Update on the Use of Pulse Wave Velocity to Measure Age-Related Vascular Changes

Abstract

Purpose of Review

Pulse wave velocity (PWV) is an important and well-established measure of arterial stiffness that is strongly associated with aging. Age-related alterations in the elastic properties and integrity of arterial walls can lead to cardiovascular disease. PWV measurements play an important role in the early detection of these changes, as well as other cardiovascular disease risk factors, such as hypertension. This review provides a comprehensive summary of the current knowledge of the effects of aging on arterial stiffness, as measured by PWV.

Recent Findings

This review highlights recent findings showing the applicability of PWV analysis for investigating heart failure, hypertension, and other cardiovascular diseases, as well as cerebrovascular diseases and Alzheimer’s disease. It also discusses the clinical implications of utilizing PWV to monitor treatment outcomes, various challenges in implementing PWV assessment in clinical practice, and the development of new technologies, including machine learning and artificial intelligence, which may improve the usefulness of PWV measurements in the future.

Summary

Measuring arterial stiffness through PWV remains an important technique to study aging, especially as the technology continues to evolve. There is a clear need to leverage PWV to identify interventions that mitigate age-related increases in PWV, potentially improving CVD outcomes and promoting healthy vascular aging.

Introduction

Age remains a primary risk factor for cardiovascular disease (CVD), playing a synergistic role with other risk factors, while also influencing CVD outcomes independently of these factors [1]. Age-related changes in arterial load imposed on the left ventricle (LV) play a particularly important role in the development of CVD. The arterial system is heterogeneous, comprised of compliance or elastic vessels (the aorta, carotid arteries, and iliac arteries) and resistance or muscular vessels (the femoral, brachial, and radial arteries). In a normal arterial system, compliance decreases gradually from the ascending aorta, descending aorta, carotid arteries, and iliac arteries to the muscular resistance arteries, which are stiffer than the compliance vessels. This “compliance gradient” is disrupted with normal aging; changes in compliance arteries may occur without changes in the resistance arteries, and vice versa.

Arterial compliance or its inverse, arterial stiffness, is assessed by determining pulse wave velocity (PWV), which plays an important role in studying the age-related development of CVD. PWV can be used to help understand vascular aging and can be a more accurate predictor of CVD risk than simple chronologic age alone [2]. PWV is not a novel technique, yet its use in clinical practice has been hampered by the need for specialized equipment and operational expertise. PWV is strongly related to not only age but also body mass index, blood pressure (BP), and physical activity [3, 4]. As increases in BP can lead to hypertension, which is a risk factor for a variety of CVDs, as well as Alzheimer’s disease [5], PWV may serve as an important early indicator of CVD risk. Nevertheless, aortic stiffness, which is measured by PWV, also exists independently from other cardiovascular conditions, highlighting its unique ability to reflect vascular aging [2]. While aortic PWV alone cannot serve as a predictor of mortality in the general population, its utilization in older individuals and clinical populations can often serve as a predictor for CVD and stroke [6]. For patients with preexisting hypertension, PWV can be a predictor of survival, more so than traditional methods such as the Framingham Risk Score, and it can also aid in monitoring response to treatment and estimating prognosis [2].

Aortic Stiffness and Aging

A seminal study evaluated the effects of age and BP on carotid-femoral PWV and established reference values for PWV across different subpopulations [7]. Since this study, our understanding of the relationships between aortic stiffness and aging has improved. We now know that arterial walls undergo structural alterations, including increased wall thickness and changes in extracellular matrix proteins, leading to reduced elasticity and increased arterial stiffness, which in turn affect PWV by accelerating the propagation of pressure waves along the arterial tree. In a large study of nearly 18,000 Chinese adults, changes in arterial stiffness, as measured by brachial-ankle PWV, were observed prior to (and may mediate) age-dependent changes in BP [8]. This suggests that PWV may serve as an early monitoring tool for BP and hypertension, which are risk factors for other CVDs, especially if arterial stiffness may be reduced to prevent or delay BP elevation [8]. PWV has also been useful for evaluating the effects of cigarette smoking on arterial stiffness mediated through factors including insulin resistance [9].

A broad spectrum of factors can affect PWV, including heart rate, sex, height, and age. Of these, age is the single most important factor influencing PWV [4]. While this limits the applicability of PWV in evaluating lifestyle risk factors, it does highlight the ability of PWV to consider cardiovascular changes in the context of age and its related pathologies. Notably, the association between age and aortic PWV is not completely linear. PWV increases rapidly after age 50 years, potentially secondary to the destruction of elastin fibers, and acts as a main contributory factor to the age-dependent development of hypertension [10]. Beyond this, there is also a sex-dependent difference, with White middle-aged females showing a greater increase in PWV with age than males [11]. Metabolic disturbances may also be associated with PWV, but these associations with aging require further elucidation [12].

Aortic Stiffness and Disease States

Aortic Stiffness and Heart Failure

Interactions between the arterial system and left ventricular function were originally studied in the 1970s [13], and soon after, Ross [14] described how heart failure is sensitive to changes in LV afterload. Despite several studies in subsequent years highlighting the need to examine ventricular-vascular relationships [15–21], evaluation of cardiac function by echocardiography continued to be the mainstay of assessment in clinical practice. More recently, however, the nexus between ventricular and vascular function has been gaining more attention, specifically with respect to aortic stiffness and heart failure.

Aortic/arterial function measured through aortic input impedance consists of aortic compliance (or stiffness), systemic vascular resistance, and wave reflections [22]. It is well known that aortic stiffness increases (or compliance decreases) with age and is enhanced in the presence of various diseases, including hypertension and diabetes. Cardiac function is dependent on preload, afterload, contractility, and heart rate [23] and is predominantly assessed with echocardiography measurements, such as ejection fraction, fractional shortening, stroke volume, and cardiac output [24]. However, these measurements do not fully represent cardiac function, as they depend on loading conditions [25]. Therefore, it is important to consider the interaction between the LV and aorta (also known as ventricular-vascular coupling (VVC)) when evaluating LV performance as a true measure of global cardiovascular efficiency [17, 26]. The VVC ratio, calculated as the aortic elastance (Ea) divided by the end-systolic elastance (Ees), has recently been recommended for risk stratification in heart failure [27]. Nevertheless, the sensitivity of Ea and Ees may be reduced in disease states, for which more sensitive parameters, such as myocardial longitudinal strain and aortic PWV or aortic impedance, may be more appropriate [27, 28].

In many studies, increased aortic stiffness, as measured by PWV, has been implicated in the development of heart failure [29]. Heart failure can be classified as either heart failure with preserved ejection fraction (HFpEF) or heart failure with reduced ejection fraction (HFrEF). While patients with HFpEF tend to be older, obese females with hypertension, diabetes, hypothyroidism, and renal disease, patients with HFrEF tend to be predominantly older males [30]. Many studies have shown that patients with HFpEF have increased arterial stiffness [31–35]. Despite the strong evidence that HFpEF is associated with increased PWV and increased pulsatile hemodynamics, treatment studies have reported mixed results [36]. In patients with HFrEF, increased PWV was significantly associated with a worse prognosis in some studies [37, 38] but not in another study [39]. Nevertheless, targeted treatments to improve arterial impedance resulted in better outcomes in patients with HFrEF [36]. Detailed reviews of ventricular-vascular interactions and the role of arterial stiffness and hemodynamics have been previously published [21, 36, 40]. Thus, ventricular-vascular interactions provide relevant prognostic options, and treatment with drugs to reduce arterial stiffness and impedance is essential for improving outcomes in patients with heart failure [36].

Aortic Stiffness and Hypertension

Aortic stiffness and hypertension often coexist in a vicious cycle. While the specific timing of events has been debated [41], Kaess et al., in their analysis of the Framingham population study, suggest that aortic stiffness predicts future incidences of hypertension and precedes, rather than follows hypertension [42]. A few studies involving animal models seem to support this viewpoint. In elastin-deficient mice, decreased aortic diameter and compliance at postnatal day 7 were followed by an increase in systolic pressure at post-natal day 14 [43]. Furthermore, the tg^sm/p22phox mouse exhibits diminished aortic compliance from the age of 6 months onward. When compared to their wild-type counterparts, this cohort of mice already exhibits higher blood pressure by the time they are 9 months old [44]. In Sod3^fl/fl Smmhc-Cre mice, marked deposition of adventitial collagen was observed by 6 months of age. This correlated with increased aortic stiffening. However, significant increases in blood pressure were delayed till they were about 9 months old [44]. Therefore, it stands to reason that therapies that improve arterial diameter or compliance are recommended as therapeutic modalities for the management of hypertension [43]. In both the tg^sm/p22phox and SOD3-deficient mice, the authors conclude that chronic vascular oxidative stress promotes fibrosis within the arteries, aortic stiffening, and subsequently hypertension [44]. An additional therapeutic strategy might focus on inhibiting the development of vascular oxidative stress and, consequently, blunt the progression of hypertension.

A second school of thought claims that high blood pressure increases the risk of aortic stiffness by causing pulsatile insults to the aorta wall [45, 46]. This view takes the approach that hypertension itself accelerates vascular aging and, consequently, aortic stiffness [41]. Indeed, acute, angiotensin II-induced increases in blood pressure in normotensive individuals elevated indices of aortic stiffness. This increase in arterial stiffening was reversed by nitroglycerin treatment [47]. Contrarily, arterial stiffness persisted in hypertensive individuals even after arterial MAP was reduced, indicating that the raised BP was not the primary cause of the stiffness but rather altered structural changes in the arterial wall [47]. Such a rise in blood pressure has the potential to hasten vascular stiffening. As a result, each condition exacerbates the others, creating a feedback loop. Blood pressure rises as a result of the heart having to work harder to pump blood through stiffened arteries, which increases resistance to blood flow. In turn, increased blood pressure puts more strain on artery walls, which contributes to their stiffening. The jury is still out on whether elevated blood pressure precedes aortic stiffness [41].

Dietary salt has also been implicated as a risk factor for arterial stiffness [48, 49]. Considering that arterial stiffness has been shown to precede hypertension, this opens up the discussion of sodium-associated arterial stiffness as a pathophysiological mechanism in salt-sensitive hypertension. Using the Na-induced, stroke-prone Dahl salt-sensitive rat model, Herrera et al. [50] investigated the causal mechanisms linking sodium and arterial stiffness. Arterial stiffness via PWV was detected in the carotid artery and aorta as early as 6 weeks of age, in conjunction with specific gene modifications of the extracellular matrix structural components, cell adhesion proteins, and epigenetic regulators of vessel walls, leading them to conclude that “a whole-vessel wall response occurs in increased salt intake-induced arterial stiffness” [50]. It would seem that increased dietary sodium drives molecular and then functional alterations in arterial stiffness. As an example, studies in humans have shown that both salt-sensitive and resistant subjects expand circulating volume and increase their cardiac output upon sodium loading equally; however, the salt-resistant subjects display a decrease in systemic vascular resistance, while the salt sensitive do not, implicating an underlying vascular dysfunction [51].

Pulse Wave Velocity and Alzheimer’s Disease

Vascular networks are affected early during the development of Alzheimer’s disease [52], underscoring the importance of PWV measurements for assessing brain hemodynamics and detecting pathology at an early stage. As both cardiovascular and cerebrovascular diseases are associated with cognitive decline, reduced blood flow to both the heart and brain may play an important role in the development of Alzheimer’s disease [53]. The cerebral vasculature is linked to cognitive deficits, including in Alzheimer’s disease, through a potential amyloid beta-dependent model [54]. Notably, data from the Baltimore Longitudinal Study of Aging revealed that arterial stiffness, as measured by PWV, correlated with cognitive decline over 14 years, even before the onset of dementia [55••]. These results highlight the applicability of PWV as an early screening tool for cerebrovascular disease and dementia.

Pulse Wave Velocity Measurements Reconsidered

Pulse Wave Velocity Measurements: Blood Vessel Selection

PWV is defined as the speed at which BP, flow, or flow velocity pulses travel in a specific segment of a blood vessel. In general, signals are measured simultaneously or sequentially at two sites along one or two blood vessels. PWV is calculated as D/PTT, where D is the distance between the two recording sites and PTT is the time for the pulse to travel between the two sites (Fig. 1). PTT is calculated as the difference in arrival times of the foot of the pulses (if measured simultaneously) or as the difference in pre-ejection times (time from the R wave peak to the foot of the pulse) of the pulses (if measured sequentially). Aortic/arterial stiffness estimated using the formula PWV = D/PTT has been used extensively and is universally accepted as a “gold standard” measurement of vessel stiffness.

Fig. 1.

Diagram of how pulse wave velocity (PWV) may be calculated from the transit of the same pulse. Notably, flow velocity signals from two sites can be measured simultaneously on the basis of distance and pulse transit time

Use of PWV to assess aortic/arterial stiffness was first introduced by Bramwell and Hill in 1922 [56], but its use increased exponentially in only the past 2 decades. Recognizing the importance of arterial stiffness, both the American Heart Association Counsel on Hypertension [57] and the European Society of Hypertension [58] recommend using PWV to assess arterial stiffness, based on evidence from multiple randomized clinical trials and meta-analyses. Despite these recommendations, PWV measurements remain predominantly a research tool. The lack of wide-spread clinical use may be at least partly attributed to ambiguous or conflicting results reported in some studies [42, 59], resulting from important measurement limitations.

The use of peripheral vessel segment combinations with properties differing from those of the aorta can lead to misinterpretation of PWV results. In humans, PWV is usually measured at carotid-femoral [60•, 61], carotid-radial [62], brachial-femoral [63], or brachial-ankle [64] arterial sites, all of which include vessels that differ significantly from the aorta. Using a multi-sensor pressure catheter, Latham et al. [65] showed that PWV increases from approximately 4.4 m/s in the ascending aorta to approximately 9.2 m/s in lower abdominal aorta in people without hypertension (average age of 42 years). PWV is 3 to 4 times higher in the femoral and brachial arteries than in the aorta [66], including these arteries that dramatically elevate PWV values, leading to substantial misinterpretation. PWV techniques that include carotid, brachial, and femoral arterial segments have been demonstrated to overestimate PWV in the aorta by approximately 34% [67], 92% [66], and 105% [66], respectively, [65] in age-matched subjects. Therefore, PWV measurements based on the aortic pressure waveform (or a representation of it, such as aortic wall motion/diameter waveforms) in a single arterial segment provide the most accurate estimate of arterial stiffness and may be the best predictor of prognosis [68]. In normal individuals, PWV based on carotid-femoral artery measurements ranged from 6.6 ± 0.8 m/s in those younger than 30 years to 11.7 ± 2.9 m/s in adults older than 70 years [69]. In contrast, PWV using aortic measurements in normal adults ranged from 4.5 ± 0.5 m/s in the 21–30-year-age group to 6.8 ± 1.0 m/s in the 61–70-year-age group [10]. These data clearly show how PWV is overestimated using carotid-femoral vessels instead of the aorta, dampening the suggestion that carotid-femoral–PWV-based aortic stiffness assessment should be considered standard for clinical practice [70].

The method used to determine the separation distance (i.e., D) between carotid-femoral sites may also affect the accuracy of PWV measurements. Estimation by two different methods may result in more than 3 m/s difference in PWV. Girerd et al. [59] compared four different methods for determining D: “direct D” (d), based on direct measurement of the distance on the surface of the body; “real D,” calculated as 0.8 × d; “subtracted D,” calculated as 1.04 × d − 0.11 × body height − 0.02; and “estimated D,” calculated as body height/4 + 7.28). PWV was 11.6 m/s, 9.3 m/s, 8.3 m/s, and 9.2 m/s, respectively, using the four different methods in the same group of subjects.

Other Issues Regarding Pulse Wave Velocity Measurements

Widespread applicability of PWV analysis, especially in clinical settings, is limited by other measurement issues as well. While carotid-femoral PWV is considered the gold standard, the need for special equipment and operational expertise limits its routine clinical use [71]. Another challenge is the variability in PWV associated with outdoor temperatures, time of the day (for females), and other common factors, which may limit the reliability of repeated PWV tests that are often necessary in clinical settings [4]. Importantly, this variability increases with age, such that 3–4 measurements may be necessary to increase precision [4]. It has also been suggested that precision can be increased by maintaining environments that reduce variability introduced by outside influences and by performing measurements in the afternoon [4]. Beyond this, there is a paucity of studies evaluating how hormonal differences, body composition, and lifestyle factors influence variations in PWV. Differences between devices used for measuring PWV may likewise contribute to variability in PWV values.

Future of Pulse Wave Velocity

Emerging Technologies

The most frequent noninvasive techniques for determining PWV involve the use of magnetic resonance imaging (MRI) or Doppler echocardiography. MRI is accompanied by potential side effects, as well as time and cost limitations [10]. Doppler echocardiography may have similar effectiveness but has fewer disadvantages and is easier to perform [10]. Ultrafast ultrasound imaging has similarly arisen as a promising technique, which can noninvasively measure PWV and is independent of age, BP, and sex [72]. Laser speckle contrast imaging [73] is a noninvasive technique that assesses only superficial blood flow, and optical coherence tomography [74] can be used to measure cerebral 3-dimensional blood flow. These two noninvasive techniques offer advantages by examining blood flow and oxygenation in the microcirculation, which can help identify early markers of heart failure and mitochondrial dysfunction. While not yet applicable to humans, arterial spin labeling allows continuous MRI of regional myocardial blood flow, and magnetic resonance techniques may be combined with phosphorus-31 magnetic resonance spectroscopy [75], a noninvasive method for continuous measurement of skeletal muscle mitochondrial oxidative phosphorylation potential. Thus, as multi-modal imaging improves, especially through noninvasive techniques for measuring PWV, there is increased potential for clinical application of PWV to better evaluate the role of mitochondria in heart failure, while improving the ability to deliver more personalized medical care.

Novel biodegradable sensors to measure PWV in the context of stents remain an important avenue of interest and may allow for better monitoring of CVD following stent implantation [76]. As wearable fitness devices, such as Fitbit and Apple Watch, become increasingly common, there is the potential to incorporate PWV analysis into these devices [77]. Textile triboelectric nanogenerators are another emerging technology. They can provide continuous monitoring through skin-surface deformation, with lower barriers to entry than traditional PWV methods, but scalability and biocompatibility limit their clinical usage at present [78]. A recent report described the creation of a flexible weaving-constructed self-powered pressure sensor with high durability that allows for continuous monitoring of PWV in addition to BP. However, its accuracy has been yet been confirmed [79•]. Another study showed that microelectromechanical sensors for measuring pulse waveforms produced results that were comparable to those obtained from invasive methods, highlighting the potential viability of these noninvasive wearables [80]. The potential use of wearable technologies for measuring PWV has been reviewed previously in detail [81], and Jin et al. demonstrated important reductions in barriers to usage, although the accuracy of these devices remains unclear.

Given the low prevalence of PWV measurements in clinical practice, the potential use of artificial intelligence to estimate PWV (ePWV) from other routinely measured parameters is particularly appealing [1]. In the Systolic Blood Pressure Intervention Trial, ePWV was utilized to predict CVD, as well as to monitor response to drugs, and was found to be a better predictor of mortality than traditional risk analysis techniques, such as the Framingham Risk Score [2]. ePWV is also a useful indicator of stroke occurrence in middle-aged men, but it has not been evaluated in other populations [82]. Of note, many current models may neglect the importance of age in estimations of PWV, skewing these measurements [1].

Nevertheless, ePWV has been predictive of CVD outcomes, as well as mortality, in US adults, highlighting that it is a valid measurement [71]. However, many studies evaluating ePWV have examined mostly White populations [71], and the relationship between age and arterial stiffness may differ between races and ethnicities, given the known effects of race on BP [83]. Moreover, ePWV continues to exhibit a false-positive rate of approximately 20%, when compared to carotid-femoral PWV [84]. It has been suggested that algorithmic methods used to determine carotid-femoral PWV mainly reflect age and BP and do not actually consider vascular aging [85]. Furthermore, while carotid-femoral PWV may not reflect vascular aging, ePWV is more related to carotid intima-media thickness, carotid stiffness, and carotid augmentation index, which are indicators of vascular aging [84]. Nevertheless, when comparing ePWV values to those obtained by invasive methods, ePWV is substantially less accurate than carotid-femoral PWV [85].

Improvements in PWV measurement methods may be further expedited by advances in artificial intelligence. A review of photoplethysmography aided by artificial intelligence to estimate BP noninvasively without a cuff noted that BP measurements are progressing to the point of allowing continuous measurements [86], whereas machine learning approaches to PWV remain limited. Recently, an artificial neural network utilized aortic PWV to identify coronary heart disease with 63–93% accuracy [87]. While this accuracy falls well below standards in the field, use of PWV in combination with other factors to diagnose age-related diseases (such as CVD) may be particularly useful to improve the accuracy of diagnostic models [87]. Another study used a recurrent neural network (publicly available) to estimate PWV based on only radial pressure waves [88].

PWV can also be used to assess cerebral blood flow, which is of special relevance for cognitive disorders [89]. Four-dimensional flow MRI is a recent technique that allows estimation of cerebral PWV within intracranial arteries [90]. Together, the above-described methodologies highlight the extensive ongoing efforts to overcome the knowledge barriers that limit the use of PWV for evaluating age-related pathologies.

Pulse Wave Velocity for Evaluating Therapies

PWV is an important technology for evaluating the efficacy of potential therapies. For example, isometric handgrip training was found to reduce arterial stiffness, as measured by PWV, in hypertensive patients [91]. Notably, endothelial dysfunction, characterized by increased oxidative stress, affects arterial properties and contributes to increased PWV [92]. Other factors, including chronic low-grade inflammation, vessel tortuosity, calcification, and the presence of various comorbidities, may also affect arterial stiffness and thus PWV [93]. However, oxidative stress may be independently associated with arterial stiffness after 45 years of age [93]. Notably, reactive oxygen species can be generated by mitochondrial dysfunction, which is further linked to accelerated vascular aging [94]. Given that aging is associated with increased oxidative stress, which increases arterial stiffness through reduced nitric oxide bioavailability [92], this suggests that mitochondrial targeting strategies may have an important role in reversing age-related increases in PWV.

Specifically, loss of the antioxidant manganese superoxide dismutase in a murine model demonstrated that mitochondria-generated oxidative stress is potentially responsible for age-related arterial stiffness [95]. Similarly, murine NADPH oxidase 4 overexpression led to oxidative stress and increased arterial stiffness, as measured by PWV [96]. A study in humans reported that mitochondria-targeted antioxidant MitoQ for peripheral artery disease improved walking ability but did not alter aortic PWV [97]. However, a murine study reported that treatment with MitoQ significantly reduced PWV, but only in older animals, in which MitoQ reduced the age-related decrease in elastin [98]. These results therefore suggest that mitochondrial-based antioxidant approaches can reduce arterial stiffness, but optimized delivery must be achieved. They also show how PWV can be used to investigate the response to oxidative stress and age-related disorders.

Conclusion and Future Perspectives

Given the applicability of PWV for measuring vascular aging and understanding age-related development of CVD, there is a need for greater healthcare reimbursement and reduced cost of PWV instrumentation to facilitate routine use of PWV in clinical practice [2]. PWV can play an important role in diagnosing conditions, but it should not necessarily exist independently from other measures. Increasingly, the literature has shown that factors predisposing to CVD, such as hypertension and potentially even diabetes mellitus, may have compounding effects on arterial stiffness, emphasizing the need to consider their synergistic effects [99]. This is highlighted by frameworks such as the Systemic Hemodynamic Atherothrombotic Syndrome (SHATS) score, which considers these combined effects [99].

While new methods of assessing PWV are being developed, there is a paucity of studies scrutinizing the accuracy of these technologies, especially in comparison to invasive measurements. A recent study reported that both finger-toe PWV and cuff-based estimated PWV are much poorer estimates of arterial stiffness and invasive PWV than carotid-femoral PWV, which remains the gold standard noninvasive measurement [85]. While some studies have supported the use of ambulatory brachial cuff-based oscillometry [100], recent studies highlight that this methodology carries no predictive power when adjusted for age and systolic BP [101]. PWV methods cannot be used clinically simply because they correlate with other factors; they must accurately capture vascular aging. Even the most commonly used method, carotid-femoral PWV, underestimates PWV when compared to invasive methods in the elderly and is less strongly associated with age than invasive PWV measurements [85]. Thus, none of the currently available noninvasive techniques is ideal for estimating vascular aging, although their accuracy may be improved by machine learning, which can make adjustments based on known issues to deliver more accurate PWV values. The combination of PWV and machine learning may help move towards identifying early biomarkers of arterial stiffness, allowing earlier initiation of potential treatments to ultimately improve outcomes.

There is also a need for more diverse reference values for PWV. Differential databases based on sex are clearly required [102]. A large Latin American cohort study reported PWV trends generally similar to those of studies containing mostly non-Hispanic participants, with arterial stiffness increasing as age increased, especially after 50 years. [103]. However, the actual standard PWV values and PWV values across various pathologies differed from those seen in non-Hispanic populations. Furthermore, many studies in all populations have relied on cross-sectional approaches, whereas longitudinal studies are more appropriate when considering the properties of the arterial system [11]. Large-scale longitudinal studies, such as the Baltimore Study of Aging, are very important, especially for diverse groups [55••].

PWV analysis remains an important methodology for understanding the progression of heart failure and other CVDs, especially those that are age-related. Future research should also explore the role of PWV measurements in monitoring the effectiveness of lifestyle modifications (such as regular exercise and a healthy diet) and pharmacologic interventions (including antihypertensive medication). There is a clear need to leverage PWV to identify interventions that mitigate age-related increases in PWV, potentially improving CVD outcomes and promoting healthy vascular aging.

Data Availability

No new data was generated for this manuscript.