. E. Ochoa
1,3
, M. M. Correa
2
, A. M. Valencia
2
, J. G. McEwen
2
,
J. A. Gallo
2
, G. Bilo
3
, P. Salvi
3
, D. Aristizabal
2
, G. Parati
1,3
1
Department of Clinical Medicine and Prevention, University of Milano-
Bicocca, Milan, Italy
2
Corporacio
´n para Investigaciones Biologicas, Clinical and Research Center,
SICOR, Medellin, Colombia
3
Department of Cardiology, S. Luca Hospital, Istituto Auxologico Italiano,
Milan, Italy
Aim: At present there is limited evidence on the relationship between
insulin resistance (IR) and measures of large artery stiffness (AS) and
wave reflections in normotensive healthy adults. Aim of the present
study was to explore this issue in 90 normotensive (Systolic(S) blood
pressure(BP) 107.19.3; diastolic (D) BP 69.67.7 mmHg), normoglyce-
mic, non-obese, otherwise healthy adults (mean age 48 10 yrs, 50%
female).
Methods: IR was assessed with HOMA-Index and subjects were classified into
IR tertiles, based on the distribution of HOMA-index values. Recordings of
pulse waveform were obtained by means of a validated oscillometric device
(Mobil-O-Graph NG, IEM, Stolberg, Germany) for ambulatory BP monitoring
with in-built transfer-function like method. Aortic pulse wave velocity
(PWV, m/s) and other measures derived from pulse wave analysis such as
augmentation index (AIx, %), central SBP (cSBP), central DBP (cDBP) and
central pulse pressure (cPP) were computed. Peripheral SBP and DBP, and
heart rate (HR) were recorded and pulse pressure (PP) calculated as the
difference between SBP and DBP.
Results: After multiple regression analysis adjusting for age, sex, HR and
BMI, there was a significant overall effect of IR on measures of large artery
stiffness and in central and peripheral BP levels. IR was associated with
increased aortic PWV, and with higher central and peripheral SBP and DBP
levels. See table.
Conclusion: our results indicate that in normotensive, healthy adults, IR
may induce significant increases in large artery stiffness (as assessed with
aortic PWV) and in central and peripheral BP levels.
Predictors of cardiac BRS (Multiple linear regression analysis)
Variable
(mean±SD)
Regression
Coefficient
95% CI Beta
Coefficient
P value R
2
PWV (6.121.53 m/s) -3.619 -5.0, -2.2 -0,503 <0,0001 0,25
HR (64.29.4 bpm) -0.426 -0.6, -0.2 -0,344 <0,0001 0,14
Sex (male) -4.373 -8.4, -0.3 -0,212 0,029 0,04
Age (4811 yrs) -0.187 -0.7, 0,3 -0.187 0,547 -
MAP (97.98.8 mmHg) -0.019 -0.4, 0.2 -0.077 0,759 -
R-Squared for the model including only significant variables (PWV, sex, HR) 0,342
Abstracts 187
Article
Full-text available
Chronic kidney disease (CKD) accelerates vascular stiffening related to age. Arterial stiffness may be evaluated measuring the carotid-femoral pulse wave velocity (PWV) or more simply, as recommended by KDOQI, monitoring pulse pressure (PP). Both correlate to survival and incidence of cardiovascular disease. PWV can also be estimated on the brachial artery using a Mobil-O-Graph; a non-operator dependent automatic device. The aim was to analyse whether, in a dialysis population, PWV obtained by Mobil-O-Graph (MogPWV) is more sensitive for vascular aging than PP. A cohort of 143 patients from 4 dialysis units has been followed measuring MogPWV and PP every 3 to 6 months and compared to a control group with the same risk factors but an eGFR > 30 ml/min. MogPWV contrarily to PP did discriminate the dialysis population from the control group. The mean difference translated in age between the two populations was 8.4 years. The increase in MogPWV, as a function of age, was more rapid in the dialysis group. 13.3% of the dialysis patients but only 3.0% of the control group were outliers for MogPWV. The mortality rate (16 out of 143) was similar in outliers and inliers (7.4 and 8.0%/year). Stratifying patients according to MogPWV, a significant difference in survival was seen. A high parathormone (PTH) and to be dialysed for a hypertensive nephropathy were associated to a higher baseline MogPWV. Assessing PWV on the brachial artery using a Mobil-O-Graph is a valid and simple alternative, which, in the dialysis population, is more sensitive for vascular aging than PP. As demonstrated in previous studies PWV correlates to mortality. Among specific CKD risk factors only PTH is associated with a higher baseline PWV. ClinicalTrials.gov Identifier: NCT02327962 .
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