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| CASE REPORT |
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| Year : 2022 | Volume
: 9
| Issue : 4 | Page : 585-587 |
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Extensive atherosclerosis associated with mobile thrombus in the left carotid bulb in an elderly
Shridhar Dwivedi, S Ashfaq, T Riyaz
Department of Cardiology, National Heart Institute, New Delhi, India
| Date of Submission | 07-Oct-2022 |
| Date of Acceptance | 10-Oct-2022 |
| Date of Web Publication | 29-Dec-2022 |
Correspondence Address:
Dr. Shridhar Dwivedi
Department of Cardiology, National Heart Institute, East of Kailash, New Delhi 110065, Delhi
India
 Source of Support: None, Conflict of Interest: None
DOI: 10.4103/mgmj.mgmj_189_22
A case of extensive atherosclerosis in an 88-year-old, chronic heavy smoker, associated with mobile thrombus in the left carotid bulb is presented. This patient also suffered from chronic obstructive pulmonary disease (COPD) and hypertension. He was fully worked up and confirmed as a case of the mobile thrombus attached to the plaque in the left carotid bulb by echocardiography and carotid Doppler. Thrombolysis of a large, mobile clot poses a theoretical risk of stroke worsening from incomplete fibrinolysis. He was prescribed anticoagulants and has been doing fine till the last follow-up. The importance of preventing premature atherosclerosis in the next generations is also discussed. We report this case to create awareness about this preventable malady and treatment options. Keywords: Aortic atherosclerosis, carotid Doppler, fibrinolysis, hypertension, mobile thrombus, thrombolysis
How to cite this article:
Dwivedi S, Ashfaq S, Riyaz T. Extensive atherosclerosis associated with mobile thrombus in the left carotid bulb in an elderly. MGM J Med Sci 2022;9:585-7 |
How to cite this URL:
Dwivedi S, Ashfaq S, Riyaz T. Extensive atherosclerosis associated with mobile thrombus in the left carotid bulb in an elderly. MGM J Med Sci [serial online] 2022 [cited 2023 Mar 28];9:585-7. Available from: http://www.mgmjms.com/text.asp?2022/9/4/585/365987 |
| Introduction | |  |
Chronic heavy smoking and dyslipidemia are often associated with accelerated atherosclerosis leading to plaque formation at various arterial sites causing intimal inflammation, necrosis, fibrosis, and calcification. After decades of relentless progression, such plaques may suddenly rupture and cause life-threatening coronary thrombosis leading to the acute coronary syndrome.[1] In the case of extensive atherosclerosis concomitant, athero-thrombosis may occur in carotid arteries together with the aorta. In such cases, the patient runs a dual risk of having a stroke and/or acute coronary syndrome. We report herewith an elderly who was a chronic heavy smoker and had extensive atherosclerosis and a mobile thrombus in the left carotid bulb along with coronary artery disease, hypertension (HTN), and chronic obstructive pulmonary disease (COPD). Echocardiography computed tomographic scan, and carotid doppler is of immense value in the workup of such cases.
| Case report | | |
An 88-year-old male belonging to a low socioeconomic strata came to the outpatient department with a history of chronic breathlessness and dry cough suggestive of COPD and HTN long. He was a chronic smoker who used to smoke 10–15 bidis per day since the age of 16 but reduced it to 5–6 bidis per day recently after being diagnosed with COPD. He also used to consume alcohol often. There was a history of dry cough. Of late he started having retrosternal chest pain which was atypical. As part of preventive work, we took a detailed family history and made a pedigree chart [Figure 1]. He picked up the habit of smoking from his father in early childhood but fortunately none of his grandchildren smoked. Curiously three of his offspring also suffer from HTN. Clinical examination was unremarkable except for occasional rhonchi in the bilateral chest. X-ray chest showed evidence of COPD and an electrocardiogram (ECG) revealed a right bundle branch block. He had no previous ECG with him. Carotid ultrasound showed thickened intima-media (IMT) in bilateral carotid arteries, the presence of bilateral plaques, and a mobile thrombus attached to the plaque in the left carotid bulb [Figure 2]. The presence of a calcified aorta was also ratified in echocardiographic examination [Figure 3]. Computed tomography chest showed a highly calcified aorta [Figure 4] He was investigated for evidence of thrombophilia. His homocysteine, protein C levels, and protein S levels were normal. His cholesterol (208 mg/dL) and low-density lipoprotein-cholesterol (136 mg/dL) levels were raised. Considering unstable plaques in the left carotid bulb and its proneness for stroke we advised immediate admission and anticoagulant therapy under supervision. However, he refused admission. We prognosticated him and prescribed aspirin, novel oral anticoagulants, heavy dose statin, conventional antianginals, and ace inhibitor immediately. He was also advised for quitting smoking immediately as it is a potent prothrombotic agent The patient was also given the option of carotid endarterectomy which he refused. He is doing well till the last follow-up.  | Figure 2: Large atherosclerotic plaque in left carotid bulb causing 80%–85% of luminal narrowing with mobile thrombus seen attached to the plaque
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 | Figure 4: Highly calcified arch and descending aorta is seen in computed tomography
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| Discussion | | |
Atherosclerotic plaque rupture is the leading cause of morbidity and mortality in developed nations. Plaques become relevant to a patient’s health when they destabilize and become vulnerable to rupture, leading to thromboembolic events. These plaques when situated in carotid arteries are significantly associated with transient ischemic attack and progressive stroke. Some workers have reported that the mobile attached plaques could disappear after anti-thrombotic therapy while other cases suggest that although giving anticoagulant therapy, the mobile plaque still progressed and led to the stroke. The internal carotid artery stands for the most prevalent site of thrombosis, in 75% of all cases.[2] An association between thrombus formation and excessive smoking with a history of HTN and COPD has been convincingly reported previously. Smoking is considered an important modifiable risk factor for the development of cardiovascular diseases such as coronary artery disease, stable angina, acute coronary syndromes, sudden death, stroke, peripheral vascular disease, congestive heart failure, erectile dysfunction, and aortic aneurysms via initiation and progression of atherosclerosis. Cigarette smoking induces oxidative stress, vascular inflammation, platelet coagulation, endothelial dysfunction, and impaired lipid profile in both current and chronic smokers. Further, active and passive smoking both result in detrimental effects on the cardiovascular system.[3] It needs no overemphasis that smoking is the major culprit behind such extensive atherosclerosis associated with a mobile large plaque. It is a matter of great relief that his children and grandchildren do not smoke and thus are less liable for such extensive atherosclerosis.[4] It is further said that carotid atherosclerosis is more prevalent in subjects with COPD. Subjects with COPD have a twofold risk of carotid wall thickening on ultrasonography. COPD being a systemic inflammatory disease, might also lead to the vulnerable plaque rupturing by inducing or aggravating the presence of a lipid core.[5]
| Conclusion | | |
Carotid arterial plaque associated with mobile thrombus is a risk factor for stroke as the thrombus can dislodge from the site and pass through the internal carotid artery to the middle cerebral artery and can cause cerebrovascular accidents. The diagnosis of such a case is confirmed by carotid ultrasonography. The thrombus can be treated by anticoagulant therapy or can be removed by carotid endarterectomy. This disease can be prevented and its ill effect minimized by quitting the habit of smoking and preventing inter-generational transmission of the smoking habit.
Ethical policy and institutional review board statement
The approval for this study was obtained after due discussion by the Scientific Advisory, Research and Ethics Committee of the All India Heart Foundation, New Delhi, India communicated vide letter of August 5, 2022.
Financial support and sponsorship
Not applicable.
Conflicts of interest
There are no conflicts of interest.
| References | | |
| 1. | Bentzon JF, Otsuka F, Virmani R, Falk E Mechanisms of plaque formation and rupture. Circ Res 2014;114:1852-66.  |
| 2. | Stewart J, Gover J, Tridgell D, Frawley J A mobile lesion in the carotid artery. Aust N Z J Surg 1996;66:639-41. |
| 3. | Siasos G, Tsigkou V, Kokkou E, Oikonomou E, Vavuranakis M, Vlachopoulos C, et al. Smoking and atherosclerosis: Mechanisms of disease and new therapeutic approaches. Curr Med Chem 2014;21:3936-48. |
| 4. | Dwivedi S, Pathak R, Agarwalla R, Ali W The intergenerational transmission of tobacco habit: Role of parents and the family. J Family Med Prim Care 2016;5:373-7. |
| 5. | Tuleta I, Farrag T, Busse L, Pizarro C, Schaefer C, Pingel S, et al. High prevalence of COPD in atherosclerosis patients. Int J Chron Obstruct Pulmon Dis 2017;12:3047–53. |
[Figure 1], [Figure 2], [Figure 3], [Figure 4]
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