Arterial Stiffness Assessed By Pulse Wave Velocity as a Predictor of Cardiovascular Risk Factors in Cancer Patients

Abstract

Background:

Cancer patients are at increased risk of coronary artery disease. Vascular dysfunction is first reflected as arterial stiffness, which can be assessed by pulse wave velocity (PWV).

Aim:

This study aims to appraise whether PWV is a clinical indicator of arterial stiffness.

Materials and Methods:

A case-control observational study was undertaken in a tertiary teaching hospital among 589 participants, including 197 cancer patients undergoing treatment and 392 age-matched controls. Arterial stiffness and hemodynamic parameters were measured noninvasively using the Diabetes Risk Profiler system based on PeriScope^® technology. Statistical analysis included comparison of means, correlation analysis, and multiple linear regression.

Results:

Cancer patients showed significantly higher heart rate, systolic and diastolic blood pressure, pulse pressure, brachial-ankle PWV, carotid-femoral PWV, aortic pulse pressure, augmentation pressure, and augmentation index than controls, while ankle-brachial index was significantly lower (all P < 0.001). In cancer patients, PWV showed strong positive correlations with age and systolic blood pressure.

Conclusion:

Cancer patients undergoing treatment have markedly increased arterial stiffness and altered vascular function compared with controls. PWV may be a useful, simple, and noninvasive marker for early cardiovascular risk assessment in cardio-oncology practice.

Introduction

Advances in cancer screening, diagnosis, and treatment have significantly improved survival among patients with malignancies, shifting attention toward long-term complications of survivorship. Among these, cardiovascular disease has emerged as a leading noncancer cause of morbidity and mortality, highlighting the growing importance of cardio-oncology.[1,2,3]

Cancer and cardiovascular disease are closely interconnected through shared risk factors such as ageing, obesity, diabetes, smoking, and chronic inflammation.[4] Beyond these common factors, malignancy itself and anticancer therapies can directly contribute to vascular injury through mechanisms including oxidative stress, endothelial dysfunction, fibrosis, thrombosis, and inflammation.[5] These processes may promote early vascular damage, even before clinically overt cardiovascular disease develops.

Arterial stiffness is a well-recognized marker of vascular ageing and a strong predictor of adverse cardiovascular outcomes.[6] Pulse wave velocity (PWV), a widely accepted noninvasive measure of arterial stiffness, provides a simple, reproducible, and clinically relevant assessment of vascular health.[7]

Emerging evidence indicates that arterial stiffness may be increased in cancer patients due to the combined influence of traditional cardiovascular risk factors, cancer-related systemic effects, and treatment-induced vascular injury.[8,9,10,11,12] However, the extent of these alterations and their relationship with cardiovascular risk factors remains insufficiently characterized, particularly in comparison with noncancer populations.

Therefore, the present study was undertaken to evaluate whether PWV can serve as a clinical indicator of arterial stiffness in cancer patients by determining PWV parameters, comparing these parameters between cancer patients and age-matched controls, and examining their association with cardiovascular risk factors.

Materials and Methods

Study design and setting

This hospital-based case–control observational study was conducted at a tertiary care teaching hospital (RLJH RC, Kolar). Participants were recruited from the Surgical Oncology Department and the general outpatient department between April 25, 2024 and December 24, 2025.

Participants

A total of 589 adults (>18 years) were enrolled, comprising 197 cancer patients undergoing treatment (cases) and 392 age-matched controls. Participants with hypertension, diabetes mellitus, hyperlipidemia, smoking history, or unwillingness to participate were excluded. Sample size was calculated using OpenEpi Version 3.01, assuming a 2:1 control-to-case ratio, 90% confidence level, 80% power, and 10% non-response rate.

Data collection and measurements

The primary outcome was brachial–ankle PWV (baPWV). Secondary variables included carotid–femoral PWV, heart–brachial PWV, heart–ankle PWV, ankle–brachial index (ABI), central aortic pressures, augmentation pressure, and augmentation index. Demographic and clinical variables included age, BMI, heart rate, and blood pressure.

Data collection included sociodemographic characteristics, anthropometry, and cardiovascular measurements. Blood pressure was recorded after 5 min of rest, and the average of three readings was used. Arterial stiffness and hemodynamic parameters were assessed noninvasively using the Diabetes Risk Profiler based on PeriScope^® technology (Genesis Medical Systems Pvt. Ltd., India). Measurements were performed after 10 min of supine rest in a temperature-controlled environment, and the mean of two readings was used for analysis.

A total of 630 participants were assessed for eligibility. Forty-one participants were excluded due to hypertension (n = 12), diabetes mellitus (n = 19), and hyperlipidemia (n = 10). Finally, 589 participants (197 cases and 392 controls) were included in the analysis [Figure 1]. Selection bias was minimized through predefined eligibility criteria and age matching, while measurement bias was reduced through standardized procedures and validated equipment.

Figure 1.

Flow diagram showing participant recruitment and selection of study participants

Statistical analysis

Data were analyzed using IBM SPSS Statistics version 22.0 (IBM Corp., Armonk, NY, USA). Continuous variables were expressed as mean ± standard deviation. Between-group comparisons were performed using the independent t-test or Mann–Whitney U test, while categorical variables were analyzed using the Chi-square test. Correlation analysis was performed using Pearson or Spearman methods, and multiple linear regression analysis was conducted with carotid–femoral PWV as the dependent variable. P < 0.05 was considered statistically significant.

Ethical considerations

Ethical approval was obtained from the Institutional Ethics Committee (IEC No. SDUAHER/KLR/R and D/CEC/S/PG/1/2024-25, dated April 17, 2024. Written informed consent was obtained from all participants.

Results

A total of 589 participants were included in the study, comprising 197 cancer patients and 392 age-matched controls. Mean age did not differ significantly between groups (58.07 ± 9.41 vs. 58.01 ± 8.04 years; P = 0.933). Gender distribution was also comparable (P = 0.467). Cancer patients had significantly higher body weight and body mass index than controls (P < 0.001) [Table 1].

Table 1.

Baseline variables of study participants

Variable		Cancer (n=197), mean±SD		Control (n=392), mean±SD		t		P
Age (years)		58.07±9.41		58.01±8.04		0.08		0.933
Weight (kg)		65.49±11.40		57.79±8.42		8.41		<0.001
Height (cm)		162.94±9.08		164.04±9.70		−1.36		0.173
BMI (kg/m2)		24.58±3.22		21.38±1.61		13.13		<0.001
Heart–brachial distance (cm)		32.75±10.26		33.99±2.34		−1.67		0.096
Heart–ankle distance (cm)		104.61±3.09		112.03±6.55		−18.68		<0.001
Male gender - 247 (41.9%)		78 (39.6)		169 (43.1)		Chi-square test: χ2=0.53, df=1, P=0.467
Female gender - 342 (58.1%)		119 (60.4)		223 (56.9)

Continuous variables are expressed as mean±SD and were compared using the independent samples t-test. Categorical variables are presented as frequencies (percentages) and were analysed using the Chi-square test. Statistical significance was defined as a two-tailed P<0.05. SD: Standard deviation; BMI: Body mass index

Peripheral hemodynamic parameters, including heart rate, systolic blood pressure, diastolic blood pressure, and pulse pressure, were significantly higher in cancer patients than in controls (all P < 0.001) [Table 2].

Table 2.

Comparison of hemodynamic and arterial stiffness parameters between cancer patients and controls

Variable		Cancer (mean±SD)		Control (mean±SD)		t/u		df		P		95% CI (Mean difference)
Heart rate (bpm)		75.74±11.63		72.53±9.95		3.310		343.3		<0.001		1.30 to 5.11
SBP (mmHg)		127.46±13.63		114.30±10.09		12.006		307.1		<0.001		11.01 to 15.32
Diastolic BP (mmHg)		73.76±10.03		69.86±8.94		4.608		355.4		<0.001		2.23 to 5.56
Pulse pressure (mmHg)		53.69±16.23		44.45±12.99		6.951		325.5		<0.001		6.63 to 11.86
Average baPWV (cm/s)		1892.95±186.33		1389.56±92.06		35.79		245.19		<0.001		475.68 to 531.10
cfPWV (cm/s)		1235.20±183.45		809.24±96.53		30.534		251.9		<0.001		398.49 to 453.44
Heart–brachial PWV (cm/s)		18.58±1.80		13.63±0.92		36.348		248.9		<0.001		4.68 to 5.22
Heart–ankle PWV (cm/s)		18.99±1.79		13.94±0.92		37.210		249.5		<0.001		4.78 to 5.32
Average ABI		1.01±0.10		1.09±0.10		−9.16		392.78		<0.001		−0.097 to−0.063
Average brachial ASI		27.39±51.08		47.46±195.18		−1.61				0.108
Average ankle ASI		35.89±64.27		75.27±247.16		−1.27				0.205
Aortic systolic pressure (mmHg)		120.65±13.83		108.79±10.35		10.633		309.6		<0.001		9.67 to 14.06
Aortic diastolic pressure (mmHg)		69.60±10.11		66.42±8.99		3.742		354.6		<0.001		1.51 to 4.86
Aortic pulse pressure (mmHg)		51.07±16.28		42.39±13.20		6.491		328.9		<0.001		6.05 to 11.31
Aortic augmentation pressure (mmHg)		18.79±6.34		6.35±2.60		26.460				<0.001
Aortic augmentation index (%)		36.69±2.97		14.93±3.59		78.089		463.8		<0.001		21.22 to 22.31

Normality of all variables was calculated using the Kolmogorov–Smirnov test. Variables with P>0.05 were normally distributed and calculated with independent t-tests, whereas variables with P<0.05 were calculated with the Mann–Whitney U-test. BaPWV: Brachial–ankle pulse wave velocity; cfPWV: Carotid–femoral pulse wave velocity; PWV: Pulse wave velocity; ABI: Ankle–brachial index; ASI: Arterial Stiffness Index; SD: Standard deviation; CI: Confidence interval; SBP: Systolic BP; BP: Blood pressure

All PWV parameters, including baPWV, carotid–femoral PWV, heart–brachial PWV, and heart–ankle PWV, were significantly higher in cancer patients compared with controls (all P < 0.001). Cancer patients also demonstrated higher aortic systolic pressure, aortic pulse pressure, augmentation pressure, and augmentation index, whereas ABI was significantly lower (all P < 0.001) [Table 2]. The violin plot illustrates the distribution and density of carotid–femoral pulse wave velocity (cfPWV) values within each group, demonstrating a clear shift toward higher cfPWV values among cancer patients compared with controls [Figure 2].

Figure 2.

Distribution of carotid–femoral pulse wave velocity (cfPWV) in cancer patients and controls

Elevated baPWV (≥1400 cm/s) was observed in all cancer patients and in 49.0% of controls. Augmentation index ≥30% was present in 97.5% of cancer patients and absent in controls. ABI <0.9 was observed in 11.7% of cancer patients and in none of the controls (all P < 0.001).

Correlation analysis demonstrated positive associations between cfPWV and systolic blood pressure, pulse pressure, and body mass index in both groups, with stronger correlations observed among cancer patients [Table 3].

Table 3.

Direct comparison of carotid–femoral pulse wave velocity correlations with cardiovascular risk factors

Cardiovascular risk factor		cfPWV (r) – Controls (n=392)		cfPWV (r) – cancer patients (n=197)		Direction of association
Age		−0.017		0.742		Strong positive in cancer patients
SBP		0.708		0.775		Strong positive in both groups
Pulse pressure		0.610		0.614		Moderate positive in both groups
BMI		0.101		0.144		Weak positive in both groups

Values represent Pearson correlation coefficients (r) between cfPWV and cardiovascular risk factors in control participants and cancer patients. SBP: Systolic blood pressure; BMI: Body mass index; cfPWV: Carotid–femoral pulse wave velocity

Cancer status showed positive correlations with baPWV (r = 0.891), carotid–femoral PWV (r = 0.836), heart–brachial PWV (r = 0.877), heart–ankle PWV (r = 0.882), augmentation pressure (r = 0.812), and augmentation index (r = 0.950), and a negative correlation with ABI (r = −0.510) (all P < 0.001).

In multivariable regression analysis, age, body mass index, and systolic blood pressure remained independently associated with carotid–femoral PWV, whereas heart rate was not significant. The model demonstrated high explanatory power (R² = 0.842; adjusted R² = 0.839; P < 0.001).

Discussion

The present study demonstrates a significant increase in arterial stiffness among cancer patients compared with age-matched controls. Cancer patients showed markedly higher baPWV (1892.95 ± 186.33 vs. 1389.56 ± 92.06 cm/s) and carotid-femoral PWV (1235.20 ± 183.45 vs. 809.24 ± 96.53 cm/s), along with elevated central hemodynamic parameters, including aortic systolic pressure (120.65 ± 13.83 vs. 108.79 ± 10.35 mmHg) and augmentation index (36.69% ± 2.97% vs. 14.93% ± 3.59%) (all P < 0.001). In contrast, ABI was significantly lower in cancer patients (1.01 ± 0.10 vs. 1.09 ± 0.10).

A high burden of abnormal arterial stiffness was observed, with elevated baPWV (≥1400 cm/s) present in all cancer patients and augmentation index ≥30% in 97.5% of cases. PWV parameters showed strong positive correlations with age and systolic blood pressure. In the control group, the correlation between age and cfPWV was weak. This finding may be related to the relatively homogeneous age distribution of the control population and the exclusion of major cardiovascular risk factors, which could have reduced age-related variability in arterial stiffness measures. In multivariable analysis, age, body mass index, and systolic blood pressure remained independently associated with cfPWV, highlighting the contribution of both demographic and hemodynamic factors to arterial stiffness.

These findings indicate that cancer and its treatment are associated with substantial vascular dysfunction, as reflected by consistently elevated PWV indices and central hemodynamic parameters. The magnitude and consistency of these changes suggest clinically meaningful arterial stiffening in this population.

These observations are consistent with previous studies reporting increased arterial stiffness in cancer patients and following anticancer therapy[8,9,10,11,12] and support the concept of accelerated vascular ageing.[6]

Potential mechanisms include endothelial dysfunction, oxidative stress, inflammation, and fibrosis associated with malignancy and its treatment.[5] Although age was identified as an independent predictor, it does not fully account for the observed differences, indicating an additional contribution from cancer-related factors.

Despite excluding participants with known hypertension, diabetes mellitus, hyperlipidemia, and smoking history, cancer patients demonstrated higher blood pressure, BMI, cfPWV, and augmentation index values than controls. All measurements were obtained using a validated PeriScope^® system under standardized conditions with duplicate measurements and averaged values. The observed differences are biologically plausible and may reflect subclinical vascular dysfunction, treatment-related vascular injury, endothelial dysfunction, oxidative stress, inflammation, and accelerated vascular ageing. Nevertheless, residual confounding and selection-related factors inherent to observational studies cannot be completely excluded.[13]

Limitations

This study has certain limitations. The cross-sectional case–control design precludes causal inference. In addition, the cancer cohort included heterogeneous malignancies and treatment modalities, and stratified analyses could not be performed. Therefore, the findings should be interpreted with appropriate caution. Future studies should evaluate arterial stiffness according to specific cancer types and treatment modalities.

Conclusion

Cancer patients undergoing treatment demonstrated significantly higher PWV parameters compared with controls, confirming increased arterial stiffness. In addition, the strong positive association of PWV with age and systolic blood pressure in cancer patients supports its relevance as a marker of vascular dysfunction. Cancer patients undergoing treatment demonstrated significantly higher PWV parameters, indicating increased arterial stiffness. PWV may serve as a useful non-invasive marker of vascular dysfunction in this population; however, further longitudinal studies are needed to confirm its prognostic value.

Conflicts of interest

There are no conflicts of interest.

Funding Statement

This study was funded by the Department of Health Research (DHR), Government of India (Grant No: MDMS24JUN-0224). The funding agency had no role in study design, data collection, analysis, interpretation, or manuscript writing.