Graphical abstract
Keywords: Acute myocardial infarction, Cystic thrombus, Hydatid cyst, Anticoagulation
Highlights
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LV thrombi after AMI are a feared complication and are not uncommon.
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LV thrombi can present unusually as cystic-like masses, warranting careful management.
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Early identification and management of LV thrombi can prevent devastating sequelae.
Introduction
Left ventricular (LV) thrombi are not uncommon following acute myocardial infarction (AMI). They are one of the most feared complications because of increased embolic risk.1 We describe our case as the largest atypical cystic LV thrombus that has been reported, which mimicked a hydatid cyst.
Case Presentation
A 40-year-old man was brought to our emergency department from prison with chest tightness and dyspnea. He was in acute distress and demonstrated signs of acute heart failure. He was stabilized as per guideline protocols. Resting electrocardiography showed ventricular tachycardia (Figure 1) that was aborted successfully using emergency electrical defibrillation. Postdefibrillation electrocardiography showed normal sinus rhythm with pathologic Q waves and ST-segment elevation in leads V1 to V3, representing anteroseptal wall myocardial infarction (Figure 2).
Figure 1.
Electrocardiogram on presentation showed ventricular tachycardia.
Figure 2.
Electrocardiogram after defibrillation showed normal sinus rhythm with pathologic Q waves and ST-segment elevation in leads V1–V3, representing anteroseptal wall myocardial infarction.
Because of respiratory distress and ongoing chest pain along with the electrocardiographic findings, the patient was intubated and shifted immediately to the cardiac catheterization laboratory. Left heart catheterization and coronary angiography were performed via the right radial approach and showed a totally occluded mid left anterior descending coronary artery (Figure 3A). The left anterior descending coronary artery thrombus was aspirated, and the procedure was completed with the successful deployment of two drug-eluting stents (Figure 3B). An intra-aortic balloon pump was inserted through the right femoral artery, and an intravenous glycoprotein IIb/IIIa inhibitor (tirofiban) was initiated and continued for 24 hours. The patient was then transferred to the coronary care unit for further stabilization and management. The next day he was successfully extubated, and the intra-aortic balloon pump was removed.
Figure 3.
(A) Left anterior oblique cranial view showing total mid left anterior descending coronary artery occlusion. (B) Left anterior oblique cranial view showing the left anterior descending coronary artery after successful primary percutaneous coronary intervention.
Transthoracic echocardiography was done on the next day and showed moderately reduced LV systolic function with an ejection fraction of 40% (by the modified Simpson method) and anterior, septal, and apical wall akinesis with no hemodynamically significant valve disease. Surprisingly, a large hyperechoic mobile cystic mass measuring 4.3 × 2.3 cm was found attached to the apical septal and inferior walls of the left ventricle (Figure 4, Video 1, Video 2, Video 3, Video 4). The differential diagnosis included but was not limited to hydatid cyst, a large atypical thrombus with central lysis, bronchogenic cyst, blood cyst, and cardiac myxoma. Echinococcus titer was measured at 1:16. Complete blood count showed leukocytes of 7.8 k/μL (normal range, 4.0–11 k/μL) and eosinophils of 0.4 k/μL (normal range, 0.0–0.8 μL). Pan computed tomography with contrast was performed to asses for extracardiac cystic lesions; results were negative except for a nonenhancing LV filling defect (Figure 5). Cardiac magnetic resonance was not available.
Figure 4.
LV cystic mass size and appearance in the standard transthoracic echocardiographic views. (A) Left parasternal long-axis view showing the LV cystic mass. (B) Left parasternal short-axis view at the level of the papillary muscles showing mass attachment to the septum. (C) Apical four-chamber view showed mass attachment to the apical septum, measuring 2.3 × 4.3 cm. (D) Apical two-chamber view showing mass attachment to the apical inferior septum.
Figure 5.
Chest computed tomography with contrast illustrating the presence of filing defects likely representing thrombus (A) with attachment to LV inferior apical septum (B).
Accordingly, in addition to routine anti-ischemic drug therapy, oral anticoagulation was started to cover the possibility of LV thrombus. Because routine international normalized ratio monitoring was not feasible in the prison, apixaban was preferred over warfarin.
One month later, the patient was brought for follow-up. He was asymptomatic, with no clinical evidence of heart failure or thromboembolism. Repeat follow-up transthoracic echocardiography showed almost complete disappearance of the cystic mass except for a small stalk (Figure 6, Video 5, Video 6, Video 7, Video 8), suggesting the diagnosis of a large atypical LV cystic thrombus.
Figure 6.
Follow-up transthoracic echocardiographic views showing complete mass disappearance in consecutive views: (A) left parasternal long-axis view, (B) left parasternal short-axis view at the level of the papillary muscles, (C) apical four-chamber view, and (D) apical two-chamber view.
Discussion
The incidence of LV thrombus has been markedly reduced with advances in AMI treatment, including primary percutaneous coronary intervention and anticoagulant therapy, reaching 2.5%–5% from 7%–46% during the previous prethrombolytic and thrombolytic eras.2
LV thrombus can occur within 24 hours up to 2 weeks after AMI. The main underlying pathogenesis is based on Virchow's triad, which comprises blood stasis, endothelial injury, and hypercoagulable state. Anterior infarction, larger infarct size, akinetic or dyskinetic wall segments, and reduced LV systolic dysfunction (ejection fraction ≤ 40%) are believed to predict LV thrombus formation.3 Thrombi mostly tend to be located apically, but they can be attached to the septal wall and to the inferoposterior wall.4 On the basis of a literature review (PubMed, Simmon), our case appears to be the largest reported. The appearance of the thrombus in our case mimicked hydatid cyst.5 Multiple cases with atypical cystic thrombi have been reported in the literature.6, 7 Therefore, it is becoming necessary to consider this type of thrombus as part of the differential diagnosis of LV cystic masses. Early thrombus identification permits early treatment and hopefully avoidance of possibly devastating sequelae.8
Absence of liver and lung lesions on computed tomography and the low Echinococcus titer, along with absence of leukocytosis and eosinophilia, made hydatidosis less likely, especially given that hydatid cyst occurs in the liver or lungs 90% of the time.9 Pan computed tomography is considered a reliable test for the diagnosis of hydatid cyst, with accuracy of 98%.10, 11
Few cases of intracardiac bronchogenic cyst, blood cyst, and atypical cardiac myxoma have been reported in the literature.12, 13 Despite being valid differential diagnoses, the clinical scenario of AMI along with the behavior of cyst disappearance after anticoagulation made these rare entities less likely.
Conclusion
LV thrombi can present as cystic masses after myocardial infarction. Early anticoagulation may be effective in managing this complication. Other cystic masses should be considered in the differential diagnosis.
Footnotes
Conflicts of interest: The authors reported no actual or potential conflicts of interest relative to this document.
Supplementary data related to this article can be found at https://doi.org/10.1016/j.case.2017.09.009.
Supplementary Data
Transthoracic echocardiography, left parasternal long-axis view, showing apical LV floating cystic mass.
Transthoracic echocardiography, left parasternal short-axis view, showing mass mobility and apical septal attachment.
Transthoracic echocardiography, apical four-chamber view, showing mass mobility and apical septal attachment.
Transthoracic echocardiography, apical two-chamber view, showing mass mobility and apical inferior wall attachment.
Follow-up transthoracic echocardiography, left parasternal long-axis view, showing almost complete mass disappearance.
Follow-up transthoracic echocardiography, left parasternal short-axis view, showing almost complete mass disappearance.
Follow-up transthoracic echocardiography, apical four-chamber view, showing almost complete mass disappearance. Note the small residual stalk in the distal septum.
Follow-up transthoracic echocardiography, apical two-chamber view, showing almost complete mass disappearance.
References
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Associated Data
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Supplementary Materials
Transthoracic echocardiography, left parasternal long-axis view, showing apical LV floating cystic mass.
Transthoracic echocardiography, left parasternal short-axis view, showing mass mobility and apical septal attachment.
Transthoracic echocardiography, apical four-chamber view, showing mass mobility and apical septal attachment.
Transthoracic echocardiography, apical two-chamber view, showing mass mobility and apical inferior wall attachment.
Follow-up transthoracic echocardiography, left parasternal long-axis view, showing almost complete mass disappearance.
Follow-up transthoracic echocardiography, left parasternal short-axis view, showing almost complete mass disappearance.
Follow-up transthoracic echocardiography, apical four-chamber view, showing almost complete mass disappearance. Note the small residual stalk in the distal septum.
Follow-up transthoracic echocardiography, apical two-chamber view, showing almost complete mass disappearance.