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Aggoun Y, Beghetti M. Noninvasive
assessment of arterial function in children: clinical applications. Images
Paediatr Cardiol 2002;13:12-18
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Service de Cardiologie Pédiatrique, Hôpital
Necker, Enfants-Malades, Paris, France, Unité INSERM 0016 and Unité
de cardiologie Pédiatrique, Département de Pédiatrie,
Genève, Hôpital des Enfants, Genève, Suisse
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| Vascular echography | Mechanical artery properties | Intima media thickness |
| Endothelial function | Pulse wave analysis | Pulse wave velocity |
Article
Mechanical properties and endothelial function
The methods include mainly 2 measurements:
Together with blood pressure measurement, this technique allows calculation of mechanical indices of the CCA: the cross sectional compliance (CSC), defined as the change in cross sectional area divided by the change in pressure (pulse pressure); the cross sectional distensibility, which is CSC divided by the diastolic cross sectional area, as a parameter of comparison of the viscoelastic properties of structures with different initial dimensions. These parameters assess the vessel as a hollow structure. The incremental elastic modulus provides information of the wall material, independent of its geometry, and defines the wall stiffness. Using the same technique, arterial endothelial and smooth muscle function are assessed. Endothelial function is determined by recording the dilator response of the brachial artery to increase blood flow generated during reactive hypereamia of the down-stream forearm, flow mediated dilation (FMD). The subject is in the supine position for 10 minutes before the first scan and remains supine throughout the study. The brachial artery is scanned in a longitudinal section, and the center of the vessel is identified when the clearest images of the anterior and posterior walls are obtained. The transmit zone is set to the level of the anterior vessel wall. Depth and gain settings are optimized to identify the lumen to vessel wall. Images are magnified with the resolution box function, leading to a television line width of 0.065 mm. Machine settings are kept constant during each study. Arterial flow velocity is measured by mean of a pulsed-Doppler signal at a 60° angle to the vessel, with the range gate (1.5 mm) in the center of the artery. Flow increase is induced by inflation of a blood pressure cuff to 300 mmHg. The cuff is released after 4 minutes, and the artery is scanned for 30 seconds before and for 90 seconds after cuff deflation, including a repeated flow velocity recording for 15 seconds after cuff release. Ten minutes later, a resting scan is recorded. Endothelium-independent dilation of the brachial artery is assessed by measuring the dilator response to a 400-µg spray of the NO donor, glyceryl trinitrate (GTN) given sublingually and the artery is scanned after 3 minutes. Results are expressed as percentage maximum change in vessel diameter from baseline.
Pulse wave analysis
The systolic and diastolic pressures represent the limits of pressure
fluctuations during the cardiac cycle. A more complete description of the
complex interaction between the left ventricle and the physical properties
of the arterial system is provided by the descriptive or quantitative analysis
of the arterial-pulse contour. The arterial-pulse contour changes with
diseases states. The arterial pressure waveform is recorded by applanating
the carotid artery with a hand-held tonometer at the site of maximal pulsation.
The tip of the tonometer contains a micromanometer that accurately records
the pressure within the artery. The morphology is determined by wave reflection
and a damped resonance, which occurs in the arterial tree, the reflected
waves originating mainly from arteries and arterioles. Morphologic change
in the arterial pulse contour eventually results in the forward incident
pressure wave summating with backward reflected pressure wave to augment
systolic blood pressure. Pulse wave analysis measures augmentation index
(Aix), a parameter that reflects the degree to which central pressure is
enhanced by wave reflection of the pulse wave. The systolic part of central
arterial waveform is characterised by two pressure peaks. The first peak
is caused by left ventricular ejection, whereas the second peak is a result
of wave reflection. The difference between both pressure peaks reflects
the degree to which central arterial pressure is augmented by wave reflection.
Aix is defined as the increment in pressure from the first systolic shoulder
(inflection point) to the second peak pressure of the aortic pressure waveform
expressed as a percentage of the peak pressure (figure 2). This index is
used to measure the additional load imposed on the left ventricle.2
Aix depends, at least in part, on aortic and large artery pulse wave velocity
(PWV). A higher PWV results in earlier arrival of reflected waves and,
hence, increased augmentation during early systole. PWV is inversely related
to arterial distensibility. Therefore, Aix has been proposed as in index
of “arterial stiffness”.3
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Obesity
Obesity has become an increasingly important medical problem in children
and adolescents. Many of the outcomes associated with obesity that were
previously thought of as diseases of adults are now affecting children
as well. Obesity is also the most common nutritional problem among children
in developed countries. There is substantial evidence that obesity in childhood
lays the metabolic groundwork for adult cardiovascular disease.6
Obesity in adolescence predicts a broad range of later health problems
including an increased risk of cardiovascular morbidity and mortality.
Our study provided evidence that severe childhood obesity is associated
with early endothelial dysfunction (FMD, 6±3 vs 8±4 %, P<0.01;
GTNMD, 17±6 vs 18±7 %, NS) and increased stiffness of elastic
arteries (2.4±0.4 vs 1±0.24 mmHg.103, P<0.001). This early
vascular dysfunction in children may be an early step in the development
of atherosclerosis.7
End stage renal disease (ESRD)
End-stage renal insufficiency in children undergoing hemodialysis was
shown to alter the mechanical properties of the common carotid artery:
a decrease of CSC (0.11±0.04 vs 0.18±0.05 mm2.mmHg-1, P<0.01)
and CSD (0.43±0.10 vs 0.82±0.20 mmHg-1.10-2, P<0.001).
The incremental elastic modulus was elevated. An impairment of endothelial
function was described and the Aix was increased (-24±8 vs 58±6
%, P<0.005) by an early return of the reflected pulse wave. This index
was well correlated with the left ventricle mass index (r=0.55, P<0.01).8
In adult patients who require hemodialysis, the arterial stiffness was
a major predictor of all-cause and cardiovascular mortality.9
Arterial dysfunction after coarctation repair
The long term course after successful coarctation repair is complicated
by late cardiovascular morbidity, which includes systemic hypertension
at rest or/and during exercise. The responsible pathophysiological mechanisms
have not been well determined. It has been reported that vascular function
was different in the upper and lower limbs. Reduced flow mediated dilation
(FMD, 5±3 vs 7±3 %, P<0.01) and glyceryltrinitrate (GTN,
16±8 vs 23±9 %, P<0.01) responses were observed in the
upper limb.10 In contrast, lower limb arteries showed preserved
FMD and GTN.11,12 This pattern of persistent abnormalities of
conduit arteries in the upper limb during long-term follow-up suggests
that aortic coarctation is associated with extensive arterial dysfunction
and that, at least in part, vascular changes are acquired as a result of
the abnormal hemodynamics present in the upper part of the body before
surgery.
Parenteral nutrition
In children, total or partial parenteral nutrition is a well-established
intervention in acute or chronic illnesses that limit oral feeding, impair
digestive function and threaten nutritional status. The repercussions of
parenteral nutrition on structure and function of arteries in children
are an increase in the CCA stiffness (1.8±0.4 vs 1.4±0.5
mmHg.103, P<0.05) associated with an impairment of the endothelium function
(FMD, 6±3 vs 8±3 %, P<0.05; GTNMD, 22±9 vs 25±9
%, NS).13 The exact mechanism through which parenteral nutrition
might accelerate the formation of atheromatous lesions is unclear. The
deleterious effects of parenteral nutrition on endothelial function and
on CCA stiffness that we observed could reflect the additive role of lipid
infusion and hyperinsulinemia. The relationship between dyslipidemia and
vascular endothelium has been well established, not only in adults but
also in children. Substrate competition during parenteral nutrition can
lead to insulin resistance.14 Insulin resistance syndrome, with
its components hyperinsulinemia, obesity, hypertension and hyperlipidemia
has been recognized as a major precursor of atherosclerostic cardiovascular
disease in adults.15
Williams syndrome
Williams syndrome, easily recognized of its typical facial appearance,
is characterised by microdeletion of chromosome 7q 11.23. The role
of disruption of elastin in producing thickening of the arterial wall has
been made evident in a mouse model lacking elastin.16,17 Elastin
not only has a structural role in the extracellular matrix, it also controls
smooth muscle proliferation during arterial development. The cross sectional
compliance of the CCA of Williams was not modified but there was evidence
of a low arterial stiffness (0.74±0.2 vs 1.4±0.5 mmHg.103,
P<0.001).18 A major increase of the intima media thickness
was described (0.6±0.07 vs 0.5±0.03 mm, P<0.001) as a
characteristic arterial phenotype (figure 3).
In conclusion, physicians need to need to be aware that measurement
of the mechanical properties of arteries and endothelial function will
provide information for guiding the clinical decision making process. The
application of the technique will contribute to assess the arterial function
in congenital or acquired abnormalities of arterial wall structures, as
seen in pathology of elastin and collagen, and in metabolic disorders such
as diabetes. The assessment of arterial function may help to define clinical
risk stratification and guide therapeutic interventions.
References
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