European Journal of Cardiovascular Medicine

Hypertension is a leading global cause of mortality, accounting for approximately 18% of deaths worldwide. With the advancement of modern technology, there has been an increase in the diagnosis of hypertension among patients. Both genetic predisposition and environmental factors of the contemporary era contribute to the development of hypertension [1].

The prevalence of hypertension rises with age, and individuals with higher blood pressure (BP) during their younger years are at an increased risk of developing hypertension. This condition heightens the risk of vascular events in the brain, heart, and kidneys. The proposed mechanism for these events involves reduced vascular compliance due to arterial stiffening in hypertension. Chronic elevated BP, often asymptomatic, is identified as a major factor in the progression of arterial stiffness and subsequent vascular damage [2].

While primary hypertension treatment commonly includes BP monitoring, it often overlooks vascular stiffness, which is a key pathological factor. Pulse wave velocity (PWV) measurements, indicative of arterial stiffness, are recognized as independent predictors of mortality in patients with cardiovascular disease (CVD) risk factors such as hypertension, diabetes, and end-stage renal disease [3]. However, PWV measurement is complex, requires technical expertise, and is time-consuming. Recent studies suggest that simple, validated non-invasive digital pulse volume (DPV) measurements can effectively monitor the progression of arterial stiffness. The stiffness index (SI) and reflection index (RI), derived from DPV, are acknowledged as independent markers of CVD [4-8]. Therefore, this study aimed to measure arterial stiffness using digital volume pulse (DVP) recordings to predict vascular events.

The primary aim of this study is to record the arterial SI and RI in subjects diagnosed with hypertension, as well as in a control group of age-matched normotensive individuals. The objectives include comparing these vascular parameters between the hypertensive subjects and the normotensive controls to identify any significant differences. Furthermore, the study seeks to classify the hypertensive subjects based on the duration of their disease and compare the arterial SI and RI among these subgroups. This classification aims to elucidate any potential correlation between the duration of hypertension and changes in vascular parameters.

This cross-sectional study was conducted on 200 individuals aged between 30 and 60 years, divided into four groups: Group 1 comprised healthy controls, while Groups 2, 3, and 4 included subjects with hypertension durations of 2, 5, and 10 years, respectively. Control group consisted of individuals aged 30–60 years with no history of cardiovascular risk factors, including hypertension, diabetes, or obesity. Subjects with a history of diabetes, angina, myocardial infarction, cerebrovascular accidents, smoking, or alcoholism were excluded from the study.

Participant identification details and clinical histories were documented in a standardized pro forma. Anthropometric measurements were taken, and blood pressure was recorded after 5 minutes of rest in a seated position. Digital volume pulse (DVP) was measured using finger pulse photoplethysmography in a quiet room. DVP recordings display two peaks: the systolic and diastolic peaks. The early systolic peak results from a pulse wave transmitted directly from the left ventricle to the finger. The diastolic peak arises from a pulse wave traveling along the aorta to the small arteries in the lower body, where it is reflected back along the aorta. This path length varies according to the subject's height (h). The pulse transit time (PTT or ∆T) [9] is the delay between the systolic and diastolic peaks and was measured using software. The magnitudes of the systolic and diastolic peaks were also determined using this tool. The stiffness index (SI) and reflection index (RI) were calculated using the following formulas:

SI (SIDVP) = Subject’s height (h) / PTT (∆T)

RI (RI) = Magnitude of Diastolic peak (b) × 100 / Magnitude of Systolic peak (a).

Table 1 summarizes the age distribution of study participants categorized by hypertension duration. It reveals a clear trend of increasing hypertension prevalence with age and longer duration of hypertension. Participants aged 40-49 years show a notable rise in hypertension prevalence across all groups compared to younger age brackets, peaking in those with hypertension for 5 and 10 years. This underscores age as a significant factor in hypertension prevalence and duration.

The Resistive Index (RI) and Stiffness Index (SI) were assessed across the four groups. Group I exhibited the lowest RI (0.50 ± 0.08) and SI (6.12 ± 0.09), indicating normal vascular function. Group II showed a significant increase in both RI (0.77 ± 0.06) and SI (10.51 ± 0.70) compared to Group I. Further elevation was observed in Group III, with RI at 0.91 ± 0.06 and SI at 10.98 ± 0.86. Interestingly, Group IV displayed a slight decrease in RI to 0.86 ± 0.03, while SI continued to increase, reaching 11.55 ± 1.18 (Table 2).

ANOVA analysis revealed significant differences in RI among the groups, with the most notable difference between Group I and Group II (F=63.225, P=0.025), followed by Group III (F=55.317, P=0.039). The difference was not statistically significant between Group I and Group IV (F=29.408, P=0.149). For SI, significant differences were observed between Group I and Group II (F=2.48, P=0.028) and Group I and Group IV (F=2.597, P=0.019), while the difference between Group I and Group III was not significant (F=1.091, P=0.536) (Table 3).

Pearson correlation analysis showed a strong positive correlation between RI and the duration of hypertension (r=0.787, P=0.037). Similarly, SI also demonstrated a significant positive correlation with the duration of hypertension (r=0.754, P=0.041), indicating that both RI and SI values increase with prolonged hypertension duration (Table 4).

Table 1: Age distribution of study participants

Table 2: RI and SI values in study groups

Table 3: ANOVA analysis for RI and SI in study groups

Table 4: Pearson Correlation between RI and SI and Duration of HTN

In this study, we evaluated arterial stiffness indices, specifically the SI and RI, using DVP measurements in both normotensive and hypertensive individuals. The RI assesses the vascular tone of small arteries, while the SI gauges the stiffness of large arteries. Our findings reveal a significant increase in SI and RI values among hypertensive subjects compared to normotensive subjects, consistent with previous research [8]. This rise in arterial stiffness indices in hypertensive individuals may be attributed to reduced arterial elasticity [10], caused by sclerotic changes and endothelial dysfunction. Grey et al. reported that endothelial dysfunction leads to decreased small artery elasticity, which is linked to cardiovascular events [11]. Persistent elevated BP induces sclerotic changes in the vessel walls, resulting in thicker arterial walls. As arteries become more rigid, pulse wave velocity increases, reducing pulse transit time (PTT) and thus increasing SI. In hypertensive patients, the magnitude of the diastolic peak also rises, elevating RI. Nichols' study on PWV measurements indicated that arterial waveforms provide valuable information on arterial stiffness [12]. Brillante et al. demonstrated that digital photoplethysmography is a simple method for measuring arterial stiffness, with BP being a significant influencing factor [13]. Chen et al. found that in untreated hypertensive individuals, SI was independently associated with vascular diseases [14]. Gunarathne et al. concluded that SI is a superior discriminator for cardiovascular disease (CVD) risk stratification compared to traditional risk factors such as total cholesterol, plasma glucose, systolic pressure, and waist-hip ratio [15].

Age-related changes in arterial stiffness have been documented in both healthy and hypertensive individuals. These changes may be due to the fragmentation of elastin fibers. Aging effects vary between elastic and muscular arteries, with central arteries becoming stiffer with age, while muscular arteries exhibit less stiffness. In our study, the control group was younger than the hypertensive groups, though age differences within the hypertensive groups were minimal [16].

The choice of antihypertensive drugs also influences arterial stiffness. ACE inhibitors, angiotensin II receptor blockers, aldosterone receptor antagonists, and calcium channel blockers have more favorable effects on arterial elasticity compared to beta blockers. Although BP reduction is immediate with treatment, reversing vascular changes due to elevated pressure takes longer. Increased arterial stiffness raises myocardial workload and ischemia, elevating cardiovascular risk. The proposed mechanism for increased arterial stiffness with elevated BP may involve higher angiotensin II levels, which induce collagen cross-link formation in the extracellular matrix, contributing to vascular stiffening. Hence, hypertension treatment should also aim to reduce arterial stiffness [17-21].

This study did not account for the antihypertensive medications used by subjects, which could influence vascular stiffness indices.

The study underscores the significance of assessing arterial stiffness in hypertensive individuals using the straightforward, non-invasive DVP method. Regular monitoring of vascular damage through this measure is crucial. Hypertensive patients exhibiting elevated stiffness indices should be considered for early interventional procedures to avert vascular complications.

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