ST-segment elevation myocardial infarction possibly caused by thromboembolism from left atrial appendage thrombus after incomplete surgical ligation

Echocardiography. 2018;35:1889–1892. wileyonlinelibrary.com/journal/echo © 2018 Wiley Periodicals, Inc.  

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1 | CASE PRESENTATION

A 70- year- old female was presented to our emergency depart-ment because of acute- onset chest pain radiating to the back and cold sweating. She underwent mechanical heart valve replace-ment for rheumatic heart disease and surgical left atrial append-age ligation 16 years ago. ECG revealed atrial fibrillation (AF) with ST- segment elevation in leads I and aVL with reciprocal ST- segment depression in the inferior leads (Figure 1A). Laboratory investigations showed initial troponin T level 0.016 ng/dL, in-creasing to 8.85 ng/dL at 12 hours and 3.3 ng/dL at 48 hours (normal reference < 0.014 ng/dL), international normalized ratio level 1.98, and the other laboratory tests were within normal lim-its. The patient’s anticoagulation therapy included warfarin treat-ment (5 mg/d), and her TTR value for the last 11 months was 60%.

Bedside transthoracic echocardiography demonstrated apical wall hypokinesis with a left ventricular ejection fraction of 50% (Movie S1), and Doppler parameters indicated normal valvular hemodynamics. Diagnostic coronary angiography was performed through right femoral access, which revealed a thromboembolic occlusion of the proximal segment of the first diagonal coronary artery (Figure 1B). After several attempts to perform thrombus aspiration, TIMI 3 flow was obtained (Figure 1C). On the follow-ing day, two- dimensional and real time three- dimensional trans-esophageal echocardiography (TEE) performed and indicated an incomplete surgical ligation of left atrial appendage (LAA) and the absence of prosthetic valve thrombosis (Figures 1D and 2, Movies S2–S5). Moreover, TEE demonstrated a 15 × 10 mm size thrombus (soft and homogeneous mass with fixed echo density similar to myocardium) in the LAA. In addition, sluggish flow as Received: 11 July 2018 

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DOI: 10.1111/echo.14123

I M A G E S S e c t i o n E d i t o r - B r i a n D . H o i t , M D

ST- segment elevation myocardial infarction possibly caused by

thromboembolism from left atrial appendage thrombus after

incomplete surgical ligation

Ahmet Guner MD

_{| Alev Kılıcgedik MD}

_{| Macit Kalçık MD}

_{| Mehmet Ozkan MD}

1_{Department of Cardiology, Kosuyolu Kartal}

Training and Research Hospital, Istanbul, Turkey

2_{Department of Cardiology, Hitit University,}

Corum, Turkey

3_{School of Health Sciences, Ardahan}

University, Ardahan, Turkey

Correspondence: Ahmet Guner, Department of Cardiology, Kosuyolu Kartal Training and Research Hospital, 34846 Kartal, Istanbul, Turkey (ahmetguner488@gmail.com).

Coronary embolism (CE) is the underlying cause of 3% of acute coronary syndromes but is frequently overlooked in the differential diagnoses of acute coronary syn-dromes. The CE may be direct (left sided from the native or prosthetic heart valve, the left atrium, left atrial appendage or pulmonary venous bed), paradoxical (from the venous circulation through a patent foramen ovale, atrial septal defect, ventricu-lar septal defects, cyanotic congenital heart defects or pulmonary arteriovenous malformations), or iatrogenic (following cardiac interventions. In patients with atrial fibrillation (AF), left atrial appendage (LAA) ligation during mitral valve surgery has long been recommended to decrease the future risk of embolic events such as myo-cardial infarction or ischemic stroke. Recently, Aryana et al reported that in patients with AF who underwent surgical ligation of LAA, the presence of incomplete ligation was associated with a significantly higher risk of stroke/systemic embolization than complete ligation (24% vs 2%).

K E Y W O R D S

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evidenced by spontaneous echo contrast (SEC) with its charac-teristic swirling and smoke- like appearance was observed in the left atrium (Movies S6, S7). The patients’ anticoagulation therapy continued with increased dose warfarin combined with 100 mg/d acetylsalicylic acid. During the 3- month uneventful follow- up, the patient’s TTR value was 100%.

2 | DISCUSSION

Coronary embolism (CE) is the underlying cause of 3% of acute coronary syndromes but is frequently overlooked in the dif-ferential diagnoses of acute coronary syndromes. The CE may be direct (left sided from the native or prosthetic heart valve, the left atrium, left atrial appendage, or pulmonary

venous bed), paradoxical (from the venous circulation through a patent foramen ovale, atrial septal defect, ventricular sep-tal defects, cyanotic congenisep-tal heart defects, or pulmonary arteriovenous malformations), or iatrogenic (following cardiac interventions).1–5

In patients with AF, LAA ligation during mitral valve surgery has long been recommended to decrease the future risk of em-bolic events such as myocardial infarction or ischemic stroke. Recently, Aryana et al6 _{reported that in patients with AF who}

underwent surgical ligation of LAA, the presence of incomplete ligation was associated with a significantly higher risk of stroke/ systemic embolization than complete ligation (24% vs 2%). The incomplete ligation of LAA creates a pouch with stagnant blood flow, which enhances the intensity of SEC and thrombus forma-tion. The high blood flow velocity jet at the small LAA orifice may F I G U R E   1   Electrocardiography depicts atrial fibrillation with ST- segment elevation in leads I and aVL with reciprocal ST- segment depression in the inferior leads (A). Coronary angiography with right cranial angiographic view indicates thromboembolic occlusion of the proximal segment of the first diagonal artery (yellow arrow) (B). After thrombus aspiration, coronary angiography with left cranial angiographic view shows TIMI III distal flow of the first diagonal artery (C). Real time three- dimensional transesophageal echocardiography demonstrates the incomplete surgical ligation of left atrial appendage (black arrows) and the absence of prosthetic valve thrombosis (D)

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promote embolization of thrombotic material into the systemic circulation. This phenomenon does occur even with high levels of anticoagulation and represents a therapeutic dilemma as even oral anticoagulation does not protect patients with incomplete LAA li-gation from thromboembolism. The cerebral circulation is about three times greater than the coronary circulation (750 mL/min vs 220 mL/min). Hence, one has to account for almost one coronary embolism per three cerebral embolisms. Yet, this is far from being represented in the literature.

In conclusion, CE caused by incomplete surgical closure of the LAA is a very rare clinical entity that may not only manifest by stroke but also by myocardial infarction. Embolic myocardial infarction is generally underdiagnosed. Intraoperative evaluation with TEE of LAA ligation during valve or other cardiac surgery is crucial to assess complete occlusion of the LAA,7 _{but later suture}

dehiscence is also possible. We present an ST- segment myocardial infarction resulting from embolism (possibly caused by a thrombus in the subtotally ligated LAA, or, less likely, by prosthetic valve thrombosis or SEC).

ORCID

Macit Kalçık http://orcid.org/0000-0002-8791-4475

Ahmet Guner http://orcid.org/0000-0002-1845-1710

Alev Kılıcgedik http://orcid.org/0000-0002-4380-7045

REFERENCES

1. Raphael CE, Heit JA, Reeder GS, et al. Coronary Embolus: an under-appreciated cause of acute coronary syndromes. JACC Cardiovasc Interv. 2018;11(2):172–180.

2. Yesin M, Karakoyun S, Kalçık M, et al. Status of the epicardial cor-onary arteries in non- ST elevation acute corYesin M, Karakoyun S, Kalçık M, et al. Status of the epicardial cor-onary syndrome in patients with mechanical prosthetic heart valves (from the TROIA- ACS Trial). Am J Cardiol. 2018. pii: S0002-9149(18)31046-4. https:// doi.org/10.1016/j.amjcard.2018.04.045

3. Windecker S, Stortecky S, Meier B. Paradoxical embolism. J Am Coll Cardiol. 2014;64(4):403–415.

4. ElRefai M, Thananayagam K, Bathula R, et al. An unusual cause of car-dioembolic stroke: paradoxical embolism due to thrombus formation on the eustachian valve. Echocardiography. 2015;32(10):1588–1591.

F I G U R E   2   Two- dimensional and real time three- dimensional transesophageal echocardiography display the incomplete surgical ligation of left atrial appendage (black arrows) and thrombus in the left atrial appendage (yellow arrow)

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heart valve thrombosis- derived coronary embolism. Turk Kardiyol Dern Ars. 2014;42(5):467–471.

6. Aryana A, Singh SK, Singh SM, et al. Association between incom-plete surgical ligation of left atrial appendage and stroke and systemic embolization. Heart Rhythm. 2015;12(7):1431–1437.

7. Oneglia C, Muneretto C, Rusconi C. Transesophageal investiga-tion of surgically ligated left atrial appendage. Echocardiography. 2004;21(7):617–619.

SUPPORTING INFORMATION

Additional supporting information may be found online in the Supporting Information section at the end of the article.

Movie S1. Transthoracic echocardiography demonstrates apical wall hypokinesis

Movies S2–S5. Two- dimensional and real time three- dimensional transesophageal echocardiography indicate an incomplete surgical ligation of left atrial appendage and the absence of prosthetic valve thrombosis

Movies S6 and S7. Two- dimensional transesophageal echocardiog-raphy shows spontaneous echo contrast with its characteristic swirl-ing and smoke- like appearance in the left atrium

How to cite this article: Guner A, Kılıcgedik A, Kalçık M, Ozkan M. ST- segment elevation myocardial infarction possibly caused by thromboembolism from left atrial appendage thrombus after incomplete surgical ligation. Echocardiography. 2018;35:1889–1892. https://doi.org/10.1111/echo.14123