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Table of Contents
CASE REPORT
Year : 2021  |  Volume : 14  |  Issue : 3  |  Page : 129-132

Coexistent left ventricular clot and self-contained pericardial haematoma: An unusual combination found in a patient post inferior ST-elevation myocardial infarction


1 Department of Internal Medicine, Rashid Hospital, Dubai, UAE
2 Department of Cardiology, Rashid Hospital, Dubai, UAE

Date of Submission28-Oct-2020
Date of Decision16-May-2021
Date of Acceptance17-May-2021
Date of Web Publication01-Oct-2021

Correspondence Address:
Rommana Mehdi
Rashid Hospital, Dubai Health Authority, P.O. BOx 4545, Dubai
UAE
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/hmj.hmj_80_20

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  Abstract 


The discovery of a left ventricular (LV) thrombus in combination with a pericardial haematoma is a rare occurrence secondary to a complicated myocardial infarction (MI). A 53-year-old male was brought to our emergency in an unresponsive state with unstable haemodynamics. Electrocardiogram showed inferior and right ventricular ST-elevation MI. The patient underwent primary percutaneous coronary intervention of the right coronary and right posterior descending arteries. Echocardiography revealed a mobile clot in the LV apex, secondary to subacute myocardial rupture, and a self-contained pericardial haematoma. Therapeutic subcutaneous enoxaparin was commenced for the LV clot. Changes in the size of the haematoma and LV clot were monitored through serial echocardiographies. The patient underwent an uneventful course where there was gradual dissolution of the clot and resolution of the haematoma. This case illustrates the clinical dilemma of administering anticoagulation for LV clot in the presence of a self-sealed haematoma that could have otherwise resulted in cardiac tamponade and LV wall rupture.

Keywords: Inferior ST-elevation myocardial infarction, left ventricular clot, pericardial haematoma, self-contained haematoma


How to cite this article:
Mehdi R, Rajani AR, Roqia S. Coexistent left ventricular clot and self-contained pericardial haematoma: An unusual combination found in a patient post inferior ST-elevation myocardial infarction. Hamdan Med J 2021;14:129-32

How to cite this URL:
Mehdi R, Rajani AR, Roqia S. Coexistent left ventricular clot and self-contained pericardial haematoma: An unusual combination found in a patient post inferior ST-elevation myocardial infarction. Hamdan Med J [serial online] 2021 [cited 2021 Dec 7];14:129-32. Available from: http://www.hamdanjournal.org/text.asp?2021/14/3/129/327429




  Introduction Top


Left ventricular (LV) thrombus is a serious complication that is known to occur after MI.[1] However, several studies have reported a decreased incidence of LV thrombus in patients who received thrombolytic therapy or underwent primary percutaneous coronary intervention (PCI).[2],[3]

Myocardial rupture is an uncommon complication of MI. After cardiogenic shock, it represents the second cause of mortality in patients with MI.[4] Pericardial haematomas can have a multitude of causes, including trauma, haemorrhagic pericarditis, myocardial or arterial rupture, aortic dissection and iatrogenic causes, which include anticoagulation, cardiac surgery and cardiac catheterisation.[5]

Some independent risk factors which could contribute towards having a myocardial rupture are female gender, advanced age, lower blood pressure, higher heart rate, delayed admission and thrombolysis.

Coronary angioplasties, when performed early, reduce the risk of myocardial rupture, while giving thrombolytic therapy is known to heighten its risk.[6]


  Case Report Top


A 53-year-old South Asian male with multiple risk factors for coronary artery disease presented to our emergency in a hypotensive and an unresponsive state. He had sustained a head injury with multiple lacerations after suddenly collapsing at work; however, there was no present or prior history of chest trauma. He received 12 min of cardiopulmonary resuscitation by the paramedics. Further to this, he was resuscitated with intravenous fluids and dopamine. The electrocardiogram (ECG) on admission showed an inferior and right ventricular ST-segment elevation myocardial infarction (MI) [Figure 1]. Once the patient was stabilised, a CT brain was performed, which revealed no evidence of an intracranial bleed or infarction.
Figure 1: Electrocardiogram on admission showing ST elevation in the inferior leads

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Upon diagnosing inferior ST-elevation MI, the patient was commenced on loading doses of oral aspirin and ticagrelor and anti-ischaemic medications. He underwent coronary angiography (CAG) for primary PCI. During the CAG procedure, the left main coronary artery appeared normal, without stenosis. There was 70%–90% stenosis involving the first diagonal artery of the proximal left anterior descending artery. The circumflex artery also showed 50%–70% stenosis. Furthermore, the proximal right coronary artery was 70%–90% stenosed. There was acute occlusion of the right posterior descending artery. Successful recanalisation of the right posterior descending artery and right coronary artery was performed with 2.25 mm × 21 mm and 4 mm × 28 mm drug-eluting stents, respectively.

Echocardiography exhibited normal valves, severe left ventricular hypertrophy, akinesia of the inferior wall, ejection fraction of 40% and a cystic, mobile left ventricular clot, measuring 0.8 cm × 0.8 cm [[Figure 2] and Video 1]; therefore, ticagrelor was discontinued in view of high bleeding risk and was changed to clopidogrel. The patient was started on a therapeutic dose of subcutaneous enoxaparin.
Figure 2: Transthoracic echocardiography showing a left ventricular clot (arrow) in the apical short-axis view

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The following day after his primary PCI, the patient developed a sudden onset of shortness of breath with hypotension; bilateral basal crackles were audible on his chest examination, suggestive of pulmonary oedema. He was managed with intravenous furosemide and dopamine infusion. Echocardiography showed a hyperechoic component in the inferior wall reflecting a self-contained pericardial haematoma, most likely secondary to the rupture of the inferior wall, measuring 1.4 cm posteriorly and 1.1 cm inferiorly, without any evidence of inferior wall perforation on transthoracic echocardiography [Figure 3] and [Figure 4]. Echocardiography performed the next day denoted an increase in the size of the left ventricular clot which now measured 2.7 cm × 1.4 cm, and there was also a progression in the size of the pericardial haematoma, measuring 1.7 cm posteriorly and 2 cm inferiorly.
Figure 3: Transthoracic echocardiography in the parasternal long-axis view showing a self-contained haematoma in the pericardial space posteriorly (arrow)

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Figure 4: Transthoracic echocardiography illustrating the self-contained pericardial haematoma inferiorly (arrow)

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Investigations

The patient's initial blood investigations revealed a white blood cell count of 12.4 × 103/uL, haemoglobin 15 g/dl and platelets 361 × 103/uL. His CK-MB fraction was elevated at 29 U/L. Furthermore, his troponin was 380 ng/L and NT-proBNP was 2244 pg/ml. Liver function tests showed alanine aminotransferase of 1835 and alkaline phosphatase of 169, suggesting ischaemic hepatitis, most likely secondary to the hypotension at admission, which required resuscitation. Lipid profile showed triglycerides of 152 mg/dl, high-density lipoprotein 32 mg/dl, low-density lipoprotein 36 mg/dl and total cholesterol 98 mg/dl. HbA1C was 7.5%.

Differential diagnoses

  • Self-contained pericardial haematoma
  • Pseudoaneurysm
  • Pericardial cyst
  • Pericardial neoplasm.1


Treatment

There was a perceived risk of embolisation with the fragile, mobile clot, and due to this reason, it was decided to start an anticoagulant. Change in sizes of both the clot and the pericardial haematoma was monitored through a series of echocardiographies which were performed daily. Over the next 2.5 weeks, the patient remained stable and underwent an uncomplicated hospital course. He did not exhibit any symptoms or signs of cardiac tamponade at any point. The left ventricular clot eventually disappeared and the haematoma gradually reduced with central lucency [Figure 5]a and [Figure 5]b.
Figure 5: Transthoracic echocardiography performed at discharge showing resolution of the haematoma to central lucency (arrows) in parasternal long-axis view (a) and short-axis view (b)

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The case illustrates the risk that accompanies the decision of giving an anticoagulant in the presence of a self-contained pericardial haematoma that could result in rupture of the myocardium, thereby leading to cardiac tamponade. However, a conservative approach leads to favourable outcomes for this individual, and the patient remained symptom free with ECG showing resolution of the ST segment on discharge [Figure 6].
Figure 6: Electrocardiogram of the patient on discharge showing resolution of the ST-segment elevation

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Outcome and follow-up

The patient demonstrated a decent response to the conservative management that we elected to provide and he was discharged in a stable condition. He was counselled about his modification of his risk factors and compliance to his dual-antiplatelet therapy (aspirin and clopidogrel) for 1 year followed by aspirin only and his other anti-ischaemic medications for life.


  Discussion Top


In the present era, with facilities for early diagnostic and therapeutic interventions, cardiac rupture remains an uncommon complication of MI, causing 7%–10% of early deaths.[7] Timely diagnosis leads to emergent life-saving procedures. The diagnosis of subacute myocardial rupture after an MI relies on the identification of a pericardial effusion (haemopericardium) on echocardiography in association with the signs of cardiac tamponade.[8]

Observational studies that were conducted in both the pre-thrombolytic and thrombolytic periods have favoured the employment of anticoagulation to reduce the risk of embolisation.[9],[10],[11] Moreover, a meta-analysis conducted in the 1990s, consisting of 11 studies, concluded that anticoagulation, compared to no anticoagulation, was associated with a reduction in the rate of embolisation.[12] Based on these data, the European Society of Cardiology and the American College of Cardiology/American Heart Association guidelines advocate the use of Vitamin K antagonist therapy in patients with an LV thrombus after MI.[13]

Literature review has shown limited case reports of cardiac rupture, which were either due to an iatrogenic cause or secondary to a blunt chest wall trauma. A case report by Helmy et al., published in the heart journal,[14] discussed the development of a contained myocardial rupture wrapped with a haematoma at the epicardium, secondary to a pseudoaneurysm, which had been managed with a surgical approach. Another report described a case of a 48-year-old man, who had an incomplete myocardial rupture after inferior MI treated by early PCI, and related a promising short-term outcome with a conservative approach.[15] However, none of these patients had coexisting left ventricular clots.

In our patient, we elected to commence a therapeutic dose of enoxaparin instead of an oral anticoagulant (warfarin) due to the presence of the self-contained haematoma and perceived risk of cardiac tamponade. Furthermore, the patient was given enoxaparin in a monitored hospital setting, where the dose of enoxaparin could easily be tailored based on results of serial echocardiographies.

No case reports were found with coexistence of a left ventricular clot with a pericardial haematoma.

Learning points/take-home messages

  • It is exceptional to find left ventricular clot coexisting with a self-sealed haematoma after an ST-elevation MI
  • Decision of giving anticoagulation to a patient for left ventricular clot in the presence of a self-sealed haematoma carries a high risk of rupture and cardiac tamponade
  • Such patients require regular monitoring with echocardiography in order to assess for changes in the sizes of both the haematoma and the left ventricular clot.


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.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Greaves SC, Zhi G, Lee RT, Solomon SD, MacFadyen J, Rapaport E, et al. Incidence and natural history of left ventricular thrombus following anterior wall acute myocardial infarction. Am J Cardiol 1997;80:442-8.  Back to cited text no. 1
    
2.
Porter A, Kandalker H, Iakobishvili Z, Sagie A, Imbar S, Battler A, et al. Left ventricular mural thrombus after anterior ST-segment-elevation acute myocardial infarction in the era of aggressive reperfusion therapy-still a frequent complication. Coron Artery Dis 2005;16:275-9.  Back to cited text no. 2
    
3.
Rehan A, Kanwar M, Rosman H, Ahmed S, Ali A, Gardin J, et al. Incidence of post myocardial infarction left ventricular thrombus formation in the era of primary percutaneous intervention and glycoprotein IIb/IIIa inhibitors. A prospective observational study. Cardiovasc Ultrasound 2006;4:20.  Back to cited text no. 3
    
4.
Figueras J, Cortadellas J, Evangelista A, Soler-Soler J. Medical management of selected patients with left ventricular free wall rupture during acute myocardial infarction. J Am Coll Cardiol 1997;29:512-8.  Back to cited text no. 4
    
5.
Brown DL, Ivey TD. Giant organized pericardial hematoma producing constrictive pericarditis: A case report and review of the literature. J Trauma 1996;41:558-60.  Back to cited text no. 5
    
6.
Qian G, Wang ZF, Liu HB, Chen YD. Clinical manifestations of 43 patients with acute myocardial infarction complicated by free wall rupture. Zhonghua Xin Xue Guan Bing Za Zhi 2011;39:812-5.  Back to cited text no. 6
    
7.
Becker RC, Gore JM, Lambrew C, Weaver WD, Rubison RM, French WJ, et al. A composite view of cardiac rupture in the United States National Registry of Myocardial Infarction. J Am Coll Cardiol 1996;27:1321-6.  Back to cited text no. 7
    
8.
Naik H, Sherev D, Hui PY. The rapid diagnosis of pseudoaneurysm formation in left ventricular free wall rupture. J Invasive Cardiol 2004;16:390-2.  Back to cited text no. 8
    
9.
Keren A, Goldberg S, Gottlieb S, Klein J, Schuger C, Medina A, et al. Natural history of left ventricular thrombi: Their appearance and resolution in the posthospitalization period of acute myocardial infarction. J Am Coll Cardiol 1990;15:790-800.  Back to cited text no. 9
    
10.
Asinger RW, Mikell FL, Elsperger J, Hodges M. Incidence of left-ventricular thrombosis after acute transmural myocardial infarction. Serial evaluation by two-dimensional echocardiography. N Engl J Med 1981;305:297-302.  Back to cited text no. 10
    
11.
Visser CA, Kan G, Lie KI, Durrer D. Left ventricular thrombus following acute myocardial infarction: A prospective serial echocardiographic study of 96 patients. Eur Heart J 1983;4:333-7.  Back to cited text no. 11
    
12.
Vaitkus PT, Barnathan ES. Embolic potential, prevention and management of mural thrombus complicating anterior myocardial infarction: A meta-analysis. J Am Coll Cardiol 1993;22:1004-9.  Back to cited text no. 12
    
13.
Delewi R, Zijlstra F, Piek JJ. Left ventricular thrombus formation after acute myocardial infarction. Heart 2012;98:1743-9.  Back to cited text no. 13
    
14.
Helmy TA, Nicholson WJ, Lick S, Uretsky BF. Contained myocardial rupture: A variant linking complete and incomplete rupture. Heart 2005;91:e13.  Back to cited text no. 14
    
15.
Hoffer E, Materne P, Lecoq E, Markov M, Boland J. Incomplete myocardial rupture following inferior myocardial infarction: A case report. Int J Cardiol 2007;116:e27-8.  Back to cited text no. 15
    


    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6]



 

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