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 Table of Contents  
AUTHORS REPLY
Year : 2015  |  Volume : 7  |  Issue : 1  |  Page : 33-35

Regional pericarditis status post cardiac ablation: A case report


1 Department of Internal Medicine, Banner Good Samaritan Medical Center, Phoenix, Arizona, USA
2 Department of Cardiology, Banner Good Samaritan Medical Center, Phoenix, Arizona, USA

Date of Web Publication27-Jan-2015

Correspondence Address:
Joseph Orme
Department of Internal Medicine, Banner Good Samaritan Medical Center, Phoenix, Arizona
USA
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Source of Support: None, Conflict of Interest: None


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How to cite this article:
Orme J, Eddin M, Loli A. Regional pericarditis status post cardiac ablation: A case report. North Am J Med Sci 2015;7:33-5

How to cite this URL:
Orme J, Eddin M, Loli A. Regional pericarditis status post cardiac ablation: A case report. North Am J Med Sci [serial online] 2015 [cited 2019 Nov 19];7:33-5. Available from: http://www.najms.org/text.asp?2015/7/1/33/150096

Dear Editor,

We sincerely appreciate the response to our recently published article [1] regarding regional pericarditis as it is a very difficult diagnosis and requires the exclusion of the more common etiologies of chest pain and ST-segment elevation.

Numerous articles [2],[3],[4],[5],[6] have confirmed the fact that the frequency of pericarditis would be underestimated if required the diagnosis of a pericardial rub; however, a pericardial rub is often present but transient in nature and is often not heard during physical exam. Although a pericardial rub was not appreciated during physical exam of our patient, it very well could have been, and likely was, present at some point during hospitalization.

Transmural post-infarction regional pericarditis (epistenocardiac pericarditis) is the most common and documented etiology resulting in regional pericarditis. [7] For this reason, our case is of great interest, as in our case regional pericarditis is due to post-atrial fibrillation ablation resulting in transmural myocardial cell death.

The electrocardiogram (ECG) prior to cardiac ablation was relatively unremarkable [Figure 1]. Patient underwent elective atrial fibrillation ablation. During the ablation, aggressive radiofrequency, and cryoablation of the pulmonary veins, left atrial posterior wall, and the left and right isthmus was required for adequate treatment of the arrhythmia. The patient was then discharged home 24 hours after the ablation. Shortly after returning home, patient developed chest pain and presented to the emergency department 36 hours after the procedure. At time of presentation, the patient had an elevated troponin of 17.2 ng/ml, which may be consistent with a post-cardiac ablation. [8] The ECG at time of presentation to the emergency department revealed normal sinus rhythm with a heart rate of 78 beats per minute with anterolateral ST-segment elevations in leads I and aVL and V2-V4, reciprocal inferior ST-segment depressions in leads III and aVF and subtle PR-segment depressions [Figure 2]. However, after coronary-artery angiography revealed no significant obstructive coronary artery disease, the ECG revealed resolving ST-segment depressions in the inferior leads and increased ST-segment elevation in leads V5-V6 [Figure 3] consistent with regional pericarditis. Furthermore, a 2D echocardiogram was performed prior to discharge, and after further review from the previous article, [1] revealed a left ventricular ejection fraction of 55-60%, no wall motion abnormalities and a new trace regional pericardial effusion around the posterolateral wall compared to the echocardiogram two days prior during the pre-procedural ischemic work-up [Figure 4]. Two-week follow-up ECG revealed normal sinus rhythm with heart rate of 81 beats per minute with a left-posterior fascicular block and no ST-segment abnormalities other than T-wave inversions isolated in leads I and aVL [Figure 5]. This is consistent with a pericarditis as T-waves may become inverted around the third week and resolve within several weeks thereafter. [6] A 3-month follow-up ECG revealed a normal sinus rhythm with heart rate of 82 beats per minute with a left posterior fascicular block and resolution of non-specific T-wave abnormalities [Figure 6].
Figure 1: ECG prior to atrial fi brillation ablation revealing normal sinus rhythm and a heart rate of 79 beats per minute and a normal early repolarization pattern with no other fi ndings

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Figure 2: ECG at time of presentation to the emergency department revealing normal sinus rhythm with heart rate 78 beats per minute with anterolateral ST-segment elevations in leads I and aVL and V2- V4, reciprocal inferior ST-segment depressions in leads III and aVF and subtle PR-segment depressions

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Figure 3: ECG status post coronary angiography at time of discharge with resolving inferior reciprocal changes and extending anterolateral ST-segment elevations to involve leads V5-V6 in adddition to leads V2-V4

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Figure 4: 2D Echocardiogram during an apical four-chamber view at end-systole revealing a trace regional pericardial effusion in the posterolateral wall

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Figure 5: Two-week follow-up ECG revealing a normal sinus rhythm with a left posterior fascicular block and isolated T-wave inversions in leads I and aVL

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Figure 6: Two-month follow-up ECG revealing a normal sinus rhythm with a left posterior fascicular block and resolution of T-wave inversions

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Oliva et al., [3],[4],[5] explained the T-wave evolution and morphology following a transmural myocardial infarction related regional pericarditis. It is known that T-wave inversions are seen during an ischemic event and accompany myocardial infarction. [3],[4],[5] However, in post-infarction regional pericarditis, the T-waves either remain positive for 48 hours despite infarction or they undergo pre-mature gradual reversal of inversion. [2],[3],[4],[5] Our patient did not have T-wave inversions at time of presentation or at time of discharge. This strongly suggests that myocardial ischemia was not the culprit for this case of regional pericarditis.

Coronary vasospasm was ruled out as seen on coronary angiography [Figure 7]. This is a likely differential diagnosis when considering regional pericarditis; however, we did not feel coronary angiography was suggestive of such a phenomenon.
Figure 7: Coronary artery angiogram, anterior-posterior caudal view, revealing no evidence of coronary artery vasospasm

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Cardiac magnetic resonance imaging (CMR) is an appropriate and great diagnostic tool and would have been beneficial in this case to confirm the diagnosis of regional pericarditis, but may not have assisted in the etiology. [7],[9]

In conclusion, all evidence as mentioned within is suggestive of a regional myo-pericarditis secondary to transmural myocardial cellular death due to an aggressive atrial-fibrillation ablation, which resolved with conservative therapy for traditional pericarditis.

 
  References Top

1.
Orme J, Eddin M, Loli A. Regional pericarditis status post cardiac ablation: A case report. N Am J Med Sci 2014;6:481-3.  Back to cited text no. 1
    
2.
Dorfman TA, Aqel R. Regional Pericarditis: A review of the pericardial manifestations of acute myocardial infarction. Clin Cardiol 2009;32:115-20.  Back to cited text no. 2
    
3.
Oliva PB, Hammill SC, Edwards WD. The electrocardiographic diagnosis of regional pericarditis in acute inferior myocardial infarction. Eur Heart J 1993;14:1683-91.  Back to cited text no. 3
    
4.
Oliva PB, Hammill SC, Edwards WD. Electrocardiographic diagnosis of postinfarction regional pericarditis. Ancillary observations regarding the effect of reperfusion on the rapidity and amplitude of T wave inversion after acute myocardial infarction. Circulation 1993;88:896-904.  Back to cited text no. 4
    
5.
Oliva PB, Hammill SC, Talano JV. Effect of definition on incidence of postinfarction pericarditis. It is time to redefine postinfarction pericarditis? Circulation 1994;90:1537-41.  Back to cited text no. 5
    
6.
Youssef G, Khouzam S, Sprung J, Bourke DL. Regional pericarditis mimicking myocardial infarction. Anesthesiology 2001;95:261-4.  Back to cited text no. 6
    
7.
Doulaptsis C, Goetschalckx K, Masci PG, Florian A, Janssens S, Bogaert J. Assessment of early post-infarction pericardial injury by CMR. JACC Cardiovasc Imaging 2013;6:411-3.  Back to cited text no. 7
    
8.
Haegeli LM, Kotschet E, Byrne J, Adam DC, Lockwood EE, Leather RA, et al. Cardiac injury after percutaneous catheter ablation for atrial fibrillation. Europace 2008;10:273-5.  Back to cited text no. 8
    
9.
Hendel RC, Patel MR, Kramer CM, Poon M, Hendel RC, Carr JC, et al., American College of Cardiology Foundation Quality Strategic Directions Committee Appropriateness Criteria Working Group; American College of Radiology; Society of Cardiovascular Computed Tomography; Society for Cardiovascular Magnetic Resonance; American Society of Nuclear Cardiology; North American Society for Cardiac Imaging; et al. ACCF/ACR/SCCT/SCMR/ASNC/NASCI/SCAI/SIR 2006 appropriateness criteria for cardiac computed tomography and cardiac magnetic resonance imaging: A report of the American College of Cardiology Foundation Quality Strategic Directions Committee Appropriateness Criteria Working Group, American College of Radiology, Society of Cardiovascular Computed Tomography, Society for Cardiovascular Magnetic Resonance, American Society of Nuclear Cardiology, North American Society for Cardiac Imaging, Society for Cardiovascular Angiography and Interventions, and Society of Interventional Radiology. J Am Coll Cardiol 2006;48:1475-97.  Back to cited text no. 9
    


    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7]



 

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