Acute myocardial infarction secondary to left main coronary embolization after the conversion of an unwanted atrial fibrillation to the sinus rhythm



    Table of Contents CASE REPORT Year : 2022  |  Volume : 11  |  Issue : 1  |  Page : 29-32

Acute myocardial infarction secondary to left main coronary embolization after the conversion of an unwanted atrial fibrillation to the sinus rhythm

Faeze Mohammadi Daniali, MohammadEsmaeil Zanganehfar, Mohammad Javad Alemzadeh Ansari, Abolfath Alizadeh Diz
Shahid Rajaee Cardiovascular, Medical and Research Center, Iran University of Medical Science, Tehran, Iran

Date of Submission26-Oct-2021Date of Decision28-Nov-2021Date of Acceptance04-Dec-2021Date of Web Publication29-Mar-2022

Correspondence Address:
Dr. MohammadEsmaeil Zanganehfar
Vali-Asr Ave. 1995614331, Tehran
Iran
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/rcm.rcm_57_21

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Atrial fibrillation (AF) is common in hypertrophic cardiomyopathy and it represents the most frequent cause of coronary artery embolism.We describe a male patient with hypertrophic cardiomyopathy with persistent AF, for which he consumed rivaroxaban. The patient received implantable cardioverter-defibrillator shocks for ventricular tachycardia, but he developed acute embolic occlusion in the left main coronary artery (LMCA) following the conversion of the AF rhythm into the sinus rhythm.

Keywords: Atrial fibrillation, hypertrophic cardiomyopathy, implantable cardioverter-defibrillator, left main artery embolus, myocardial infarction


How to cite this article:
Daniali FM, Zanganehfar M, Ansari MJ, Diz AA. Acute myocardial infarction secondary to left main coronary embolization after the conversion of an unwanted atrial fibrillation to the sinus rhythm. Res Cardiovasc Med 2022;11:29-32
How to cite this URL:
Daniali FM, Zanganehfar M, Ansari MJ, Diz AA. Acute myocardial infarction secondary to left main coronary embolization after the conversion of an unwanted atrial fibrillation to the sinus rhythm. Res Cardiovasc Med [serial online] 2022 [cited 2022 Mar 29];11:29-32. Available from: https://www.rcvmonline.com/text.asp?2022/11/1/29/341265   Introduction Top

Atrial fibrillation (AF) is common in hypertrophic cardiomyopathy with a prevalence of 22–32%,[1] and it represents the most frequent cause of coronary artery embolism. Coronary artery embolism is a rare cause of acute myocardial infarction. The prevalence of this entity remains unknown because of its difficult diagnosis in the acute setting. Arterial embolism can be an undesirable event of AF rhythm cardioversion.

  Case Report Top

A 66-year-old man was referred to our tertiary center to receive an implantable cardioverter-defibrillator (ICD). The patient was a known case of hypertrophic cardiomyopathy (HCM) and chronic kidney disease, with an estimated creatinine clearance rate of 38 mL/min. He had experienced episodes of sustained monomorphic ventricular tachycardia (VT), which were cardioverted into the AF rhythm with external direct cardioversion. Subsequently, because of positive cardiac troponin and arrhythmia, he underwent coronary angiography, which revealed no significant coronary involvement [Figure 1].

Figure 1: The coronary angiography shows no significant coronary involvement

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The patient had no history of syncope or familial history of sudden cardiac death. His basic electrocardiogram (ECG) illustrated atrial fibrillation (AF) with a left ventricular (LV) hypertrophy pattern [Figure 2]. He was on metoprolol (25 mg BID), amiodarone (200 mg OD), aspirin (80 mg OD), and rivaroxaban, which was discontinued 24 h before the procedure (15 mg daily for the AF rhythm).

Figure 2: The patient's electrocardiogram depicts atrial fibrillation with a left ventricular hypertrophy pattern

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Transthoracic echocardiography (TTE) showed normal left and right ventricles in size and function, a hypertrophied interventricular septum, and asymmetrical septal hypertrophy (anteroseptal wall thickness = 2.2 cm and posterior wall thickness = 1.3 cm) with mild-to-moderate mitral regurgitation but without any gradient in the LV cavity or the LV outflow tract. No clots or smoky patterns were observed in the LV or the left atrium (LA).

The patient was scheduled to receive an intracardiac ICD for secondary prevention. The implantation of an ICD-VR was done with no complications. In the ward, about 20 h after the ICD implantation, he developed palpitation; before our visit, the ICD detected VT and delivered shocks. After some minutes, the patient complained of severe retrosternal chest pain with nausea, which was followed by a drop in his blood pressure. ECG revealed the sinus rhythm with diffuse ST depression and aVR and V1 ST elevation [Figure 3]. Bedside TTE revealed severe LV systolic dysfunction (ejection fraction = 15%–20%) with global hypokinesia without LV outflow tract obstruction.

Figure 3: The electrocardiogram illustrates the sinus rhythm with diffuse segment depression and aVR and V1 segment elevation, tall R wave in V2 may depict a concomitant posterior wall infarction

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Given the patient's condition, an emergent coronary angiography was performed in the catheterization laboratory after clopidogrel loading (600 mg). An intra-aortic balloon pump (IABP) was inserted, and coronary injection showed a frightening scene [Figure 4]: an abrupt total occlusion of the left coronary system from the distal part of the left main coronary artery (LMCA). Eptifibatide was promptly started, and the left anterior descending and the left circumflex were wired. Then, predilation and thrombosuction were performed. Next, the stenting of the LMCA to the left anterior descending and the left circumflex was carried out, with acceptable results [Figure 5]. The patient's pain was relieved, and the ECG changes were reversed. Heparin (500 unit/h) and eptifibatide (13 mL/h) infusion, as well as ASA (80 mg daily) and clopidogrel (75 mg daily), was continued.

Figure 4: The image demonstrates total occlusion of the left main coronary artery

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The next day, the IABP was removed. On the 3rd postprocedural day, coronary angiography was performed for the evaluation of the results, and plain balloon angioplasty was done on the previous stent of the LMCA, with good final results. Triple antithrombotic therapy, including aspirin (81 mg daily), clopidogrel (75 mg daily), and apixaban (2.5 mg BID), was prescribed. After 5 days, the patient was discharged in good condition. At 1-year follow-up, he was asymptomatic.

  Discussion Top

AF, LV thrombi, septic emboli from infective endocarditis, tumors, and paradoxical embolism due to patent foramen ovale can be the sources of emboli to coronary arteries.[2] The prevalence of thromboembolic events after the direct-current cardioversion of AF is 2.0%, and it is even higher in patients with diabetes and heart failure (9.8%).[3] Most embolic events occur within 3 days after cardioversion.[4] The duration of AF prior to direct-current cardioversion is an important risk factor for the early formation of the LA appendage thrombus in the case of subtherapeutic anticoagulation. When AF lasts more than 48 h following direct-current cardioversion, there is an electromechanical dissociation in the LA due to its tachycardia-mediated stunning,[5] causing blood stasis and leading to thrombogenesis and embolization.[3]

AF is a major complication and reason for worse outcomes in patients with HCM. In contrast to patients without HCM, no validated risk scores exist to define patients who benefit from oral anticoagulation. Even if the CHA₂DS₂-VASc score is 0, patients with HCM are at high risk for embolic events. Parameters such as LA size, mitral regurgitation, and LV outflow gradient may contribute to higher stroke risk, but they do not contribute to the CHA₂DS₂-VASc score. In unselected patients with HCM, stroke and peripheral embolism occur with a prevalence rate of 6% and an incidence rate of 0.8%/year.[6] However, a cohort study on HCM patients who received a cardiac rhythm management device reported a much higher incidence rate of thromboembolic stroke (18%).[7],[8] Compared with warfarin, patients with HCM and AF on novel oral anticoagulants had similar stroke and major bleeding risks but lower all-cause mortality and composite fatal cardiovascular events.[9] Pretreatment with low-dose oral amiodarone increases electrical cardioversion efficacy and reduces AF recurrence. Oral amiodarone boosts the efficacy of direct-current cardioversion in the restoration of the sinus rhythm in patients with chronic AF.[10]

Our patient was a known case of HCM and AF on rivaroxaban. He underwent external VT cardioversion, but his atrial rhythm remained AF. He was given amiodarone and referred to our tertiary center, where we implanted a single-chamber ICD. After a day, he experienced intracardiac shocks due to an episode of VT. What transpired was an acute myocardial infarction secondary to total occlusion in the LMCA after the conversion of an unwanted AF to the sinus rhythm. We succeeded in saving the patient's life with an emergent angioplasty.

At 1-year follow-up, the patient was in good condition, with acceptable functional capacity. In addition, he had not experienced any chest pain.

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.

Ethical clearance

Ethical committee is approved by patients hospitalization in October 2020.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

 

  References Top
1.Patten M, Pecha S, Aydin A. Atrial fibrillation in hypertrophic cardiomyopathy: Diagnosis and considerations for management. J Atr Fibrillation 2018;10:1556.  Back to cited text no. 1
    2.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
    3.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. 3
    4.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. 4
    5.Manning WJ, Silverman DI, Katz SE, Riley MF, Come PC, Doherty RM, et al. Impaired left atrial mechanical function after cardioversion: Relation to the duration of atrial fibrillation. J Am Coll Cardiol 1994;23:1535-40.  Back to cited text no. 5
    6.Olivotto I, Maron BJ, Cecchi F. Clinical significance of atrial fibrillation in hypertrophic cardiomyopathy. Curr Cardiol Rep 2001;3:141-6.  Back to cited text no. 6
    7.Wilke I, Witzel K, Münch J, Pecha S, Blankenberg S, Reichenspurner H, et al. High incidence of de novo and subclinical atrial fibrillation in patients with hypertrophic cardiomyopathy and cardiac rhythm management device. J Cardiovasc Electrophysiol 2016;27:779-84.  Back to cited text no. 7
    8.Haruki S, Minami Y, Hagiwara N. Stroke and embolic events in hypertrophic cardiomyopathy: Risk stratification in patients without atrial fibrillation. Stroke 2016;47:936-42.  Back to cited text no. 8
    9.Jung H, Yang PS, Jang E, Yu HT, Kim TH, Uhm JS, et al. Effectiveness and safety of Non-Vitamin K antagonist oral anticoagulants in patients with atrial fibrillation with hypertrophic cardiomyopathy: A nationwide cohort study. Chest 2019;155:354-63.  Back to cited text no. 9
    10.Capucci A, Villani GQ, Aschieri D, Rosi A, Piepoli MF. Oral amiodarone increases the efficacy of direct-current cardioversion in restoration of sinus rhythm in patients with chronic atrial fibrillation. Eur Heart J 2000;21:66-73.  Back to cited text no. 10
    
  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5]
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