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ARTERIAL STIFFNESS
Dr.R.V.S.N.Sarma., M.D., M.Sc., (Canada)
Consultant Physician and Chest Specialist
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Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings
The Blood Vessels and the Cardiovascular SystemThe Blood Vessels and the Cardiovascular System
Figure 15-1: Functional model of the cardiovascular system
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Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings
• Endothelium
• Elastic tissues
• Rebounds
• Evens flow
• Smooth muscles
• Fibrous tissue
• Tough
• Resists stretch
Make Up of Bllod Vessels: Arteries and ArteriolesMake Up of Bllod Vessels: Arteries and Arterioles
Figure 15-2: Blood vessels
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Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings
Blood Pressure: Generated by Ventricular ContractionBlood Pressure: Generated by Ventricular Contraction
Figure 15-4: Elastic recoil in the arteries
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Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings
More Blood Pressures: Pulse and Mean Arterial PressuresMore Blood Pressures: Pulse and Mean Arterial Pressures
Figure 15-5: Pressure throughout the systemic circulation
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Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings
Factors Controlling MAP : The Driving Pressure for Blood FlowFactors Controlling MAP : The Driving Pressure for Blood Flow
Figure 15-10: Factors that influence mean arterial pressure
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Arterioles as a group have a greater cross sectional area than the large vessels.
How can their resistance be greater?
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r = 1A= 3.14Res=1
B and C in parallel have a combined resistance of 2 and a cross sectional area of 3.14
A
r = .707A= 1.57Res=4
B
C
Resistance ~ ( r4)Area ~ (r 2 )
Branching to smaller radius vessels increases resistance
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The heart pumps in short spurts. The compliant aorta stores this energy during ejection and releases it during diastole so that flow into the periphery continues throughout the cardiac cycle
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The bagpipe player blows into the bag in short spurts. That energy is stored in the bag and the air escapes through the pipes in a continuous stream thanks to the bag's compliance.
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If the vessels were rigid pipes then all forward flow would have to occur during the ejection period which is only about 1/3 of the cardiac cycle.
Blood pressure would have to be 3 times higher during that period to maintain the cardiac output.
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Why is aortic pressure pulsatile?
With each ejection the aortic volume increases by one stroke volume
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If aortic compliance were to decrease, pulse pressure will increase.
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Pulse pressure = stroke volume/compliance
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Aging reduces aortic compliance
Pulse pressure naturally increases with age
Compliance = volume/ pressure
120/80
Systolic hypertension >140
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Mean and Pulse Pressure
P P +1
3P - P )a d s d (
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Mean Arterial Pressure
Q =P P
Ra v
P - P = Q Ra v
MAP = cardiac output x total resistance
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Arterial Elasticity Stores Pressure and Maintains Flow
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Factors Controlling Blood Pressure
Peripheral resistance mean arterial pressure
Cardiac output mean arterial pressure
Stroke volume pulse pressure
Arterial compliance pulse pressure
Heart Rate pulse pressure
Blood Volume arterial & venous
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• Conduits– To conduct blood to the organs and periphery
• Impedance matching– Minimise cardiac work– Minimise pulse pressure– Control flow according to demand
What are arteries for?
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• What are arteries made of?
• Why do large arteries become stiffer with age (and disease)?
• Why are some people affected more than others?
QuestionsConduit arteries: large arteries near the heart and their main branches
• Why are conduit arteries distensible?
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Arteries are distensible because:
80
100
120
1 sec
• The wheel has yet to evolve in the animal kingdom (bacteria have propellers)
• Therefore(?) the heart is a pulsatile pump.
• Its output consists of a pulse wave superimposed on a steady component.
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Systolic pressure
Diastolic pressure
Mean Arterial Pressure
Pulse pressure = systolic pressure - diastolic pressure
80
100
120
1 second
Pre
ssur
e [m
mH
g]Aortic pulse wave
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• MAP determined by resistance of peripheral arteries = Pd +1/3 PP
• Pulse pressure determined by elasticity of large arteries
Pulse pressure = systolic pressure - diastolic pressure
Systolic pressure
Diastolic pressure
Mean Arterial Pressure
80
100
120
1 second
Pre
ssur
e [m
mH
g]
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The pulse is a wave of dilatation
With thanks to Chris Martyn
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Speed of the wave is related to the stiffness of the artery it is
traveling in
The stiffer the artery;
the higher the wave speed
Wave speed is proportional to the square root of arterial stiffness
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Stress, strain and elastic modulus
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• Stress (, sigma)– Force per unit area = (F/A)
• Strain (, epsilon)– Change in length per unit length = (L/L0)
• Elastic (Young’s) modulus (E)– stress/strain =
F L0
A L=
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2001000
Pressure (mmHg)
Rela
tive R
ad
ius
1.0
1.5
2.0
P
P
R R
P
P
R R
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2.62.42.22.01.81.61.41.21.0
R/Ro
0
5
10
15
Einc [Nm-2 x 105]
Variation of Einc with stretch
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WHY THE ARTERY?
Epidemiological studies have shown that:
• Cardiovascular disease is the first cause of morbidity and mortality in western countries.
• Cardiovascular morbidity and mortality are principally related to arterial pathology.
• Arterial wall alterations are usually associated with: age, smoking, diabetes, dyslipidemia and hypertension.
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WHY THE ARTERY?
• Arterial alterations can be observed at early stages in both small and large arteries.
• Alterations of the arterial wall properties favor development of arterial lesions:
• Arteries constitute the target, the battleground and the common denominator of cardiovascular complications.
– Kidney nephroangiosclerosis
– Cerebral stroke
– Coronary angina, M.I.
– Peripheral stenosis, aneurysm
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WHY THE ARTERY?
• Cardiovascular morbidity and mortality are principally due to arterial lesions.
• Treatments differ by their effect on the arterial wall.
• The evaluation of cardiovascular prevention and its impact on the arterial wall is important as an intermediate marker
• Large therapeutic trials including arterial evaluation are required.
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WHY PULSE WAVE VELOCITY?
• Arterial pathology is a major contributor to cardiovascular disease, morbidity and mortality.
• Most non-invasive methods to assess large arteries are ultrasound based:
– Doppler velocity measurement– Echography– High resolution Echo-tracking
Sophisticated, costly and reserved for a few clinical research labs.
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WHY PULSE WAVE VELOCITY?
• Clinical assessment of large arteries requires a simple, practical method.
Pulse wave velocity = Index of arterial stiffness
• Arterial stiffness will– Play a potential etiologic role in cardiovascular disease.
– Help to recognize arterial changes.
– Constitute an "early risk marker" .
– Be useful in assessing the arterial effects of drugs.
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PULSE WAVE VELOCITY
• A simple method to assess arterial stiffness and distensibility.
• A long-established and widely used technique.
• Non-invasive, accurate and reproducible.
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PULSE WAVE VELOCITY
Principles
L.V.E. generates a pulse wave which will propagate along the arterial walls at a certain speed.
Propagation alongthe arterial tree
Systole
L.V.
Blood = incompressible fluid
Artery = elastic conduit }
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PULSE WAVE VELOCITY
• The propagation velocity is determined by:
– the elastic and geometric properties of the arterial wall – the characteristics of the arterial wall structure.
Higher velocity = higher stiffness
= lower distensibility.
Principles
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PULSE WAVE VELOCITY
Intermittent cardiac output
Systole Diastole
Large arteries store a part of the ejection volume during systole and restore it during diastole.
Arterial Buffering function
Continuous peripheral flow
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•
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PULSE WAVE VELOCITY
The Complior® device
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COMPLIOR
Automatic Measurement (The Complior®)
• Transducer = large frequency band (0.1 - 100 Hz)
• Signal gain adjustment (manual or automatic)
• Acquisition frequency = 4 kHz
• Waveforms = entire exam stored in memory (signal data & parameters)
• Pedal for trigger acquisition
• Automatic detection and calculation of propagation delay between the 2 pulse waves
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PULSE WAVE VELOCITY
• Plasma cholesterol
• Glycemia
• Smoking status
• Gender
• Atherosclerosis
• Genetic Factors
Determining Factors
•Age
•Blood pressure
+++ From + to ++
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ARTERIAL STIFFNESS
Clinical Implications and Epidemiological Data
Arterial Stiffness Cardiovascular risk
Compliance
Distensibility
PWV
Pulse pressure
Atherosclerosis
LVH
Systolic HT
Stroke
CHD
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ARTERIAL DISTENSIBILITY
Arterial distensibility in coronary heart desease (CHD).
CHDn = 24
Normaln = 18
Systolic pressure(mmHg)
Distensibility(cm² x dynes-1)
117+ 4 121 + 4 NS
1.6 + 0.1 3.4 + 0.4 P < 0.001
Stefanadis C et al. Am J Cardiol. 1987
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PULSE WAVE VELOCITY
Aortic P.W.V. is an independent determinant of L.V.H.
1.9
1.5
1.0
0.6
5 10 15
r = 0.61p < 0.001
PWV m/sec
Left ventricularmass/volume
= NT (normotensive)
= HTA
(Bouthier et al, Am Heart J 1985)
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Relationship between arterial stiffness and number of atheromatous vessels
Common carotid artery
0
10
20
30
N 0-VD 1-VD 2-VD 3-VD
Sti
ffne
ss in
dex
*
*
adapted from Hirai et al.
VD: vessel disease
Abdominal aorta
0
10
20
30
N 0-VD 1-VD 2-VD 3-VD
Sti
ffne
ss in
dex
(
*
**
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AORTIC PWV AND DISTENSIBILITY IN STROKE PATIENTS AND CONTROL SUBJECTS
adapted from Lehmann
0
5
10
15
controls stroke
Aor
tic P
WV
(m/s
)0
5
10
controls stroke
Aor
tic d
iste
nsib
ility
(Arb
itra
ry u
nit)
*** **
8.2
4.9
9.4
13.8
Carotid Radial PWV Carotid Femoral PWV
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ARTERIAL DISTENSIBILITY IN PATIENTS WITH ABDOMINAL AORTIC ANEURYSM (AAA)
5
10
15
20
25
Normotensives Hypertensives AAA Normotensives Hypertensives Supra-aneurysm Aneurysm
Art
eria
l dis
tens
ibil
ity
(Kpa
-1.1
0-3 )
AAA
*
*
CAROTID AORTA
*
adapted from Boutouyrie et al.
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CAROTID-RADIAL PWV IN DIABETIC SUBJECTS
4
6
8
10
12
14
16
1 to 10 11 to 20 21 to 30 31 to 40 41 to 50 51 to 60
Age (years)
Car
otid
-rad
ial P
WV
(m
/sec
)
Healthy
Diabetics
adapted from Woolam et al
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PULSE WAVE VELOCITY
P.W.V. in normotensives and borderline hypertensives.
HT = Borderline hypertensives
NT = Normotensives
10
9
8
7
6
5
70 90 110 130
Mean Blood Pressure (mmHg)
Ca
rotid
-Fe
mo
ral P
WV
(m
/s)
(Girerd et al, J of Hyper, 1989)
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13
14
15
No Unilateral Bilateral
13
14
15
1 2 3 4 5
PWV AND ATHEROSCLEROSIS INDICATORSValues are adjusted for age, sex, mean BP and pulse rate
Quintiles of carotid artery wall thickness Plaques in carotid artery
Car
otid
-fem
oral
PW
V (
m/s
)
Car
otid
-fem
oral
PW
V (m
/s)
p < 0.001 p = 0.001
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PWV AND ATHEROSCLEROSIS INDICATORSValues are adjusted for age, sex, mean BP and pulse rate
13
13.5
14
14.5
1 2 3 4 5
Quintiles of ankle-brachial pressure index
Car
otid
-fem
oral
PW
V (
m/s
)
p = 0.02
13
14
15
16
no mild moderate severe
Calcified plaques in the aorta
Car
otid
-fem
oral
PW
V (
m/s
)
p < 0.001
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CONCLUSION
• Arterial stiffness must be taken into consideration in clinical practice.
• The Complior system is an accurate device to assess the arterial stiffness using pulse wave velocity measurements.
• The examination procedure is simple, and the method is accurate and reproducible.
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Which is important ? SBP or DBP
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The Impact of the Early The Impact of the Early Wave ReflectionWave Reflection
• This earlier return to the heart of This earlier return to the heart of the reflected pressure wave (due the reflected pressure wave (due to stiffening of the arteries) to stiffening of the arteries) changes the aortic root pressure changes the aortic root pressure waveform, waveform, … with 3 key clinical … with 3 key clinical implicationsimplications
• Central pulse pressure Central pulse pressure increases ... increases ... increasing risk of increasing risk of stroke and renal failurestroke and renal failure
• LV Load increases…. LV Load increases…. increasing increasing LV massLV mass, and accelerating , and accelerating progress towards LV hypertrophy progress towards LV hypertrophy and heart failureand heart failure
• Coronary artery perfusion Coronary artery perfusion pressure in diastole reduces…. pressure in diastole reduces…. increasing risk of myocardial increasing risk of myocardial ischemiaischemia
PP
Increased CentralPulse Pressure
Increased LV Load
Decreased Coronary ArteryPerfusion Pressure in Diastole
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Treatment of Arterial Stiffness
• Currently approved drugs for arterial stiffness
• ACEi, ARBs
• Nitrates
• Diuretics
• Statins
• Aspirin
• Certain beta blockers
• Certain Ca channel blockers
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Treatment of Arterial Stiffness
• Promising Drugs
• Endopeptidase inhibitors (Omiprilait)
• PDE inhibitors (Sildenafil group)
• Methyl Xanthines (with better safety window)
• NO donors (novel drugs avoiding tolerance)
• Drugs breaking AGE cross links (ALT 711)
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PulseMetricPulseMetric
Brachial Artery Distensibility, SVR, CO, LV dP/dtUses Oscillometric BP cuff
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SphygmocorSphygmocor
Pulse Wave Velocity & Augmentation Index
Uses Arterial tonometer (radial)
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