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ORIGINAL ARTICLE |
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Year : 2019 | Volume
: 21
| Issue : 2 | Page : 134-137 |
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Evaluation of carotid plaque vulnerability using shear-wave elastography: An observational comparative study
Rajeev Sivasankar1, Ramandeep Singh2, PI Hashim1, Brijesh Kumar Soni3, Rajneesh Kumar Patel4, Amit Bajpai1
1 Department of Radiodiagnosis, INHS Asvini, Colaba, Mumbai, Maharashtra, India 2 Department of Radiodiagnosis, Bombay Hospital, Mumbai, Maharashtra, India 3 Department of Radiodiagnosis, INHS Sanjivani, Kochi, Kerala, India 4 Department of Radiodiagnosis, INHS Kalyani, Vishakapatnam, Andhra Pradesh, India
Date of Submission | 29-Apr-2019 |
Date of Acceptance | 02-Jun-2019 |
Date of Web Publication | 07-Oct-2019 |
Correspondence Address: Dr. Rajeev Sivasankar Department of Radiodiagnosis, INHS Asvini, Next to RC Church, Colaba, Mumbai - 400 005, Maharashtra India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/jmms.jmms_31_19
Objectives: This prospective observational, comparative study was aimed at assessing our results of shear-wave elastography (SWE) in evaluating carotid plaque vulnerability. Subjects and Methods: Sixty patients were prospectively studied over 2 years in a tertiary hospital setting and divided into two groups of 30 each. The first group consisted of patients with atherosclerotic plaques with a history of stroke, whereas the second group consisted of 30 patients with atherosclerotic plaques without stroke. Carotid plaques in both groups were studied for plaque length, morphology, and SWE measurements. All data analysis was performed using SPSS software (version 22, IBM SPSS statistics). Results: Both groups showed no statistical difference with respect to comorbidities, addictions, or anthropometry. The internal carotid artery was involved in 24 (80%) and 13 (43.33%) patients in Groups A and B, respectively. Mean length and width of the plaque were more in Group A patients than that of Group B patients on both right and left sides. Proximal stiffness (kpa) was 32.27 and 42.86; mid stiffness was 32.92 and 45.77, while distal stiffness was 26.57 and 38.15 in Groups A and B, respectively. The proximal, mid, and distal stiffness values of the plaque in Group A were less on stroke side as compared to nonstroke side with a statistically significant difference. Conclusion: SWE is a noninvasive, reproducible, and reliable imaging technique which could be used as a tool for the early detection of vulnerable carotid artery plaques.
Keywords: Carotid, plaque, shear-wave elastography
How to cite this article: Sivasankar R, Singh R, Hashim P I, Soni BK, Patel RK, Bajpai A. Evaluation of carotid plaque vulnerability using shear-wave elastography: An observational comparative study. J Mar Med Soc 2019;21:134-7 |
How to cite this URL: Sivasankar R, Singh R, Hashim P I, Soni BK, Patel RK, Bajpai A. Evaluation of carotid plaque vulnerability using shear-wave elastography: An observational comparative study. J Mar Med Soc [serial online] 2019 [cited 2022 Jul 2];21:134-7. Available from: https://www.marinemedicalsociety.in/text.asp?2019/21/2/134/268619 |
Introduction | |  |
Cardiovascular diseases (CVDs) account for the maximum number of deaths worldwide contributing to over 17 million annual deaths according to the World Health Organization.[1] CVDs make up 48% of deaths caused by noncommunicable diseases, which is more than deaths due to cancer, respiratory disease, and diabetes put together. CVDs related to atherosclerosis include coronary artery disease, carotid artery disease, intracranial atherosclerotic disease, and peripheral arterial disease. The CVDs due to cerebrovascular disease account for approximately one-third of the cardiovascular deaths and are second to ischemic heart disease.[1] The development of atherosclerotic plaques may cause changes in the local mechanical properties of the vessel involved, thereby leading to the causation of stroke, which is a major outcome of atherosclerosis with high morbidity and mortality.[2],[3] Nearly 15%–20% of all strokes are caused due to carotid artery disease.[4] Current recommendations and guidelines for stroke management are based on the severity of stenosis to determine the need for surgical intervention.[5] However, it is also extremely important to recognize that small embolizations from atherosclerotic plaques may occur over multiple occasions, leading to numerous small infarcts and thereby causing cerebral atrophy. Various modalities that have been utilized to determine the instability of plaques include magnetic resonance imaging, computed tomography, ultrasonography (USG), and thermography.[5] Conventional high-frequency carotid USG has been widely used to quantify carotid plaques as a fast, inexpensive, and tolerable modality.[6]
Shear-wave elastography (SWE) is a relatively new application of USG and is used to assess the tissue elasticity. This, in turn, helps to differentiate diseased from normal tissue. Real-time SWE uses acoustic wave force for shear-wave propagation in tissues and enables the measurement of plaque stiffness by quantification of Young's modulus.[7] Although SWE has been used widely in various types of tissue, including the breast, liver, etc.; very few studies have considered its vascular applications. In order to validate and optimize the use of SWE in the clinical vascular setting, a considerable effort is required.[8] The present study was conducted with the aim of measuring carotid plaque stiffness using SWE and to discuss how stiffness measurements could be linked with plaque vulnerability to provide diagnostic information for stroke prediction and management.
Subjects and Methods | |  |
The study was an observational, prospective pilot study conducted over 2 years, from November 2016 to 2018. The study population included patients with stroke referred to the Department of Radiodiagnosis and other nonstroke patients with plaques found by screening in geriatric, cardiac, neurology, and oncology wards, fulfilling the inclusion and exclusion criteria. The study population comprised 60 patients with atherosclerotic plaques. These were divided into two groups. The first group (Group A) consisted of patients with atherosclerotic plaques with stroke, whereas the second group (Group B) patients with atherosclerotic plaques without stroke. Each of the groups contained 30 patients. Patients were included in the study if they met the following criteria: age group between 40 and 80 years, atherosclerotic plaque involvement was of the common carotid and/or internal carotid and/or external carotid artery/arteries, plaques had to be >1 cm in length and homogeneous on USG (hyper or hypoechoic). Exclusion criteria were patients with age <40 years and >80 years, plaques of length <1 cm, heterogeneous plaques, and critically ill patients requiring continuous monitoring or uncooperative patients.
The study was performed on a USG/Doppler machine Siemens Acuson S3000 and high-frequency linear array ultrasound probe 9L4. Patients were examined in the lying position, with the necks relaxed and turned away by 45° from the side being examined. SWE of the carotid artery plaques were measured at the proximal shoulder, peak middle site, and distal shoulder of the plaque [Figure 1]. | Figure 1: Measurement of carotid plaque for shear-wave elastography at proximal shoulder, mid peak, and distal shoulder
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Results | |  |
The mean age in Groups A and B was 67.16 and 59.33 years, respectively. Both groups had the maximum number of patients belonging to the seventh decade of life. There was a significant difference in both groups with respect to age (P = 0.03). The study population comprised 52 males (86.67%) and 8 females (13.33%) with no significant difference between the two groups in this regard (P = 0.78).
[Table 1] shows the distribution of anthropometric data in patients in both groups. No statistically significant difference between both groups with respect to weight, height, and body mass index was found on analysis with the Chi-square test (P > 0.05).
[Figure 2] shows the distribution of comorbidities distribution in both groups. Hypertension was present in 11 (36.67%) in the group of patients who had a stroke, whereas six (20%) patients were hypertensive in the group without stroke. There was no statistically significant difference between both groups with respect to comorbidities such as hypertension, diabetes mellitus, and dyslipidemia (P > 0.05).
[Table 2] shows the distribution of substance use in the two groups. The Chi-square test showed no statistically significant difference between both groups with respect to substance use such as smoking, tobacco use, and alcohol (P > 0.05).
[Table 3] shows the distribution of atherosclerotic plaques and their morphology. The internal carotid artery (ICA) was involved in 24 (80%) in the group of patients who had a stroke (Group A) and 13 (43.33%) patients in the group which did not have a stroke (Group B), respectively. The Chi-square test showed a statistically significant difference between both groups with respect to internal carotid involvement (P < 0.05). | Table 3: Distribution according to the site of carotid plaque among two groups*
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On the right side, the mean length of the plaque was 1.68 mm and 1.26 mm and the mean width of the plaque was 0.31 mm and 0.21 mm in Groups A and B, respectively. The length and width of the plaque were more in the group of patients who had a stroke versus the group that did not have a stroke with a statistically significant difference (P < 0.05). On the left side, the mean length of the plaque was 1.29 mm and 1.16 mm, and the mean width of the plaque was 0.22 mm and 0.21 mm in Groups A and B, respectively. The length of the plaque was more in the group of patients who had a stroke versus the group that did not have a stroke with a statistically significant difference (P < 0.05). Plaque dimensions in the group of patients that had suffered a stroke (Group A) and with bilateral plaques were as follows: mean plaque length was 1.82 mm and 1.21 mm on the left and right sides, respectively, mean plaque width was 0.22 mm and 0.22 mm on the left and right sides, respectively. The length of the plaque was more on the right side as compared to the left side with a statistically significant difference (P < 0.05). In the same group, the mean dimensions of the plaque on the stroke versus nonstroke side were as follows: the mean length was 1.60 mm and 1.42 mm on the stroke and nonstroke side, respectively, the mean plaque width was 0.23 mm and 0.22 mm on the stroke and nonstroke side, respectively, the mean plaque length was more on the side of the stroke as compared to the nonstroke side with a statistical significant difference (P < 0.05).
The mean stiffness values (kpa) on the right side in the two groups were as follows: proximal stiffness was 32.27 and 42.86 kpa, mid stiffness of the plaque was 32.92 and 45.77 kpa, and distal stiffness of the plaque was 26.57 and 38.15 kpa in Groups A and B, respectively. The proximal, mid, and distal stiffness values of the plaque were more in the group of patients who did not have a stroke (Group B) as compared to the group of patients who had a stroke (Group A) with a statistically significant difference when analyzed using the Chi-square test (P < 0.05) [Figure 3]. Mean plaque stiffness in Group A patients with bilateral plaques showed a proximal stiffness of 26 and 37.87 kpa on stroke and nonstroke side, respectively. Mid plaque stiffness was 24.05 and 42.67 kpa and the distal stiffness of the plaque was 24.01 and 43.97 kpa on stroke and nonstroke sides, respectively. The proximal, mid, and distal stiffness values of the plaque were less on the side on which the stroke had occurred as compared to the nonstroke side with a statistically significant difference (P < 0.05). | Figure 3: Comparison of plaque stiffness on the left and right sides in Group A
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Discussion | |  |
SWE is a relatively new application of USG and is used to assess the tissue elasticity. Information with respect to tissue elasticity and stiffness yielded by examination using this technique can be utilized in various pathologies to aid diagnoses as well as guide therapeutic decision-making in different patients.[9],[10],[11],[12],[13],[14],[15],[16],[17],[18],[19]
The present study showed homogeneity between both groups with respect to comorbidities such as hypertension, diabetes mellitus, and dyslipidemia, substance use, or anthropometric data.
The concept of the “vulnerable plaque” has always been of interest to researchers in order to try and predict which plaque would cause problems of clinical consequence.[20],[21],[22],[23],[24],[25] The present study showed ICA involvement by atherosclerotic plaque in 24 (80%) and 13 (43.33%) patients in Groups A and B, respectively, showing a significantly higher ICA involvement by atherosclerotic plaque in stroke patients. The results of the study also show that the length and width of the plaque burden were more in Group A patients on both sides with a statistically significant difference. This probably signifies that the more the plaque burden more is the risk of stroke.
Findings of plaque stiffness in the present study corroborate well with the findings of the study by Li et al. who assessed the stiffness of arteries in patients with acute ischemic stroke (AIS) with SWE and compared it to the control group, which showed that the patients with AIS had markedly higher intima-media thickness and pulse-wave velocity values (P < 0.05).[4] The elasticity modulus, MEmean, MEmax, and MESD were also greater in the AIS group (P < 0.05), which reveals markedly hardened and nonuniform arterial wall in the AIS group.[4] This again supports the fact that softer the plaques more are the chances of rupture, thereby leading to an ischemic stroke.
The proximal, mid, and distal stiffness values of the plaque were more on the left side as compared to the right side with a statistically significant difference (P < 0.05). This difference is likely due to the differences in hemodynamic stress suffered by both sides.
The present study shows that the statistically significant difference in the SWE characteristics of the carotid artery plaques in the stroke versus nonstroke group probably means that softer plaques are more vulnerable to embolize and thus lead to stroke. This would help treating physicians decide as to which patients should be candidates for aggressive medical management and also help select candidates for preemptive intervention to prevent the occurrence of ischemic events. Further, this modality could possibly be also used in future to assess the success of medical management by assessing temporal changes in plaque stiffness following optimization of medical management and control of risk factors.
The present study had several limitations. The study evaluated only homogeneous plaques, which is not always the case in the clinical scenario. This was done, as this was an initial pilot, observational study and due to the fact that there exist no normograms with regard to SWE plaque stiffness in the carotid arteries in the Indian population. Further, the sampling size to acquire SWE values within the region of interest, vary among various device manufacturers. This needs to be standardized for more consistent and reproducible results across various studies. In conclusion, SWE is a promising tool to evaluate the “stiffness” of plaques and can help guide management strategy in the management of stroke.
Conclusion | |  |
In conclusion, SWE is a promising tool to evaluate the “stiffness” of plaques and can help guide management strategy in the management of stroke. The modality possibly has potential in prognostication, by assessing temporal changes in plaque stiffness following optimization of medical management and control of risk factors.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
References | |  |
1. | World Health Organization. Fact Sheets about Stroke Manual. World Health Organization; 2013. p. 1-12. |
2. | Tatar IG, Kurt A, Hekimoglu B. Ultrasound elastography: A new era for vulnerable carotid plaque? J Cardiovasc Surg 2013;1:20-4. |
3. | Maurice RL, Soulez G, Giroux MF, Cloutier G. Noninvasive vascular elastography for carotid artery characterization on subjects without previous history of atherosclerosis. Med Phys 2008;35:3436-43. |
4. | Li Z, Du L, Wang F, Luo X. Assessment of the arterial stiffness in patients with acute ischemic stroke using longitudinal elasticity modulus measurements obtained with shear wave elastography. Med Ultrason 2016;18:182-9. |
5. | Ramnarine KV, Garrard JW, Dexter K, Nduwayo S, Panerai RB, Robinson TG. Shear wave elastography assessment of carotid plaque stiffness: In vitro reproducibility study. Ultrasound Med Biol 2014;40:200-9. |
6. | Lei Z, Qiang Y, Tianning P, Jie L. Quantitative assessment of carotid atherosclerotic plaque: Initial clinical results using shear wave TM elastography. Int J Clin Exp Med 2016;9:9347-55. |
7. | Ramnarine KV, Garrard JW, Kanber B, Nduwayo S, Hartshorne TC, Robinson TG. Shear wave elastography imaging of carotid plaques: Feasible, reproducible and of clinical potential. Cardiovasc Ultrasound 2014;12:49. |
8. | Widman E, Maksuti E, Larsson M. Shear Wave Elastography of the Arterial Wall-where we are Today. Lab on Cardiovascular Imaging and Dynamics. Department of Cardiovascular Sciences, KU, Leuven, Belgium; 2014. |
9. | Gennisson JL, Deffieux T, Fink M, Tanter M. Ultrasound elastography: Principles and techniques. Diagn Interv Imaging 2013;94:487-95. |
10. | Shiina T, Nightingale KR, Palmeri ML, Hall TJ, Bamber JC, Barr RG, et al. WFUMB guidelines and recommendations for clinical use of ultrasound elastography: Part 1: Basic principles and terminology. Ultrasound Med Biol 2015;41:1126-47. |
11. | Kamaya A, Machtaler S, Safari Sanjani S, Nikoozadeh A, Graham Sommer F, Pierre Khuri-Yakub BT, et al. New technologies in clinical ultrasound. Semin Roentgenol 2013;48:214-23. |
12. | Bamber J, Cosgrove D, Dietrich CF, Fromageau J, Bojunga J, Calliada F, et al. EFSUMB guidelines and recommendations on the clinical use of ultrasound elastography. Part 1: Basic principles and technology. Ultraschall Med 2013;34:169-84. |
13. | Tang A, Cloutier G, Szeverenyi NM, Sirlin CB. Ultrasound elastography and MR elastography for assessing liver fibrosis: Part 1, principles and techniques. AJR Am J Roentgenol 2015;205:22-32. |
14. | Bhatia KS, Lee YY, Yuen EH, Ahuja AT. Ultrasound elastography in the head and neck. Part I. Basic principles and practical aspects. Cancer Imaging 2013;13:253-9. |
15. | Choi YJ, Lee JH, Baek JH. Ultrasound elastography for evaluation of cervical lymph nodes. Ultrasonography 2015;34:157-64. |
16. | Nightingale K. Acoustic radiation force impulse (ARFI) imaging: A review. Curr Med Imaging Rev 2011;7:328-39. |
17. | Friedrich-Rust M, Nierhoff J, Lupsor M, Sporea I, Fierbinteanu-Braticevici C, Strobel D, et al. Performance of acoustic radiation force impulse imaging for the staging of liver fibrosis: A pooled meta-analysis. J Viral Hepat 2012;19:e212-9. |
18. | Cosgrove D, Piscaglia F, Bamber J, Bojunga J, Correas JM, Gilja OH, et al. EFSUMB guidelines and recommendations on the clinical use of ultrasound elastography. Part 2: Clinical applications. Ultraschall Med 2013;34:238-53. |
19. | Thim T, Hagensen MK, Bentzon JF, Falk E. Pathology of vulnerability caused by high-risk (vulnerable) arteries and plaque. In: Naghavi M, editor. Asymptomatic Atherosclerosis: Pathophysiology, Detection, and Treatment. New York: Springer; 2010. |
20. | Redgrave JN, Gallagher P, Lovett JK, Rothwell PM. Critical cap thickness and rupture in symptomatic carotid plaques: The oxford plaque study. Stroke 2008;39:1722-9. |
21. | Lutgens E, de Muinck ED, Kitslaar PJ, Tordoir JH, Wellens HJ, Daemen MJ. Biphasic pattern of cell turnover characterizes the progression from fatty streaks to ruptured human atherosclerotic plaques. Cardiovasc Res 1999;41:473-9. |
22. | Libby P. Inflammation in atherosclerosis. Nature 2002;420:868-74. |
23. | Feldman CL, Chatzizisis YS, Coskun AU, Koskinas C, Naghavi M, Stone PH. Vulnerable anatomy; the role of coronary anatomy and endothelial shear stress in the progression and vulnerability of coronary artery lesions: Is anatomy destiny? In: Naghavi M, editor. Asymptomatic Atherosclerosis: Pathophysiology, Detection, and Treatment. New York: Springer; 2010. |
24. | Wald NJ, Morris JK, Rish S. The efficacy of combining several risk factors as a screening test. J Med Screen 2005;12:197-201. |
25. | Naghavi M, Falk E, Hecht HS, Jamieson MJ, Kaul S, Berman D, et al. From vulnerable plaque to vulnerable patient – Part III: Executive summary of the screening for heart attack prevention and education (SHAPE) task force report. Am J Cardiol 2006;98:2H-15H. |
[Figure 1], [Figure 2], [Figure 3]
[Table 1], [Table 2], [Table 3]
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