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Year : 2021  |  Volume : 22  |  Issue : 2  |  Page : 137-140  

Acute myocardial infarction attributed to coronary artery embolism in a patient with atrial fibrillation secondary to thyrotoxicosis - An underrecognized entity: A case report and literature review

1 Department of Cardiology, Heart Hospital, Hamad Medical Corporation, Doha, Qatar
2 Department of Internal Medicine, Hamad Medical Corporation, Doha, Qatar

Date of Submission23-Mar-2021
Date of Acceptance04-Jul-2021
Date of Web Publication19-Aug-2021

Correspondence Address:
Dr. Abdul Rahman Arabi
Department of Cardiology, Heart Hospital, Hamad Medical Corporation, Doha
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Source of Support: None, Conflict of Interest: None


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Nonatherosclerotic causes of acute myocardial infarction (MI) are infrequent, with atrial fibrillation as the most common etiology in cases of embolic MI. This entity, however, along with other causes of coronary embolus remains underappreciated as a probable cause of acute coronary syndromes.[1] Our case delineates a rare presentation of STEMI due to cardioembolic origin secondary to atrial fibrillation in a patient with thyrotoxicosis, previously undiagnosed to have an abnormal cardiac rhythm.

Keywords: Atrial fibrillation, coronary artery embolism, myocardial infarction, percutaneous coronary intervention, thyrotoxicosis

How to cite this article:
Abed H, Sardar S, Abdelghani MS, Abdullatef WK, Arabi AR. Acute myocardial infarction attributed to coronary artery embolism in a patient with atrial fibrillation secondary to thyrotoxicosis - An underrecognized entity: A case report and literature review. Heart Views 2021;22:137-40

How to cite this URL:
Abed H, Sardar S, Abdelghani MS, Abdullatef WK, Arabi AR. Acute myocardial infarction attributed to coronary artery embolism in a patient with atrial fibrillation secondary to thyrotoxicosis - An underrecognized entity: A case report and literature review. Heart Views [serial online] 2021 [cited 2023 Dec 5];22:137-40. Available from: https://www.heartviews.org/text.asp?2021/22/2/137/324104

   Introduction Top

ST-segment elevation myocardial infarction (STEMI) of nonatherosclerotic etiology is uncommon and in a few cases, emboli to coronary arteries may be seen due to left ventricular thrombus, atrial fibrillation, septic embolic owing to infective endocarditis, tumors, or patent foramen ovale, resulting in paradoxical embolism.[2]

A few case reports have documented nonatherosclerotic causes of acute MI attributed coronary artery embolism.[2],[3],[4],[5],[6],[7],[8],[9],[10],[11],[12],[13],[14] Our case elucidates the significance of early recognition of atrial fibrillation secondary to thyrotoxicosis as a cause of acute MI in a patient found to have a thrombus in the left atrial appendage, which has been previously reported as an alternative trigger site in the initiation of atrial fibrillation in some cases rather than the pulmonary veins.[15]

   Case Presentation Top

A 52-year-old man, known to have hypertension and dyslipidemia for 5 years, experienced acute chest pain radiating to his left arm and shoulder associated with nausea and sweating. He did not have any prior history of similar symptoms or cardiac disease. The ambulance electrocardiogram showed atrial fibrillation with ST-segment elevation in the inferior leads and reciprocal ST-segment depression in lateral leads [Figure 1]. The diagnosis of ST-segment elevation MI (STEMI) was confirmed, and he was loaded with 600 mg clopidogrel, 5000 units of IV heparin, and 300 mg of aspirin in the ambulance.
Figure 1: Initial electrocardiogram showing atrial fibrillation with ST-segment elevation in the inferior leads and reciprocal ST-segment depression in lateral leads

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Subsequently, upon hospital arrival, he was transported directly to the catheterization laboratory for percutaneous coronary intervention (PCI). Focused physical examination revealed a height of 174 cm and a weight of 78 kg. He was afebrile with blood pressure of 171/109 mmHg and had irregularly irregular pulse rate of 105 beats/min. Auscultation of the heart and lungs revealed no abnormalities.

Coronary angiography (CAG), performed through the right radial artery, revealed a normal dominant right coronary artery, and an abrupt occlusion of the distal LAD denoted as 100% with TIMI 0 [Figure 2]a. The intervention was performed, using a 6F Launcher EBU3.5, and a Runthrough NS 180 cm. Plain Balloon was performed, using a Maverick 2.75 mm × 15 mm compliant balloon. The inflation pressure was 6 ATM for the duration of 60.0 s. Following the intervention, there was a 60% residual stenosis. There was TIMI 0 flow before the procedure and TIMI 2 flow following the procedure [Figure 2]b.
Figure 2: (a) Thrombus in distal LAD causing abrupt occlusion of the vessel. (b) Distal LAD after POBA

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At this point, the clinical suspicion of coronary artery embolism as the cause of the STEMI was high. The angiographic appearance in conjunction with atrial fibrillation was highly suggestive. Heparin was given intravenously during the procedure and continued after as well. A rate-control strategy was initiated for the atrial fibrillation since the duration of the abnormal rhythm was unclear. Transthoracic echocardiography showed an ejection fraction of 33%, and the left atrium was severely dilated [Figure 3].
Figure 3: LV 2-chamber TTE showing severely dilated left atrium and ejection fraction of 33%

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During the same admission, transesophageal echocardiography revealed a definite thrombus in the left atrial appendage [Figure 4]. The patient was started on rivaroxaban 20 mg and clopidogrel 75 mg daily. Moreover, the laboratory investigations revealed a new diagnosis of hyperthyroidism with a TSH value of <0.01 mIU/L, FT4 of 34 pmol/L, and FT3 of 9 pmol/L.
Figure 4: (a) LV 4-chamber view on TEE. (b-d) TEE showing definite thrombus in left atrial appendage

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In liaison with endocrinology assessment, carbimazole 20 mg once daily was initiated. Thereafter, he was discharged home in good clinical condition.

   Discussion Top

Coronary artery embolism is known as a rare etiology of acute MI, while the accurate diagnosis presents as a challenge for interventional cardiologists, it is imperative to emphasize the possibility of nonatherosclerotic cause of MI, especially in patients lacking evidence of atherosclerotic coronary disease on CAG. Atrial fibrillation is the most common underlying etiology in acute MI attributed to coronary embolism, followed by cardiomyopathy and valvular heart disease.[16] Coronary embolism may be suspected based on the National Cerebral and Cardiovascular Center clinical criteria for the diagnosis of coronary artery embolism as proposed by Shibata et al.[16]

As nonatherosclerotic etiology of acute MI remains challenging to diagnose in acute clinical setting, its exact prevalence remains unclear. One study reported the absence of atherosclerotic coronary disease on CAG or autopsy findings in 4%–7% of patients with acute MI,[17] while another study documented coronary artery embolic infarcts in 13% of patients upon autopsy.[18]

After direct current cardioversion of atrial fibrillation, the prevalence of thromboembolic events is 2.0%,[19] of which most thromboembolic events present within 3 days postcardioversion.[20] Patients with diabetes and heart failure have a greater prevalence of 9.8% of thromboembolic events after cardioversion of atrial fibrillation.[21]

In another retrospective study of patients with acute MI, the prevalence of coronary artery embolism was 2.9%, of which 73% were attributed to atrial fibrillation. Nonvalvular atrial fibrillation accounted for 58% of patients with AF-induced coronary artery embolism.[16]

The incidence of arterial embolism in patients with thyrotoxicosis and atrial fibrillation is alarming. In the study of patients with thyrotoxicosis and atrial fibrillation, Staffurth et al. reported 8% of patients (21 out of 262) with 26 episodes of arterial embolism and 11 patients with concurrent atrial fibrillation and hyperthyroidism had embolic events.[22] Yuen et al. identified 24% of thyrotoxic patients with systemic embolism in the hyperthyroid state.[23] Hurley et al. described arterial embolism in eight patients out of 381 cases of thyrotoxicosis.[24] Owing to the increasing incidence of thromboembolic complications in patients with thyrotoxic atrial fibrillation, the ACC/AHA recommends anticoagulation therapy in these cases.[25]

It must be noted that the thyroid status of the patients affects the anticoagulative effect of warfarin. Hyperthyroidism with elevated levels of thyroid hormone increases the anticoagulative effect while the patients on antithyroid agents such as methimazole or propylthiouracil may experience diminished anticoagulative effect. Therefore, these patients with thyrotoxic atrial fibrillation must be monitored closely to ensure INR within recommended range.[24]

Initial studies reported a higher prevalence of rheumatic valvular disease[18] and bacterial endocarditis[26] in patients with acute MI attributed to coronary artery embolism. The prevalence of rheumatic valvular heart disease and bacterial endocarditis as an underlying etiology of coronary artery embolism has decreased, likely due to the advancements in primary PCI and the use of thrombectomy devices over the past three decades.

Aging results in a significant increase in the prevalence of atrial fibrillation, approximately 4% in those in their seventies, and 10% in individuals older than 80 years of age.[27]

The 5-year recurrence rate for thromboembolism including coronary artery embolism after the primary event of coronary embolism was 8.7%, with 35 months of median time until recurrence.[16]

   Conclusion Top

Our case emphasizes the importance of early recognition of acute MI due to coronary artery embolism in a patient with atrial fibrillation secondary to thyrotoxicosis. As these cases seldom appear in clinical practice, physicians must be vigilant to timely identify this underrecognized entity as a cause of acute MI due to coronary embolism, especially in patients without angiographic evidence of atherosclerotic involvement.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

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Conflicts of interest

There are no conflicts of interest.

   References Top

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Camaro C, Aengevaeren WR. Acute myocardial infarction due to coronary artery embolism in a patient with atrial fibrillation. Neth Heart J 2009;17:297-9.  Back to cited text no. 2
Nuqali A, Shafiq Q, Syed MM, Sheikh M. A suspected case of acute embolic myocardial infarction following direct-current cardioversion of atrial fibrillation. Am J Case Rep 2018;19:1306-10.  Back to cited text no. 3
Jiao ZY, Zhang DP, Xia K, Wang LF, Yang XC. Clinical analysis of acute myocardial infarction caused by coronary embolism. J Thorac Dis 2017;9:2898-903.  Back to cited text no. 4
Sinha SK, Jha MJ, Razi M, Chaturvedi V, Erappa YB, Singh S, et al. Acute myocardial infarction due to coronary artery embolism in a 22-year-old woman with mitral stenosis with atrial fibrillation under warfarinization: Successful management with anticoagulation. Am J Case Rep 2017;18:361.  Back to cited text no. 5
Daoud H, Abugroun A, Erramilli S, Kumar S. Acute coronary syndrome (ACS) due to coronary artery embolism in a patient with atrial fibrillation. Case Rep Cardiol 2019;2019:9347198.  Back to cited text no. 6
Van de Walle S, Dujardin K. A case of coronary embolism in a patient with paroxysmal atrial fibrillation receiving tamoxifen. Int J Cardiol 2007;123:66-8.  Back to cited text no. 7
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Hernández F, Pombo M, Dalmau R, Andreu J, Alonso M, Albarrán A, et al. Acute coronary embolism: Angiographic diagnosis and treatment with primary angioplasty. Catheter Cardiovasc Interv 2002;55:491-4.  Back to cited text no. 10
Taniike M, Nishino M, Egami Y, Kondo I, Shutta R, Tanaka K, et al. Acute myocardial infarction caused by a septic coronary embolism diagnosed and treated with a thrombectomy catheter. Heart 2005;91:91:e34.  Back to cited text no. 11
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Di Biase L, Burkhardt JD, Mohanty P, Sanchez J, Mohanty S, Horton R, et al. Left atrial appendage: An underrecognized trigger site of atrial fibrillation. Circulation 2010;122:109-18.  Back to cited text no. 15
Shibata T, Kawakami S, Noguchi T, Tanaka T, Asaumi Y, Kanaya T, et al. Prevalence, clinical features, and prognosis of acute myocardial infarction attributable to coronary artery embolism. Circulation 2015;132:241-50.  Back to cited text no. 16
Waller BF. Atherosclerotic and nonatherosclerotic coronary artery factors in acute myocardial infarction. Cardiovasc Clin 1989;20:29-104.  Back to cited text no. 17
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Gallagher MM, Hennessy BJ, Edvardsson N, Hart CM, Shannon MS, Obel OA, et al. Embolic complications of direct current cardioversion of atrial arrhythmias: Association with low intensity of anticoagulation at the time of cardioversion. J Am Coll Cardiol 2002;40:926-33.  Back to cited text no. 20
Airaksinen KE, Grönberg T, Nuotio I, Nikkinen M, Ylitalo A, Biancari F, et al. Thromboembolic complications after cardioversion of acute atrial fibrillation: The FinCV (Finnish CardioVersion) study. J Am Coll Cardiol 2013;62:1187-92.  Back to cited text no. 21
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Hurley DM, Hunter AN, Hewett MJ, Stockigt JR. Atrial fibrillation and arterial embolism in hyperthyroidism. Aust N Z J Med 1981;11:391-3.  Back to cited text no. 23
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Staffurth JS, Gibberd MC, Fui SN. Arterial embolism in thyrotoxicosis with atrial fibrillation. Br Med J 1977;2:688-90.  Back to cited text no. 25
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  [Figure 1], [Figure 2], [Figure 3], [Figure 4]


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