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| REVIEW ARTICLE |
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| Year : 2017 | Volume
: 14
| Issue : 2 | Page : 65-70 |
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Arterial stiffness in health and disease
Noha Hassanin Hanboly
Department of Cardiovascular, Cairo University, Cairo, Egypt
| Date of Web Publication | 26-Oct-2017 |
Correspondence Address:
Noha Hassanin Hanboly
Department of Cardiovascular, Cairo University, Cairo
Egypt
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/njc.njc_3_17
The incidence of cardiovascular (CV) diseases is increasing worldwide raising the urgency for early detection of the underlying pathological processes. Early identification of risk factors is important to avoid hospitalization and to reduce CV morbidity and mortality rates. Cardiovascular risk can be assessed by history taking (age, gender, smoking habits), clinical examination (body mass index, heart rate, respiratory rate, blood pressure (BP), temperature and pulse oximetry), laboratory analysis (cholesterol, glucose, triglycerides, potassium, sodium) and with novel techniques like pulse wave velocity (PWV) and augmentation index. Pulse wave velocity is an emerging technique used for CV risk stratification, assessment of arterial stiffness and follow the efficiency of the therapeutic intervention. Pulse wave velocity proved to have independent predictive value when evaluated in conjunction with standard risk factors for CV diseases. However, the field of arterial stiffness research, which evolutes over the past 20 years, lacks guidance for research investigators. This review summarizes the mechanisms of arterial stiffness, various methodologies to assess arterial stiffness and the latest scientific statements regarding its clinical applications. Keywords: Augmentation index, cardiovascular risk, pulse wave velocity
How to cite this article:
Hanboly NH. Arterial stiffness in health and disease. Nig J Cardiol 2017;14:65-70 |
| Introduction | |  |
Large arteries of the human body are normally elastic to maintain a steady blood flow. During systole, the arterial walls expand and absorb energy, which is released during diastole. With aging, the large arteries gradually lose their elasticity and become stiffer. The systolic blood pressure (SBP) consequently tends to increase with age, whereas the diastolic blood pressure (DBP) generally starts to decline after 60 years of age which results in wide pulse pressure (PP) and stiff arteries.
PP is the pressure difference between systolic and diastolic pressures.[1] It is directly proportional to the volume of blood ejected from the left ventricle (LV) during systole (stroke volume) and inversely proportional to the compliance of the aorta [2] [Figure 1]. | Figure 1: Pulse pressure is the systolic blood pressure minus diastolic blood pressure
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A prospective study of 12,763 people living in the United States, Japan, Italy, Greece, Finland, former Yugoslavia, and the Netherland found that PP values followed by DBP and SBP were the best predictors of cardiovascular (CV) disease mortality over the 25-year follow-up period.[3]
| What Determines Arterial Wall Stiffness? | | |
It depends on the structural elements within the arterial wall (smooth muscle fibers, elastin, and collagen). It reflects the structure of the arterial wall which can be modulated by endothelial function, smooth muscle tone, or by alterations in the integrity of the extracellular matrix [Figure 2].
Normally, the pressure load in large conduit arteries is borne by the elastin and collagen components, with less contribution from smooth muscle in the muscular arteries. Because of the anatomic arrangement of the elastin and collagen fibers, elastin engages at low pressure and collagen at higher pressure.[5]
During systolic contraction, 40% of stroke volume is forwarded directly to peripheral tissues, while the remainder is stored in capacitive arteries (mainly aorta and elastic-type arteries). Approximately 10% of the energy produced by the heart is diverted for the distension of arteries and “restored” during diastole to recoil the aorta, squeezing the stored blood forward into the peripheral tissues, thereby ensuring continuous perfusion of organs and tissues. The part of energy used for arterial distension and recoil should be as low as possible. Therefore, the arterial wall must be distensible, i.e., for a given volume change (stroke volume), the developed pressure (PP) should be as low as possible. The arterial stiffness expresses the relationship between pressure response (ΔP) and change in volume (ΔV).[6]
With aging, the cardiac load tends to increase because of a disproportional augmentation of central than brachial arterial stiffness that raises central PP and reduces peripheral PP augmentation.[7] This process favors the development of cardiac hypertrophy.[8]
| Premature Arterial Stiffening | | |
It occurs in association with several important CV risk factors including hypertension, diabetes mellitus, and cigarette smoking,[9] which are also associated with endothelial dysfunction.[10] Hypercholesterolemia is also associated with endothelial dysfunction.[11]
Arterial stiffness can be evaluated by ultrasonography or by the measure of the pulse wave velocity (PWV) over a given arterial segment which increases with arterial stiffness. The principal consequences of arterial stiffening are an increase in systolic pressure and a decrease in diastolic pressure with resulting high PP.[12]
| Increased Arterial Stiffness and Pulse Wave Velocity | | |
Ejection of blood into the aorta generates a pressure wave that is propagated to other arteries throughout the body. This forward traveling (incident) pressure wave is reflected at any point of structural and functional discontinuity in the arterial tree, thereby generating a reflected wave traveling backward the ascending aorta. Incident and reflected pressure waves interact and summed up in the measured pressure wave.[13]
Young human subjects have distensible arteries and low PWV; the reflected waves affect central arteries during diastole after LV ejection has ceased. This timing is desirable since the reflected wave causes an increase in ascending aortic pressure during early diastole and not during systole, resulting in aortic systolic and PPs which are lower than in peripheral arteries.
This is advantageous since the increase in early DBP has a boosting effect on coronary perfusion, without increasing LV after load.[13] With increased PWV, the reflected waves occur earlier. The earlier return means that the reflected wave affects the central arteries during systole rather than diastole, thus increasing aortic pressures during systole and reducing aortic pressure during diastole [13] [Figure 3]. | Figure 3: Schematic representation of pulse pressure amplification. Typical pressure tracings from the brachial artery (a) and central aorta (b) are shown. When the large arteries are compliant, such as in a normal healthy young subject (waveforms on the left), the arterial waveform is amplified as it travels toward the periphery. As the large arteries stiffen, for example, with increasing age, diabetes, or other cardiovascular risk factors, this amplification is reduced (waveforms on the right). The two subjects have similar BP at the brachial artery despite striking differences at the aorta, demonstrating the importance of assessing central BP in individuals. When the large arteries are compliant the initial systolic pressure wave, P1, traveling from the heart to the periphery, is responsible for peak SBP. Reflected pressure waves, P2, arrive at the central aorta in diastole, augmenting DBP and coronary artery filling. As large arteries stiffen, wave reflection occurs earlier so that SBP is augmented and DBP falls. Augmentation index is calculated as the difference between the second (P2) and first (P1) systolic peaks (ΔP) as a percentage of the PP. Augmentation index is negative in healthy young people, but with aging or increasing cardiovascular risk, arteries stiffen and it becomes increasingly positive. [14]
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| Pulse Wave Velocity | | |
It is defined as the velocity at which the pressure waves generated by the systolic contraction of the heart propagate along the arterial tree. The evaluation of PWV provides complementary information about the elastic properties of arterial system. The higher PWV corresponds to lower vessel compliance and higher arterial stiffness.
| Is Measuring Arterial Stiffness Important? | | |
The arterial stiffness is responsible for several pathological processes, which can lead to many CV diseases. Recently, the European Society of Cardiology guidelines for the management of arterial hypertension and the American Heart Association Council on Hypertension considered PWV as the gold standard method for assessing arterial stiffness.[15],[16]
Measurements of PWV are undertaken with several methodologies; some devices use a probe or tonometer to record the pulse wave with a transducer, and other devices use cuffs placed around the limbs or the neck that record arrival of the pulse wave oscillometrically or other devices that use ultrasonography or magnetic resonance imaging (MRI) approaches.[15]
Carotid-femoral PWV is a simple, noninvasive, robust, and reproducible method that is regarded as the gold standard for measuring arterial stiffness since epidemiological studies have found it to be an independent predictor of CV events.[17]
The complior system uses two mechanotransducers applied to the skin and measures real-time pulse waves at carotid and femoral points. The test is performed in supine position, placing sensors at the carotid and femoral pulses [Figure 4].[17] | Figure 4: Measurement principle of pulse wave velocity with complior analyze. Carotid femoral velocity is measured form the carotid-femoral distance and the transit time between the carotid and the femoral pulse recorded simultaneously. Pulse wave velocity = carotid − femoral distance/T
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SphygmoCor uses an applanation tonometer to calculate the central pressure and augmentation index.[18]
Complior system records both waves simultaneously, whereas SphygmoCor records consecutively using electrocardiogram (ECG). In this case, changes in heart rate between two recordings may determine a variation in transit time (TT). These mechanical methods have the disadvantages that there is a prolonged learning period to become an experienced observer.[19]
| Doppler Ultrasound in the Measurement of Pulse Wave Velocity | | |
Doppler ultrasonography may be used to record flow waveforms from accessible sites. Waveforms may be recorded either sequentially with ECG gating or simultaneously.[20]
Using a linear array (6.6 MHz) probe, synchronized with ECG, the examination begins with the patient in a supine position after locating the carotid artery with B-mode at the supraclavicular level (1–2 cm of the bifurcation). The process is repeated on the common femoral artery in the groin. To find the TT, the time from the R-wave of QRS to the foot of the waveform using digital calipers is measured [17] [Figure 5]. The foot of the flow wave from each of the recording sites is used and the time elapsed in milliseconds is calculated.[21] | Figure 5: Time measurement in femoral artery gating with electrocardiogram[17]
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| Magnetic Resonance Imaging-Based Approaches | | |
MRI can be applied in much the same way as ultrasonography to determine PWV. It has the advantage of being able to assess any vessel and providing more accurate distance and area estimates. However, poorer time and spatial resolution and cost are main disadvantages.[15]
| Normal and Abnormal Carotid-Femoral Pulse Wave Velocity | | |
Many previous cohort studies have demonstrated that higher carotid-femoral PWV is associated with increased risk for a first or recurrent major CV disease event.[22] [Table 1] summarizes the results obtained in multiple studies. | Table 1: Studies of pulse wave velocity carotid-femoral measurement and reference values in different population
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Hypertension
A stiffened vasculature is less able to buffer short-term alterations in flow. Increased aortic stiffness is also associated with impaired baroreceptor sensitivity which will result in potentially marked alterations in BP as cardiac output changes during normal daily activities such as changes in posture and physical exertion.[31]
Cardiac disease
Excessive arterial stiffness represents a compound insult on the heart. Aortic stiffening increases LV systolic load, which contributes to ventricular remodeling and reduced mechanical efficiency. This leads to an increase in myocardial oxygen demand.[32]
Central nervous system
Aortic stiffening is also associated with increased risk for large-vessel stroke, either ischemic or hemorrhagic. This may be mediated through atherosclerosis, with increased stiffness contributing to both atherogenesis and risk for plaque rupture.[33]
Kidney disease
The kidneys are low-impedance organs that are exposed to obligate high flow throughout the day. In the presence of increased aortic stiffness, the microvasculature of the kidney is exposed to excessive pressure which can damage the glomerulus, leading to proteinuria and loss of function.[34] Some studies have demonstrated modest associations between increased PWV and reduced glomerular filtration rate.[35]
| Pitfalls and Limitations of Arterial Stiffness Measurements | | |
Physiological confounders
A recent study demonstrated that an increase in heart rate results in a modest but significant increase in PWV; this must be taken into consideration when undertaking measurements of arterial stiffness so that large meals, caffeine-containing food and drinks, and smoking should be suspended for at least 2–4 h before the measurements.[36]
Methodological confounders
It was found that two devices yielded different values of carotid femoral PWV within the same individual attributable to the algorithm used by each device to derive the time of travel (foot-to-foot method with the SphygmoCor system versus maximum-slope method with the complior system); thus, the same waveforms analyzed by the two devices could result in differences in PWV values of 5%–15%.[37] Moreover, some of the techniques are highly operator dependent.
| Conclusion | | |
Arterial stiffness is accepted as one of the most useful parameters for assessment of the CV system. PWV as the gold standard to measure it was extensively studied in different groups of patients with distinct pathologies. The imaging methods, such ultrasonography and MRI, take advantage of the pulse wave path length direct measurement. However, these methods are very expensive. Nonimaging methods based on the pressure mechanotransducers are available and extensively studied in different populations although this method has problems on signal acquisition in obese patients. Future studies are needed to provide novel methods for arterial stiffness assessment easy to use in daily clinical practice, simple, not expensive and more efficient.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
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[Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5]
[Table 1]
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