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 Table of Contents  
Year : 2020  |  Volume : 6  |  Issue : 1  |  Page : 33-39

Significance of aortic propagation velocity in patients with coronary artery disease – A novel echocardiographic parameter of atherosclerosis

Department of Cardiology, Osmania General Hospital, Hyderabad, Telangana, India

Date of Submission01-Dec-2019
Date of Decision21-Jan-2020
Date of Acceptance14-Feb-2020
Date of Web Publication17-Apr-2020

Correspondence Address:
Nagula Praveen
Department of Cardiology, First Floor, Quli Qutubshah Building, Osmania General Hospital, Afzalgunj, Hyderabad - 500 012, Telangana
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/jpcs.jpcs_76_19

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Background: Optimal risk stratification of patients with coronary artery disease (CAD) is of paramount importance to deliver appropriate care. As the age increases and with an increase in risk factors for CAD, the stiffness of the vascular system increases. The aortic propagation velocity (APV) may decrease with an increase in the stiffness and decrease in the strain and distensibility. Aim: To correlate the Aortic Propagation Velocity (APV) with the presence and severity of CAD. Subjects and Methods: Patients with diagnosis of Acute coronary syndrome (ACS) have been enrolled. APV, Aortic strain (AS) and aortic distensbility (AD) have been assessed in them. The correlation of the parameters with severity of CAD was assessed. Results: A total of 100 consecutive patients were studied. The patients were divided into two groups after coronary angiography (Group A – with CAD and Group B – normal coronaries). The male-to-female ratio in the whole cohort was 2.3:1. The mean age of presentation for Group A was 54 ± 10.8 years and for Group B was 51.1 ± 7.37 years (t = 1.56, P = 0.122). The AS, AD, and APV were significantly decreased in patients with CAD (P < 0.0001). There was significant decrease in APV as there is increase in syntax score (SS) (SS <22 [20] – 65.15 ± 9.25 vs. SS 22–32 [16] – 55.88 ± 10.14 vs. SS >32 [14] – 37.09 ± 8.02, respectively, P < 0.0001). On receiver operating characteristic curve analysis, the cutoff of APV for the prediction of CAD was 60 cm/sec (area under the curve: 0.813) with a sensitivity of 72.5% and specificity of 62%. Conclusion: APV is a reliable, simple echocardiographic parameter of aortic stiffness which is feasible for noninvasive cardiovascular risk stratification during the evaluation of CAD.

Keywords: Aortic distensibility, aortic propagation velocity, aortic strain, coronary artery disease

How to cite this article:
Vamsikrishna M, Naidu OA, Praveen N, Srinivas R, Reddy PK. Significance of aortic propagation velocity in patients with coronary artery disease – A novel echocardiographic parameter of atherosclerosis. J Pract Cardiovasc Sci 2020;6:33-9

How to cite this URL:
Vamsikrishna M, Naidu OA, Praveen N, Srinivas R, Reddy PK. Significance of aortic propagation velocity in patients with coronary artery disease – A novel echocardiographic parameter of atherosclerosis. J Pract Cardiovasc Sci [serial online] 2020 [cited 2022 Jan 29];6:33-9. Available from: https://www.j-pcs.org/text.asp?2020/6/1/33/282813

  Introduction Top

Coronary artery disease (CAD) and its result, myocardial infarction (MI), continue to be a significant cause of mortality and morbidity in the present era. Optimal risk stratification of patients with acute MI is of paramount importance to deliver appropriate care. Risk prediction is based on clinical, electrocardiography (ECG), two-dimensional echocardiography (2D ECHO) and biochemical parameters.

As the age increases and with an increase in risk factors for CAD, the stiffness of the vascular system increases. The aortic propagation velocity (APV) may decrease with an increase in the stiffness and decrease in the strain and distensibility.

Atherosclerosis is a chronic and multifactorial disease that affects the whole arterial system.[1] Atherosclerotic plaque begins early in life and grows slowly over decades. Evidence of some atherosclerosis is almost ubiquitous in the modern world, yet most plaque remains asymptomatic throughout the lifetime. Traditional risk factors and consequent chronic inflammation promote much of the development of atherosclerosis, although some patients have a systemic predisposition to plaque erosion that is independent of traditional risk factors. Plaque disruption exposes substances that promote platelet activation and aggregation. Ischemic heart disease is the leading cause of death globally. India has the highest burden of acute coronary syndrome (ACS) in the world due to the early occurrence of ischemic heart disease compared to counterparts around the world.[2],[3]

Vascular stiffness

The stability, resilience and compliance of the vascular wall are dependent on the relative contribution of its two prominent scaffolding proteins – collagen and elastin. The relative content of these molecules is normally held stable by a slow but dynamic process of production and degradation. Dysregulation of this balance, mainly by stimulation of an inflammatory milieu, leads to the overproduction of abnormal collagen and diminished quantities of normal elastin, which contribute to vascular stiffness. Increased luminal pressure, or hypertension, also stimulates excessive collagen production.[4]

In addition to structural changes, arterial stiffness is strongly affected by endothelial cell signaling and vascular smooth muscle cell tone.[5],[6],[7] Endothelial dysfunction is secondary to various factors such as the local imbalance between vasodilator nitric oxide and vasoconstrictors, increased expression of asymmetrical dimethylarginine, and activation of reactive oxygen species.

In patients with diabetes and metabolic syndrome, the cause of arterial stiffening seen across all age groups appears to be insulin resistance. It is positively correlated with central arterial stiffness. Chronic hyperglycemia and hyperinsulinemia increase the local activity of the renin–angiotensin–aldosterone system and expression of angiotensin type I receptor in vascular tissue, promoting the development of wall hypertrophy and fibrosis. Importantly, increased arterial stiffness in the metabolic syndrome is not the consequence of fully established diabetes but rather caused by subtle hormonal and metabolic abnormalities present from the very beginning of an insulin-resistant state.[8]

Arterial stiffening increases in patients with chronic renal insufficiency, and aortic pulse wave velocity (PWV), a marker of stiffening, is a strong independent predictor of mortality in this population. Arterial stiffening in renal disease involves several mechanisms. Intima–medial thickening increased extracellular matrix collagen content, increased age formation secondary to uremia, and increased osteoblast-like cells promoting calcification of the arterial walls which are some of the proposed mechanisms.[9]

Vascular stiffening results in widening of the arterial pulse pressure (PP), which can profoundly influence blood vessel and heart biology. In arteries, the impact is primarily related to changes to mechanical vascular stimulation caused by increased pulsatile shear and pressure.[10] Local regions near bifurcations have more turbulent flow and experience a higher amplitude of oscillatory shear stress with elevated stress, magnifying endothelial dysfunction, and vascular disease.

Clinical implications

Isolated systolic hypertension (defined as systolic blood pressure ≥140 and diastolic blood pressure <90 mm Hg) and elevated PP (PP is systolic blood pressure-diastolic blood pressure) are the two clinical manifestations of decreased vascular distensibility. Approximately 60% of people >65 years have isolated systolic hypertension. Unlike in young, isolated systolic hypertension, elevated PP, and increased PWV pose more significant risks for stroke, MIs, heart failure, and overall mortality in older adults. Elevation of peripheral vascular resistance combined with increased arterial stiffness in older subjects leads to the development of isolated systolic hypertension. It is reported that every 2-mmHg increase in systolic blood pressure increases the risk of fatal stroke by 7% and fatal coronary heart disease event by 5%.[11] Chronic elevation of mean blood pressure also leads to the thickening of the arterial wall, mostly in media.


The role of 2D ECHO in ischemic heart disease includes diagnosing, detecting complications, and assessing prognosis. Resting blood flow to the myocardium is preserved until coronary stenosis approaches 90% diameter narrowing. The easiest and most commonly identified abnormality is abnormal mitral valve inflow, with the reduction in E-wave velocity and an increase in A-wave velocity which occurs within seconds of total coronary occlusion. There will be loss of systolic thickening and decreased endocardial excursion in the region perfused by the obstructed coronary artery.

As the extension and severity of CAD increase, the distensibility and strain of the aorta decrease. Parameters such as aortic strain (AS), aortic distensibility (AD), PP, and augmentation index(AI), pulse wave propagation velocity in the detection of aortic stiffness were used in previous studies, and a relationship with CAD was detected.[12],[13],[14] Yildiz et al. showed a relation between the presence and severity of CAD and AS.[15] Güneş et al. described the APV and used it for the determination of the aortic stiffness.[16] In their study, the color M-mode-derived propagation velocity of the descending thoracic aorta (APV) was associated with coronary and carotid atherosclerosis and brachial endothelial function.

APV can be a simple, easy available novel echocardiographic parameter for the risk stratification in the evaluation of CAD. In this study of evaluation for the presence of CAD and aortic stiffness, APV is measured and compared with other conventional aortic stiffness parameters such as AS and AD.

Aims and objectives

  1. To assess the relationship between APV with the severity of lesion by syntax score (SS) in patients with CAD
  2. To compare APV in patients with and without CAD
  3. To compare AS and AD in patients with and without CAD.

  Patients and Methods Top

It is a hospital-based observational study done between June 2015 and December 2016.

Inclusion criteria

Patients with age >18 years and a diagnosis of ACS based on clinical features, ECG, and 2D ECHO were included in the study.

Exclusion criteria

Patients with moderate and severe valvular stenosis and/or regurgitation, cardiomyopathy, atrial fibrillation, atrial flutter, bundle branch blocks, congenital heart disease, symptomatic heart failure, and aortic aneurysm were excluded from the study.


One hundred consecutive patients of age >18 years presenting with chest pain and with a diagnosis of ACS were included in the study. The patients were divided into two groups. One group included patients with significant CAD defined as at least 50% stenosis in the epicardial coronaries (Group A) and the other group included patients with normal epicardial coronaries (Group B).

The ACS describes the range of myocardial ischemic states that includes unstable angina (UA), non-ST-elevated MI (NSTEMI), or ST elevated MI (STEMI).[17] UA is defined by the presence of ischemic symptoms without elevations in biomarkers and transient if any ECG changes.[18] The term MI is used when there is evidence of myocardial necrosis in the setting of acute myocardial ischemia.[19] STEMI is differentiated from NSTEMI by the presence of persistent ECG findings of ST-segment elevation.[20]

All patients underwent transthoracic echocardiographic examination by Philips iE33 2D ECHO device (Philips Medical Systems, Andover, MA, USA) with a 2.5–3.5 MHz transducer. Echocardiography was performed by an experienced echocardiographer who was blinded to the group of patients. The ejection fraction (EF) of the left ventricle was assessed by Simpson's method. The systolic and diastolic diameters of the ascending aorta were measured on M-mode, 3 cm above the aortic valve. The aortic systolic diameter was measured when the aortic valve was fully open, whereas the diastolic diameter was measured in relation to the peak of QRS on the electrocardiography gating. Five consecutive measurements were made and the average of the readings was calculated. After routine echocardiographic examination, color M-mode Doppler recordings were obtained with the cursor parallel to the main flow of direction in the descending aorta from the suprasternal window. The Nyquist limit was set at 30–50 cm/s. A flame-shaped M-mode spatiotemporal velocity map was displaced by switching to M-mode with the recorder sweep rate of 100 mm/s. Then, aliasing velocity was adjusted to get clear delineation of the velocity slope. The APV was calculated by the division of the distance by time of the propagation slope just by tracing the velocity slope. The mean of at least three consecutive measurements was recorded as the APV value. AS and AD were calculated from the echocardiographically derived aortic diameters and the clinical blood pressure. Aortic PP was calculated by subtracting diastolic aortic pressure from systolic aortic pressure. AS and AD were used as aortic elasticity parameters. The formulas used to calculate the above-mentioned parameters were as follows.[21]

Coronary angiography

Coronary angiography was performed through the femoral or radial artery using the standard technique. Significant CAD was defined as a >50% reduction of the internal diameter of epicardial coronary arteries and side branches with a diameter >1.5 mm. The SS was used to quantify the severity of CAD, low SS with the value of ≤22, intermediate as between 23 and 32, and high SS as ≥33.[22] Coronary angiography was performed in the catheterization laboratory (Siemens AXIOM-Artis [Siemens, Munich, Germany]), equipped with quantitative coronary analysis software.

Statistical analysis

All data were evaluated by the SPSS (Statistical Package for the Social Sciences for Windows, version 17.0, Chicago, IL, USA). Data were expressed as mean ± standard deviation (continuous variables) or number and percentages (categorical variables). A comparison of quantitative variables between the groups has been done using Student's t-test, and the Chi-square test has been applied for categorical variables. P ≤ 0.05 has been considered statistically significant to determine the association between variables. The correlation of the parameters was assessed with Pearson's® correlation test.

Ethical considerations

ECG and 2D ECHO are noninvasive tests. A coronary angiogram is an invasive study. The study protocol was approved by the institutional ethical committee. Written informed consent was obtained from all the patients after discussion of the study process with them. All patients gave consent for the study.

  Results Top

A total of 100 patients with a diagnosis of ACS were studied. After coronary angiography the patients were divided into two groups (Group A with significant CAD and Group B normal epicardial coronaries).

There was no significant difference in the mean age of presentation between the two groups (Group A 54 ± 10.8 years vs. Group B 51.1 ± 7.37 years, [t = 1.56, P = 0.122]) [Table 1]. A majority of patients were in the age group of 51–60 years (Group A 34% vs. Group B 46%). A study conducted by Sen et al. also showed that there were no significant differences between the ages of both the study groups.[23]
Table 1: Demographic and clinical characteristics of the study population

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The male-to-female ratio was 2.3: 1. In both the groups, there were more male with 66% and 74% constituting males in Groups A and B, respectively. The value of P was 0.383.

In the present study, it was observed that body mass index (BMI), urea, creatinine, total cholesterol, low-density lipoprotein (LDL) cholesterol, and triglycerides were significantly higher in Group A compared to Group B (P < 0.05). There was a statistically significant decrease observed in high-density lipoprotein (HDL) in Group A compared to Group B (P < 0.05) [Table 2].
Table 2: Comparison of body mass index and biochemical parameters between the two groups

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On comparison of the aortic stiffness parameters between the two groups, AS and distensibility and APV were significantly low in the CAD group (P < 0.0001), though there was no much difference in the aortic diameters between the two groups [Table 3]. The assessment of the aortic systolic and diastolic diameters in parasternal long axis view is shown in [Figure 1]. The color M mode picture of the APV in patient with normal coronaries and with CAD is shown in [Figure 2]. The APV among the two groups with bar diagram shown in [Figure 3].
Table 3: Aortic measurements, strain, distensibility, and propagation velocity between the two groups

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Figure 1: Measurements of the aortic dimensions in systole and diastole on M-mode at 100mm/sec speed 1: Systole, 2: Diastole.

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Figure 2: Aortic propagation velocity as measured on color M-mode in the aorta left: In a patient with normal coronaries, right: In a coronary artery disease patient.

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Figure 3: Bar diagram showing the aortic propagation velocity between the two groups.

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APV among the patients with CAD correlated inversely with the severity of CAD as assessed by the SS (r = −0.801, P < 0.0001) [Table 4].
Table 4: Comparison of the present study aortic propagation velocity and aortic stiffness with previous studies

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The ROC curve analysis of the APV showed that AUC was 0.813, and an APV cutoff value of 60 cm/sec predicted the presence of CAD with a sensitivity of 72.5% and specificity of 62% [Figure 4].
Figure 4: Receiver operating characteristic curve analysis of aortic propagation velocity cutoff value for predicting coronary artery disease.

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  Discussion Top

Aortic stiffness is associated with cardiovascular risk factors such as smoking, obesity, hypertension, glucose tolerance, diabetes, and older age.[26],[27],[28] As the extent and the severity of the atherosclerosis increase, AD and AS decrease. Atherosclerosis increases arterial wall thickness and the stiffness of the aorta.[27] As atherosclerosis progresses, tunica media increases in thickness and tunica media get stiffer.[29] Therefore, it is very valuable to detect atherosclerotic disease before its manifestations via a noninvasive method. Endothelial dysfunction is the first stage of atherosclerosis. The arterial resistance will increase as the arterial wall gets stiff and thick.[29] An increase in arterial resistance decreases the flow and APV. In our study, AS, AD, and APV were significantly lower in the CAD group compared to the non-CAD group.

Furthermore, our study showed that APV was statistically correlated with the other conventional aortic stiffness parameters, i.e., AS and AD. APV is one of the easiest echocardiographic parameters which correlates with significant CAD and aortic stiffness and distensibility. While aortic stiffness and AD are more correlated with conventional risk factors such as hypertension and increased age, APV correlates much with the extent of CAD and left ventricular dysfunction. As the severity of LV dysfunction increases, the APV decreases. It can be used for follow-up studies to see for the increment in APV as the systolic function of the patient improves following treatment with ACE inhibitors, beta-blockers, and antianginal therapies.

Demographic data

The male to female ratio was 2.3:1. In both groups males were more than females. A study conducted by Sen et al.[23] also showed that there were more male patients when compared to female patients. In their study, there were 25 and 26 male patients when compared to 18 and 24 females in CAD group and non-CAD groups, respectively.

Risk factors and aortic propagation velocity

In the present study, it was observed that there was a higher occurrence of diabetes in the study group compared to controls, but the increase was not statistically significant P > 0.05. BMI was higher in the study group when compared to the control group. Renal parameters were within the normal limits in both the groups but slightly higher in the study group. Patients with grossly elevated renal parameters with chronic kidney disease were excluded from the study. In the present study, it was observed that there was no statistically significant difference in the presence of hypertension between groups P > 0.05. Although there were more hypertensives in Group B (50%) when compared to GroupA (42%), the difference was not statistically significant. In a study conducted by Sen et al.,[23] hypertensives in CAD and the non-CAD group were not statistically significant (66.7% vs. 59.5%). In the study by Vasudeva Chetty et al.,[24] there were more hypertensive and smokers in the significant CAD group compared to nonsignificant and normal coronaries group (P = 0.008, P = 0.04 respectively). AD was lower in patients with hypertension, diabetes, smoking, and alcoholism, indicating that the vascular system responds to these risk factors resulting in increased stiffness leading to decreased distensibility. In their study also, the AD was significantly lower in patients with hypertension and diabetes.

Coming to the lipid parameters although the total cholesterol, LDL, and triglycerides were higher in the study group, there was no statistical difference between the two groups of patients. HDL was higher in the non-CAD group, but there was no statistical difference between the two groups. In a study by Sen et al.,[23] there was no statistically significant difference between the lipid parameters of two groups.

The best clinical utilization of APV would be in noninvasive cardiovascular risk stratification and management of patients and for a better selection of cardiovascular high-risk individuals. In the present study, it was shown that EF in patients with CAD was lower than when compared to patients with insignificant CAD. Multivessel disease involving significant lesions is more than a single vessel that is the double-vessel and triple-vessel diseases were more common in patients with CAD group. APV was much lower in patients with multivessel disease involving two and three coronary arteries.

The present study is compared to the previous studies in the literature in [Table 5].
Table 5: Comparison of aortic propagation velocity among Group A stratified according to the syntax score

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In the present study, we determined that the APV is significantly lower in the CAD group compared to the normal coronaries group. This was similar to previous studies [Table 5]. The findings support that the APV has a role in arterial stiffness and can be useful in predicting atherosclerotic events. It can be an early marker of asymptomatic patients. Major finding in this study was that there was a significant negative correlation of APV with SS (which has a greater agreement with the present guidelines in the management of CAD patients regarding revascularization), which was also used in Ghaderi et al.[25] and Vasudeva Chetty et al[24]; whereas Sen et al.[23] and Güneş et al.[16] could not show significant negative correlation and have used Gensini score. The number of patients in the present study is more than that of Ghaderi et al.[25] and Vasudeva Chetty et al.[24] The AS is less in CAD patients compared to non-CAD patients as was seen in the previous studies (Sen et al.,[23] Ghaderi et al.[25]). The more number of patients in the present study compared to the previous studies was more. It is the first study in the Indian population to correlating the AD and APV with SS in CAD patients.


The study was conducted in a small number of patients.

  1. This is not a follow-up study
  2. This is a single-center study
  3. The suprasternal images of some of the patients were not suitable enough to get a clear measurement of APV
  4. The sample size may not be large enough to generalize the results.

  Conclusion Top

APV, a novel non-invasive easily available echocardiographic marker, can be used in risk stratification of patients being evaluated for CAD. A decrease in APV, AS, and AD will indicate the presence of significant CAD.

Ethics clearance

Institutional Ethical Committee has approved for the conduct of the study.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

  References Top

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  [Figure 1], [Figure 2], [Figure 3], [Figure 4]

  [Table 1], [Table 2], [Table 3], [Table 4], [Table 5]


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