The Evaluation Value of Non-Invasive Indices of Arterial Stiffness in the Early Stage of Coronary Artery Disease: Preliminary Results from an Exploratory Study
by
and
Fei Wang
1, 
Hui Zhang
1,
Kotaro Uchida
2,
Takuya Sugawara
2,
Shintaro Minegishi
2,
Hiroshi Doi
2,
Rie Nakashima-Sasaki
2,
Lin Chen
1,2,* and
Tomoaki Ishigami
2,* 
1
Department of Cardiology, Sir Run Run Hospital, Nanjing Medical University, Long Mian Avenue 109 Jiangning, Nanjing 211000, China
2
Department of Medical Science and Cardio-Renal Medicine, Yokohama City University, Graduate School of Medicine, 3-9 Fukuura, Kanazawa-ku, Yokohama 236-0027, Japan
*
Authors to whom correspondence should be addressed.
J. Vasc. Dis. 2024, 3(3), 278-289; https://doi.org/10.3390/jvd3030022
Submission received: 8 May 2024
/
Revised: 22 July 2024
/
Accepted: 5 August 2024
/
Published: 8 August 2024
(This article belongs to the Section Peripheral Vascular Diseases)
Abstract
:Background: Recently, the arterial velocity pulse index (AVI) and arterial pressure volume index (API) have been used to evaluate arterial stiffness and endothelial function. As arterial stiffness and endothelial injury are risk factors for coronary artery disease (CAD), these two indexes are therefore expected to predict and evaluate the future risk of CAD and cardiovascular events before clinical manifestations. Methods: A total of 90 consecutive patients with coronary angiography (CAG) were enrolled. After excluding normal patients and acute coronary syndrome patients, forty-seven patients with CAD and thirty-two patients with coronary atherosclerosis, and baseline characteristics data were collected. A multifunctional blood pressure monitoring device, AVE-1500 (Shisei Datum, Tokyo, Japan), was used to measure the AVI and API before CAG, and immediately and 2 h, 24 h, and 48 h after CAG and (or) PCI in all the selected participants. Results: After adjusting for various variables using stepwise multiple linear regression analyses, we found that the AVI in the CAD subjects was significantly higher than that in the coronary atherosclerosis subjects before CAG (p = 0.02), immediately after CAG/PCI (p = 0.01), and 48 h after CAG/PCI (p = 0.01), whereas the AVI decreased 24–48 h rather than immediately after CAG/PCI in the CAD group. Moreover, we also found that the API clearly changed in both groups during the periprocedural period of CAG (p = 0.01). Conclusions: In accordance with the results, we propose that the API and AVI may be useful for predicting the early stage of CAD and may be promising as indicators to assess the effect of early revascularization.
1. Introduction
Coronary artery disease (CAD) is one of the leading causes of mortality worldwide. It is a major public health epidemic that places an enormous burden on the population. With the development of society and the advancement of medicine, multiple factors likely have contributed to the decline of the incidence, morbidity, and mortality of CAD, including better control of risk factors, standardized drug treatment, and improvement of interventional therapy [1,2]. However, the total prevalence of obstructive (symptomatic and asymptomatic) CAD is unclear because lots of undiagnosed asymptomatic patients are ignored. An accurate determination of the prevalence of silent obstructive CAD would require coronary arteriography (CAG) or coronary angiography by computed tomography (CT) of a very large number of people of various ages without any clinical evidence of CAD. Such an investigation is impossible but would be highly useful, especially since the average age of CAD incidence is gradually becoming younger due to unhealthy dietary habits exacerbated by excessive social pressure [3]. It is well known that arterial stiffness and endothelial dysfunction are both evident in atherosclerosis before the development of cardiovascular events [4,5]. Therefore, an early diagnosis of subclinical atherosclerosis with less invasive clinical devices is of particular concern in public health.
Non-invasive vascular function tests for predicting atherosclerosis have shown valuable clinical prospects. Various devices have been extensively validated in various populations, such as pulse wave velocity (PWV) and carotid intima-media thickness (IMT), which have been shown to be associated with various cardiovascular risk factors and have been used to evaluate atherosclerosis [6,7,8]. However, their applications remain challenging and limited due to the requirement of technology expertise and complex equipment. The AVE-1500 (Shisei Datum, Tokyo, Japan) is a multifunctional blood pressure monitoring device used to non-invasively measure the new indexes arterial velocity pulse index (AVI) and arterial pressure volume index (API). These indices are measured using a cuff oscillometric technique developed to assess arterial stiffness and endothelial function. The AVI reflects the arterial stiffness of the central artery, and the API reflects the arterial stiffness of the peripheral artery [9,10].
It is known that the AVI and API are correlated with each other and cardiovascular outcomes [11,12,13]. Our own and other previous studies in healthy subjects have revealed that both indexes are significantly correlated with the brachial–ankle pulse wave velocity (baPWV) and the API was significantly correlated with the severity of CAD and complexity of the coronary artery [14]. These convenient and feasible indexes are therefore expected to be clinically useful for predicting and evaluating the future risk of atherosclerotic diseases. However, the clinical significance of these two indexes in the early stages of atherosclerosis and CAD is unknown. Therefore, in the present study, we aimed to evaluate the clinical significance of the AVI and API in patients with different degrees of coronary stenosis severity to explore the predictive ability of these two indexes for atherosclerosis in actual clinical settings.
2. Materials and Methods
2.1. Study Population
This research was a single-center observational cohort study. Ninety subjects aged 36 to 86 years, hospitalized in the Department of Cardiovascular Disease at Sir Run Run Hospital, Nanjing, Jiangsu, China were enrolled from August 2023 to October 2023. The patients with typical or clinically suspected CAD, such as chest tightness, chest pain, retrosternal discomfort, or palpitations, and those who were informed and consented to elective CAG were registered. After excluding the patients with normal coronary or coronary microvascular disease, and those with acute coronary syndrome (ACS), they were transferred to the catheterization laboratory to undergo an emergency cardiac catheterization and could not complete the study. Finally, 79 patients were included and assigned into two groups. The study protocol was registered and approved by the hospital’s ethical committee (ethical approval code: 2023-SR-022). The study protocol also complied with the requirements of the Helsinki Declaration of the World Medical Association and the International Ethics Guide for Human Biomedical Research of the Council for International Organizations of Medical Sciences. In addition, due to the non-invasive observational nature of the study design, we did not request additional informed consent from the participants. The purpose and procedures of this study were explained to the subjects.
Data for each subject’s general status, past medical history, results of blood tests and imaging tests, and concomitant medications were collected retrospectively from hospital electronic medical records. Chronic kidney disease (CKD) was defined as an estimated glomerular filtration rate (eGFR) of <60 mL/min. Chronic heart failure (CHF) was defined as a B-type natriuretic peptide (BNP) level of ≥40 pg/mL caused by CV disease. Hypertension was defined as an SBP of ≥140 mmHg, diastolic blood pressure (DBP) of ≥90 mmHg, or ongoing medical treatment for HT. Diabetes mellitus (DM) was defined as a blood glucose level ≥ 200 mg/dL (11.1 mmol/L), a hemoglobin A1c level ≥ 6.5%, or ongoing medical treatment for DM. Dyslipidemia was defined as a low-density lipoprotein (LDL) cholesterol level of ≥140 mg/dL (3.63 mmol/L), a triglyceride level of ≥150 mg/dL (1.69 mmol/L), a high-density lipoprotein (HDL) cholesterol level of ≤40 mg/dL (1.03 mmol/L), or ongoing medical treatment for DL [15]. Plasma glucose and triglyceride levels were measured by routine blood sampling without overnight fasting.
2.2. CAG
CAG was performed for each patient by an experienced cardiologist using the standard procedure via the right radial artery. CAD was diagnosed based on the existence of significant narrowing (≥50%) in any of the main coronary arteries, according to the coronary artery lesion classification of the European Society of Cardiology/European Association for Cardiothoracic Surgery [16,17,18]. The statistical population of this study was assigned into one of two groups: (1) CAD group and (2) non-CAD group. The CAD group was the population with definite vascular stenosis ≥ 50% and included patients who had previously undergone coronary artery stent or drug balloon implantation, while the non-CAD group was described as presenting coronary atherosclerosis, which coronary artery stenosis was confirmed by coronary angiography < 50% of the population. And for those patients with significant stenosis of the coronary arteries who required PCI treatment, after obtaining informed consent from the patients and or patients’ families, we performed PCI treatment.
2.3. AVI and API Measurement
Both the AVI and API were measured for each subject using the AVE-1500 multifunctional blood pressure monitoring device in the sitting position in a quiet and temperature-controlled room (24–26 °C). The measurement principles for the AVI and API have been previously described elsewhere [12,14]. The API and AVI were measured before CAG and immediately, 2 h, 24 h, and 48 h after the CAG and (or) PCI. The AVI, API, systolic blood pressure (SBP), diastolic blood pressure (DBP), and pulse rate (PR) were evaluated in a single measurement. Measurements were taken twice for each participant; the average was used for subsequent analyses.
2.4. Statistical Analysis
Descriptive data are presented as mean ± (standard deviation) or median (IQR). Statistical significance was inferred at p < 0.05. First, the Shapiro–Wilk test was used to test the normality of the AVI and API in each group. If all the data met the criteria for a normal distribution, the group t-test was used to compare the differences between the groups of AVI and API; otherwise, the Kruskal–Wallis test was used to test the differences between the groups. Variables with statistically significant differences between groups (p < 0.05) were included in a stepwise multifactor linear regression, and then variables with p < 0.05 in a univariate analysis were included in a multivariate analysis. The correlation between the AVI and API and the degree of coronary lesions (number of lesions and degree of stenosis) was analyzed by binary and multicategorical logistic regression. The Friedman rank sum test was used to analyze the difference in the AVI and API between the two groups during the periprocedural period. For variables with statistically significant differences between groups, the signed rank sum test was used for a dual comparison, and the FDR method was used to correct the multiple comparisons. The statistical analysis was performed using R version 4.1.3 (The R Foundation for Statistical Computing, Vienna, Austria).
3. Results
3.1. Baseline Characteristics
A total of 79 patients were included and assigned to the CAD group (n = 47) and the non-CAD group (n = 32), in the CAD group, 22 patients had a single-vessel lesion, 12 had a two-vessel lesion, and 13 had a three-vessel lesion, and a total of 19 patients underwent PCI treatment. The baseline characteristics of the patients in the different groups are shown in Table 1, Table 2 and Table 3. There were significant differences between the two groups in terms of sex (p = 0.046), age (p = 0.007), body mass index (BMI, p = 0.005), blood urea nitrogen (BUN, p = 0.028), creatinine (Cr, p = 0.007), glomerular filtration rate (eGFR, p = 0.004), and brain natriuretic peptide (BNP, p = 0.035), and, in addition, the use of ASA (aspirin, p = 0.001), P2Y12 receptor antagonist (p = 0.037), statins (p = 0.002), and beta-blockers (p = 0.023) also displayed significant differences with the number of coronary diseased vessels during the periprocedural period in the CAD group.
3.2. Comparison of AVI and API between Two Groups during the Periprocedural Period
In this study, we monitored the changes in the API and AVI during the periprocedural period of CAG and (or) PCI for the first time. Table 4 shows the comparison of the AVI and API between the two groups during the periprocedural period. The univariate analysis showed that the AVI in the CAD group was significantly higher than in the non-CAD group in the preprocedural period (p = 0.034), immediate postprocedural period (p = 0.003), and 48 h post-procedural (p < 0.001), but the API was only statistically significantly higher 2 h post-procedural (p = 0.019) in the CAD group.
In addition, after adjusting for confounders and variables with statistically significant differences in the univariate analysis by multivariate linear regression, there also were statistically significant differences between the preprocedural AVI (p = 0.02), immediately postprocedural AVI (p = 0.01), and 48 h postprocedural AVI (p = 0.01) in the different groups. However, the difference in the 2 h postprocedural API between the two groups could not be considered statistically significant (Figure 1 and Table 5).
3.3. Comparison of AVI and API at Different Time Points during the Periprocedural Period within Groups
In order to explore the role of the API and AVI in the evaluation of the revascularization efficacy, we analyzed the AVI and API during the periprocedural period within the groups. The results showed that in the CAD group, there was a statistically significant difference in the AVI at different time points (p = 0.031), but there was no difference seen in a pairwise comparison within the group. There was also a statistically significant difference in the API at different time points in the CAD group (p < 0.001). After adjusting the results using the FDR method, the results showed that the immediately postprocedural AVI was significantly higher than the 24 h postprocedural AVI (p = 0.034) and 48 h postprocedural AVI (p = 0.012); the preprocedural API was significantly higher than the 48 h postprocedural API (p = 0.045); the immediately postprocedural API was significantly higher than the 24 h postprocedural API (p = 0.003) and 48 h postprocedural API (p = 0.004); and the 2 h postprocedural API was significantly higher than the 24 h postprocedural API (p < 0.001) and 48 h postprocedural API (p = 0.003). Meanwhile, in the non-CAD group, there was a statistically significant difference in the API at different time points (p = 0.001); the immediate postprocedural measurement was significantly higher than the 24 h postprocedural measurement (p = 0.004). However, there was no significant difference in the AVI at different time points (p = 0.283). In addition, for the patients treated with PCI in the CAD group, there was a statistically significant difference in the AVI at different time points (p = 0.03); the immediately postprocedural AVI was significantly higher than the 48 h postprocedural AVI (p = 0.013). Whereas there was no significant difference in the API at different times in the PCI-treated subgroup (p = 0.077) (Table 6).
3.4. Correlations of API and AVI with the Severity of Coronary Atherosclerosis during the Periprocedural Period
In order to further clarify the relationship between the AVI and API and the number of diseased vessels and degree of stenosis, a multi-categorical logistic regression analysis was performed in the CAD group. The results showed that, compared with single-vessel lesions, the patients with double-vessel lesions had a higher 2 h postprocedural AVI (OR: 1.12, 95%CI: 1.01–1.25, p = 0.035) and 24 h postprocedural AVI (OR: 1.15, 95%CI: 1–1.32, p = 0.043). Meanwhile, the patients with triple-vessel lesions were also observed with a higher 2 h postprocedural AVI (OR: 1.12, 95%CI: 1–1.24, p = 0.042) (Table 7).
4. Discussion
In this study, we monitored the changes in API and AVI during the periprocedural period of CAG and (or) PCI between non-CAD and CAD patients for the first time and found that the AVI in the CAD subjects was significantly higher than the coronary atherosclerosis subjects before CAG and decreased after PCI. Moreover, the API was also changed in both groups during the periprocedural period. These data indicate that the API and AVI, as non-invasive markers of coronary atherosclerosis, may be useful for predicting the early stages of CAD, and as a preliminary evaluation of the efficacy of early revascularization.
The AVE-1500 can measure the BP and the two indexes (AVI and API) in a single procedure without requiring technology expertise and complex equipment. The device is a reproducible non-invasive method for assessing the stiffness of the arterial system [9,10,14]. The AVI is an index calculated from the characteristics of the pulse wave pattern under high cuff pressures exceeding the SBP. We found that the AVI in the CAD subjects was significantly higher than in the non-CAD subjects. Moreover, there were statistically significant differences in the preprocedural AVI, immediately postprocedural AVI, and 48 h postprocedural AVI. Our previous studies have shown that the AVI and API were significantly higher in patients with ≥75% arterial stenosis than in those with <75% arterial stenosis [13]. However, data were scarce for healthy participants and those with mild to moderate atherosclerosis. Therefore, in this study, we compared CAD and non-CAD subjects and found that the AVI was significantly correlated with the severity and complexity of coronary atherosclerosis. In addition, we found that there was no significant difference in the API between the non-CAD group and the CAD group. Although the API and AVI are correlated, this may be due to the pathophysiological implications of these two indexes being different. As analyzed and reported previously, the API is derived from the pressure–volume relationships of the brachial artery, representing the peripheral arterial stiffness, while the AVI is derived from waveform analyses, calculated from the pulse wave pattern of the brachial artery under suprasystolic pressure, reflecting the central arterial stiffness and cardiac afterload. Therefore, the AVI, and not the API, may more accurately estimate the coronary artery function and contribute to diagnosis in the early stage of CAD.
We first observed the change in the indexes before and after catheterization, which has not been examined in previous trials. The results showed that the API changed in both the non-CAD group and CAD group in the periprocedural period. At 24 h postprocedure, the API decreased compared with the immediately postprocedural API, particularly in the CAD group; the immediately postprocedural API was significantly higher than the 24 h postprocedural API and 48 h postprocedural API. Previous studies have demonstrated the influence of radial sheath insertion on the structure and function of the radial artery and indicated that transradial catheterization causes physical damage to the vascular endothelium [19,20,21]. It is well known that flow-mediated vasodilation (FMD) of the brachial artery (BA) represents one of the most widely accepted non-invasive standard methods for the assessment of endothelial dysfunction. Recently, Ellen A. Dawson et al. reported that there was a significant reduction in FMD in catheterized arms from before catheterization to the day after catheterization; the placement of a catheter sheath inside the radial artery disrupted vasodilator function, which recovered after 3 months [19]. Moreover, Christian Heiss et al. showed that transradial catheterization not only led to dysfunction of the radial artery but also the upstream brachial artery, which was more severe and sustained with increasing numbers of catheters. FMD was significantly decreased in the intervention arm at 6 h, and at 24 h, it recovered significantly but was still impaired in comparison with baseline values [22]. Our data are largely consistent with these findings. In our study, the immediate postprocedural API was significantly higher in the CAD group patients, which may be due to their treatment with a greater number of catheters and more complex procedures. It is known that the API is derived from the pressure–volume relationships of the brachial artery. Therefore, the values of the API were significantly correlated with peripheral arterial stiffness and endothelial function.
In this study, we also observed that the AVI changed before and after catheterization in the CAD group and found that the 24 h postprocedural AVI and 48 h postprocedural AVI were significantly lower than the immediately postprocedural AVI. However, the AVI was not significantly changed in the non-CAD group subjects. A previous study has shown that PCI with a stent implantation or drug balloon dilation could restore blood flow to the downstream myocardium [23]. In our CAD group, some subjects were subjected to coronary artery stenting or drug balloon dilation, which relieved the narrowing of the coronary artery vessels and caused the AVI to decline significantly 24 h and 48 h after the intervention procedures. In the sub-PCI group, the AVI also showed a downward trend 24 and 48 h after interventional therapy, but there was no statistical significance 24 h after therapy, which was considered to be related to the small sample size. In addition, we also found that double-vessel or triple-vessel lesions had a higher 2 h postprocedural AVI, which indicated that, compared with multi-vessel lesions, the vascular improvement of single-vessel patients is faster and more obvious in the short term after surgery. Therefore, these data indicated that the AVI may be promising as an indicator to evaluate coronary artery endothelial function after interventional therapy earlier and in a more convenient manner, and we could use it to assess the risk of early postoperative complications and the benefits of vascular reperfusion.
The present study has some potential limitations. First, the preliminary results from an exploratory study are detailed herein. Therefore, the number of patients in the present study was relatively small and the indexes may not have been sufficient to provide accurate cut-off points for different people. In addition, in this study, patients with acute coronary syndromes and healthy subjects with completely normal coronary arteries were excluded; to better reflect the average vascular endothelial status, a more comprehensive population should be monitored. Second, previous studies have shown that both the AVI and API effectively predicted major adverse cardiovascular events, hospitalization due to HF, and CV events. In addition, the follow-up time in our current study was not extensive enough to observe the long-term outcomes and prognosis of the patients after revascularization. Further studies with larger sample sizes and longer follow-ups are needed to confirm our results and to evaluate the values of the AVI and API to predict early and late risks in CAD patients with PCI and the efficacy of revascularization. Our results using the AVI and API will provide evidence for their use in preliminary interventions and treatments. Their use is an important method for recognizing high-risk patients. For patients with a clearly abnormal AVI and API, we are prompted to refine the current complex tests to reduce the missed diagnoses of occult coronary artery disease, especially in younger patients. At the same time, because the method used in this study is simple and non-invasive, it can be used widely in medical examinations.
5. Conclusions
The results of our study indicated that the API and AVI may be useful for predicting the early stages of CAD and may be promising as indicators for assessing the effect of early revascularization. Further studies are needed to establish the optimal clinical usage of these indexes.
Author Contributions
The conception or design of the work, T.I. and L.C.; the acquisition of data, F.W. and H.Z.; the analysis of data, L.C.; the interpretation of data, K.U., T.S., H.D. and R.N.-S.; Drafting the work, F.W. and L.C.; revising it critically for important intellectual content, S.M.; Final approval of the version to be published all of the authors. All authors have read and agreed to the published version of the manuscript.
Funding
This research was funded by the National Natural Science Foundation of China, grant number 81900388, the Nanjing Health Science and Technology Development Special Fund Project, grant number YKK20222, JSPS KAKENHI Grant Number JP22K16110 and Science and Technology Development Foundation of Nanjing Medical University, grant number NMUB20230259, Fujian Science and Technology Innovation Joint Fund Project, grant number 2023Y9248.
Institutional Review Board Statement
The study was conducted in accordance with the Declaration of Helsinki, and approved by the Ethics Committee of Sir Run Run Hospital (protocol code 2023-SR-022 and 31 July 2023).
Informed Consent Statement
Due to the non-invasive observational study design, we did not request additional informed consent from the participants. And the exemption from informed consent, were approved by the ethics committee of Sir Run Run Hospital (ethical approval code: 2023-SR-022 and 31 July 2023).
Data Availability Statement
The data that support the findings of this study are available from the corresponding author upon reasonable request. The data are not publicly available due to privacy regulations.
Conflicts of Interest
AVE-1500 was kindly lent to us by Shisei Datum, Tokyo, Japan.
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Figure 1.
The distribution and comparison of AVI and API measurement at different times between two groups. (A): After adjusting for confounders and variables with statistically significant differences in the univariate analysis by multivariate linear regression, there also were statistically significant differences between the preprocedural AVI, immediately postprocedural AVI, and 48 h postprocedural AVI in the two groups; (B): The univariate analysis showed that the API in the CAD group was significantly higher than in the non-CAD group in the 2 h postprocedure (p = 0.019), however, after adjusting for confounders and variables with statistically significant differences in the univariate analysis by multivariate linear regression, the difference in the 2 h postprocedural API between the two groups could not be considered statistically significant. * p < 0.05. CAD, coronary artery disease; AVI, arterial velocity pulse index; API, arterial pressure volume index.
Figure 1.
The distribution and comparison of AVI and API measurement at different times between two groups. (A): After adjusting for confounders and variables with statistically significant differences in the univariate analysis by multivariate linear regression, there also were statistically significant differences between the preprocedural AVI, immediately postprocedural AVI, and 48 h postprocedural AVI in the two groups; (B): The univariate analysis showed that the API in the CAD group was significantly higher than in the non-CAD group in the 2 h postprocedure (p = 0.019), however, after adjusting for confounders and variables with statistically significant differences in the univariate analysis by multivariate linear regression, the difference in the 2 h postprocedural API between the two groups could not be considered statistically significant. * p < 0.05. CAD, coronary artery disease; AVI, arterial velocity pulse index; API, arterial pressure volume index.
Table 1.
Baseline characteristics of the study population.
| Characteristics | Non-CAD n = 32 | CAD n = 47 | p Value |
|---|---|---|---|
| Sex, (female, %) | 19 (59.4) | 16 (34.0) | 0.046 |
| Age, mean (SD) | 57.34 (10.79) | 64.09 (10.45) | 0.007 |
| BMI, mean (SD) | 25.95 (3.84) | 23.82 (2.72) | 0.005 |
| Smoking (%) | 0.28 | ||
| No | 26 (81.2) | 33 (70.2) | |
| EX | 6 (18.8) | 11 (23.4) | |
| Current | 0 (0.0) | 3 (6.4) | |
| Alcohol consumption (%) | 0.441 | ||
| Never | 27 (84.4) | 36 (76.6) | |
| EX | 5 (15.6) | 9 (19.1) | |
| Current | 0 (0.0) | 2 (4.3) | |
| HR (bpm), mean (SD) | 75.50 (14.21) | 69.77 (12.80) | 0.065 |
| SBP (mmHg), median (IQR) | 132.00 (121.00, 141.50) | 131.00 (124.00, 147.50) | 0.61 |
| DBP (mmHg), median (IQR) | 80.00 (73.75, 91.00) | 80.00 (71.50, 89.50) | 0.484 |
| LVEF (%), median (IQR) | 63.00 (61.00, 65.00) | 62.00 (60.00, 64.00) | 0.107 |
CAD, coronary artery disease; BMI, body mass index; HR, heart rate; SBP, systolic blood pressure; DBP, diastolic blood pressure; LVEF, left ventricular ejection fraction (detected by the M-type method and Simpson’s method); Ex-smoking, completely stopped smoking for at least 6 months; Ex-alcohol consumption, completely stopped drinking for at least 6 months; Data are presented as mean ± (standard deviation) or median (IQR) or %. Significant p values are presented.
Table 2.
Serum Biochemical Parameters of the study population.
| Characteristics | Non-CAD n = 32 | CAD n = 47 | p Value |
|---|---|---|---|
| Glu (3.9–6.1; mmol/L), median (IQR) | 5.24 (4.62, 5.90) | 5.78 (5.34, 5.78) | 0.304 |
| Hb1Ac (4.0–6.0; %), median (IQR) | 6.10 (5.35, 6.20) | 6.10 (5.65, 6.50) | 0.208 |
| TC (≤5.18; mmol/L), mean (SD) | 4.26 (3.54, 4.83) | 4.15 (3.65, 4.70) | 0.818 |
| TG (≤1.7; mmol/L), median (IQR) | 1.64 (1.09, 2.53) | 1.47 (0.96, 2.55) | 0.529 |
| HDL-C (1.0–3.1; mmol/L), mean (SD) | 1.14 (0.96, 1.36) | 1.14 (0.90, 1.35) | 0.869 |
| LDL-C (≤3.37; mmol/L), mean (SD) | 2.36 (1.98, 2.87) | 2.48 (1.98, 3.06) | 0.664 |
| ALT (7–40; μ/L), median (IQR) | 19.00 (14.75, 28.25) | 16.00 (13.00, 22.00) | 0.12 |
| AST (13–35; μ/L), median (IQR) | 20.00 (17.00, 24.50) | 17.00 (14.00, 22.50) | 0.083 |
| γ-GGT (7–45; μ/L), median (IQR) | 25.00 (15.75, 50.50) | 22.00 (14.00, 28.87) | 0.219 |
| ALB (40–55; g/L), mean (SD) | 42.63 (3.20) | 42.86 (3.84) | 0.78 |
| Glob (20–40; g/L), mean (SD) | 25.26 (3.74) | 25.64 (3.33) | 0.634 |
| TBIL (≤21; μmol/L), median (IQR) | 10.40 (7.45, 15.95) | 9.70 (7.60, 11.05) | 0.281 |
| DBIL (≤8.0; μmol/L), median (IQR) | 4.15 (3.10, 5.65) | 3.80 (2.95, 4.50) | 0.263 |
| IBIL (3.4–17.0; μmol/L), median (IQR) | 6.45 (4.25, 8.95) | 5.70 (4.40, 7.15) | 0.393 |
| BUN (2.6–7.5; mmol/L), median (IQR) | 4.80 (4.18, 5.95) | 5.60 (4.85, 6.95) | 0.028 |
| Cr (41–73; μmol/L), median (IQR) | 59.00 (52.00, 67.75) | 68.00 (62.50, 82.00) | 0.007 |
| eGFR (mL/min/1.73 m2), median (IQR) | 107.99 (82.43, 124.77) | 87.52 (66.20, 102.61) | 0.004 |
| UA (155–357; μmol/L), mean (SD) | 327.41 (82.47) | 320.00 (83.97) | 0.699 |
| K (3.5–5.3; mmol/L), median (IQR) | 3.82 (3.68, 3.95) | 3.94 (3.68, 4.19) | 0.128 |
| Na (137–147; mmol/L), median (IQR) | 141.00 (140.00, 142.00) | 140.00 (139.00, 142.00) | 0.627 |
| Cl (99–110; mmol/L), median (IQR) | 105.00 (102.60, 105.95) | 104.70 (102.45, 106.95) | 0.964 |
| WBC (3.5–9.5; 109/L), median (IQR) | 5.66 (4.99, 6.20) | 5.84 (4.42, 6.99) | 0.78 |
| NEUT (40–75; %), mean (SD) | 59.30 (9.85) | 62.30 (11.19) | 0.224 |
| LYMPH (20–50; %), median (IQR) | 30.45 (24.65, 38.00) | 28.40 (22.10, 35.30) | 0.272 |
| EO (0.4–8.0; %), median (IQR) | 1.40 (0.95, 2.32) | 1.70 (1.05, 2.65) | 0.529 |
| RBC (3.8–5.1; 1012/L), mean (SD) | 4.28 (0.51) | 4.37 (0.45) | 0.421 |
| HGB (115–150; g/L), mean (SD) | 129.16 (15.18) | 128.62 (12.00) | 0.861 |
| CRP (0–10; mg/L), median (IQR) | 3.58 (0.80, 3.96) | 1.95 (0.80, 3.96) | 0.376 |
| BNP (0–100; pg/mL), median (IQR) | 65.81 (38.33, 65.81) | 82.30 (26.60, 93.96) | 0.035 |
CAD, coronary artery disease; GLU, glucose; HBA1C, glycated hemoglobin; TC, total cholesterol; TG, triglyceride; HDL-C, high-density lipoprotein; LDL-C, low-density lipoprotein; ALT, alanine aminotransferase; AST, aspartate aminotransferase; γ-GGT, gamma glutamyl transpeptidase; ALB, serum albumin; Glob, serum globulins; TBIL, serum total bilirubin; DBIL, direct bilirubin; IBIL, indirect bilirubin; BUN, blood urea nitrogen; Cr, creatinine; eGFR, glomerular filtration rate; UA, uric acid; K, potassium; Na, sodium; Cl, chloride; WBC, white blood cell; NEUT, neutrophil; LYMPH, lymphocyte; EO, eosinophil; RBC, red blood cell; HGB, hemoglobin; CRP, C-reactive protein; BNP, brain natriuretic peptide. Data are presented as mean ± (standard deviation) or median (IQR). Significant p values are presented.
Table 3.
Medical history and concomitant medications of the study population.
| Characteristics | Non-CAD n = 32 | CAD n = 47 | p Value |
|---|---|---|---|
| Medical history | |||
| CKD (%) | 0 (0.0) | 3 (6.4) | 0.391 |
| CHF (%) | 0 (0.0) | 2 (4.3) | 0.651 |
| Stroke (%) | 4 (12.5) | 8 (17.0) | 0.818 |
| Hypertension (%) | 17 (53.1) | 36 (76.6) | 0.053 |
| DM (%) | 2 (6.2) | 12 (25.5) | 0.057 |
| Dyslipidemia (%) | 3 (9.4) | 2 (4.3) | 0.655 |
| AF (%) | 4 (12.5) | 3 (6.4) | 0.592 |
| Medications | |||
| ASA (%) | 2 (6.2) | 20 (42.6) | 0.001 |
| P2Y12 receptor antagonist (%) | 2 (6.2) | 13 (27.7) | 0.037 |
| DOACs/VKA (%) | 1 (3.1) | 3 (6.4) | 0.9 |
| Statin (%) | 5 (15.6) | 25 (53.2) | 0.002 |
| ACEI/ARB/ARNI (%) | 8 (25.0) | 19 (40.4) | 0.239 |
| Beta-blocker (%) | 2 (6.2) | 14 (29.8) | 0.023 |
| CCB (%) | 11 (34.4) | 16 (34.0) | >0.999 |
| Diuretics (%) | 4 (12.5) | 10 (21.3) | 0.482 |
CAD, coronary artery disease; CKD, chronic kidney disease; CHF, chronic heart failure; DM, diabetes mellitus; AF, atrial fibrillation; ASA, aspirin; DOACs/VKA, direct oral anticoagulants/vitamin k antagonists; ACEI/ARB/ARNI, angiotensin-converting enzyme inhibitors/angiotensin receptor blockers/Angiotensin receptor enkephalase inhibitors; CCB, calcium channel entry blockers; Data are presented as %. Significant p values are presented.
Table 4.
Comparison of AVI and API between two groups during the periprocedural period.
| Time | Non-CAD n = 32 | CAD n = 47 | p Value | |
|---|---|---|---|---|
| AVI | before, median (IQR) | 20.00 (16.00, 26.50) | 25.00 (20.25, 31.00) | 0.034 |
| t0, median (IQR) | 19.00 (16.00, 27.25) | 25.00 (21.00, 32.50) | 0.003 | |
| t2h, median (IQR) | 23.00 (18.00, 27.25) | 24.00 (21.00, 29.25) | 0.172 | |
| t24h, mean (SD) | 21.71 (7.81) | 23.68 (6.18) | 0.215 | |
| t48h, median (IQR) | 19.71 (17.75, 20.25) | 23.33 (21.50, 25.50) | <0.001 | |
| API | before, mean (SD) | 25.61 (7.85) | 27.21 (8.07) | 0.385 |
| t0, median (IQR) | 26.00 (21.00, 32.25) | 27.00 (23.50, 33.75) | 0.322 | |
| t2h, median (IQR) | 23.00 (19.00, 26.50) | 28.00 (23.00, 33.50) | 0.019 | |
| t24h, median (IQR) | 22.25 (19.00, 26.25) | 25.24 (20.50, 29.50) | 0.148 | |
| t48h, median (IQR) | 25.19 (20.00, 25.89) | 25.02 (21.00, 26.00) | 0.574 |
CAD, coronary artery disease; AVI, arterial velocity pulse index; API, arterial pressure volume index; t0, immediately postprocedural; t2h, 2 h postprocedural; t24h, 24 h postprocedural; t48h, 48 h postprocedural; data are presented as mean ± (standard deviation) or median (IQR). Significant p values are presented.
Table 5.
Multivariate linear regression analysis of AVI and API at different times in two groups.
| Time | Beta | Std Error | T Value | p Value | |
|---|---|---|---|---|---|
| AVI | before | 4.47 | 1.80 | 2.48 | 0.02 |
| t0 | 4.51 | 1.73 | 2.61 | 0.01 | |
| t48h | 2.73 | 1.09 | 2.50 | 0.01 | |
| API | t2h | 0.92 | 1.36 | 0.67 | 0.50 |
AVI, arterial velocity pulse index; API, arterial pressure volume index; t0, immediately postprocedural; t2h, 2 h postprocedural; t48h, 48 h postprocedural. Significant p values are presented.
Table 6.
Comparison of AVI and API at different time points during the periprocedural period within groups (FDR).
Table 6.
Comparison of AVI and API at different time points during the periprocedural period within groups (FDR).
| Variables | Before Median (IQR) | t0 Median (IQR) | t2h Median (IQR) | t24h Median (IQR) | t48h Median (IQR) | Friedman Chi-Squared | p Value |
|---|---|---|---|---|---|---|---|
| CAD (n = 47) | |||||||
| AVI | 25 (20.25, 31) | 25 (21, 32.5) | 24 (21, 29.25) | 23 (19, 27) 2 | 23.33 (21.5, 25.5) 2 | 10.63 | 0.031 |
| API | 26 (20.5, 32.5) | 27 (23.5, 33.75) | 28 (23, 33.5) | 25.24 (20.5, 29.5) 2,3 | 25.02 (21, 26) 1,2,3 | 22.19 | <0.001 |
| non-CAD (n = 32) | |||||||
| AVI | 20 (16, 26.5) | 19 (16, 27.25) | 23 (18, 27.25) | 20.5 (16.75, 25) | 19.71 (17.75, 20.25) | 5.05 | 0.283 |
| API | 24 (19, 29) | 26 (21, 32.25) | 23 (19, 26.5) | 22.25 (19, 26.25) 2 | 25.19 (20, 25.89) | 18.04 | 0.001 |
| CAD (PCI-treated subgroup, n = 19) | |||||||
| AVI | 26 (21.25, 30.5) | 25 (22, 29.5) | 24 (22.25, 29.25) | 23 (19, 25.5) | 22 (19, 25) 2 | 10.68 | 0.03 |
| API | 29 (20, 33) | 28 (23.75, 31.75) | 25 (23, 33.5) | 24 (19.5, 32) | 25.02 (19.5, 28.5) | 8.43 | 0.077 |
CAD, coronary artery disease; PCI, percutaneous coronary intervention; AVI, arterial velocity pulse index; API, arterial pressure volume index; t0, immediately postoperative; t2h, 2 h postprocedural; t24h, 24 h postprocedural; t48h, 48 h postprocedural. 1: There was a statistically significant difference between the perioperative measured value and the preoperative measured value. 2: There was a statistically significant difference between the perioperative measured value and the immediately postprocedural measured value. 3: There was a statistically significant difference between the periprocedural measured value and the 2 h postprocedural measurement. Multiple comparisons were corrected using the FDR method. Significant p values are presented.
Table 7.
Correlations of API and AVI with the number of coronary diseased vessels during the periprocedural period in the CAD group.
Table 7.
Correlations of API and AVI with the number of coronary diseased vessels during the periprocedural period in the CAD group.
| Time | Two vs. One | Three vs. One | |||
|---|---|---|---|---|---|
| OR (95%CI) | p Value | OR (95%CI) | p Value | ||
| AVI | before | 1.08 (0.97, 1.19) | 0.165 | 0.99 (0.89, 1.09) | 0.787 |
| t0 | 1.09 (0.98, 1.21) | 0.095 | 1.08 (0.98, 1.19) | 0.144 | |
| t2h | 1.12 (1.01, 1.25) | 0.035 | 1.12 (1, 1.24) | 0.042 | |
| t24h | 1.15 (1, 1.32) | 0.043 | 1.14 (1, 1.31) | 0.05 | |
| t48h | 1.16 (0.95, 1.42) | 0.135 | 1.14 (0.94, 1.38) | 0.17 | |
| API | before | 1.06 (0.97, 1.17) | 0.18 | 0.96 (0.87, 1.06) | 0.419 |
| t0 | 1.07 (0.97, 1.18) | 0.206 | 0.96 (0.87, 1.07) | 0.486 | |
| t2h | 1.07 (0.97, 1.17) | 0.191 | 0.99 (0.9, 1.09) | 0.839 | |
| t24h | 1.01 (0.9, 1.13) | 0.875 | 0.94 (0.84, 1.05) | 0.29 | |
| t48h | 1.11 (0.98, 1.25) | 0.10 | 0.96 (0.84, 1.09) | 0.494 | |
AVI, arterial velocity pulse index; API, arterial pressure volume index; t0, immediately postprocedural; t2h, 2 h postprocedural; t24h, 24 h postprocedural; t48h, 48 h postprocedural. Significant p values are presented.
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MDPI and ACS Style
Wang, F.; Zhang, H.; Uchida, K.; Sugawara, T.; Minegishi, S.; Doi, H.; Nakashima-Sasaki, R.; Chen, L.; Ishigami, T. The Evaluation Value of Non-Invasive Indices of Arterial Stiffness in the Early Stage of Coronary Artery Disease: Preliminary Results from an Exploratory Study. J. Vasc. Dis. 2024, 3, 278-289. https://doi.org/10.3390/jvd3030022
AMA Style
Wang F, Zhang H, Uchida K, Sugawara T, Minegishi S, Doi H, Nakashima-Sasaki R, Chen L, Ishigami T. The Evaluation Value of Non-Invasive Indices of Arterial Stiffness in the Early Stage of Coronary Artery Disease: Preliminary Results from an Exploratory Study. Journal of Vascular Diseases. 2024; 3(3):278-289. https://doi.org/10.3390/jvd3030022
Chicago/Turabian StyleWang, Fei, Hui Zhang, Kotaro Uchida, Takuya Sugawara, Shintaro Minegishi, Hiroshi Doi, Rie Nakashima-Sasaki, Lin Chen, and Tomoaki Ishigami. 2024. "The Evaluation Value of Non-Invasive Indices of Arterial Stiffness in the Early Stage of Coronary Artery Disease: Preliminary Results from an Exploratory Study" Journal of Vascular Diseases 3, no. 3: 278-289. https://doi.org/10.3390/jvd3030022
