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Year : 2021  |  Volume : 5  |  Issue : 1  |  Page : 78-80

Pericardial Effusion Secondary to Dressler's Syndrome Leading to Intractable Ventricular Tachycardia: Pericardio (Centesis) - Cardioversion of an Electrical Tamponade

Department of Cardiology, Yashoda Hospitals, Hyderabad, Telangana, India

Date of Submission25-Mar-2020
Date of Decision07-Apr-2020
Date of Acceptance10-Apr-2020
Date of Web Publication04-Feb-2021

Correspondence Address:
Dr. Pankaj Jariwala
Department of Cardiology, Yashoda Hospitals, Somajiguda, Raj Bhavan Road, Hyderabad - 500 082, Telangana
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/jiae.jiae_12_20

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Post infarction pericarditis, Dressler's syndrome is a well-recognized condition, but its incidence has decreased in the present interventional era due to early reperfusion strategy. We encountered an unusual association of large pericardial effusion secondary to Dressler's syndrome and intractable ventricular tachycardia that reverted upon pericardiocentesis. We coined a term “electrical tamponade” to describe an electrical storm or high-grade ventricular arrhythmias secondary to pericardial effusion.

Keywords: Acute myocardial infarction/adverse effects, Dressler's syndrome, pericardial effusion/etiology, ventricular tachycardia/etiology

How to cite this article:
Jariwala P, Jadhav K. Pericardial Effusion Secondary to Dressler's Syndrome Leading to Intractable Ventricular Tachycardia: Pericardio (Centesis) - Cardioversion of an Electrical Tamponade. J Indian Acad Echocardiogr Cardiovasc Imaging 2021;5:78-80

How to cite this URL:
Jariwala P, Jadhav K. Pericardial Effusion Secondary to Dressler's Syndrome Leading to Intractable Ventricular Tachycardia: Pericardio (Centesis) - Cardioversion of an Electrical Tamponade. J Indian Acad Echocardiogr Cardiovasc Imaging [serial online] 2021 [cited 2021 Jul 23];5:78-80. Available from: https://www.jiaecho.org/text.asp?2021/5/1/78/308724

  Introduction Top

A gradually accumulating pericardial effusion can present in many atypical ways. Our patient had frequent ventricular premature complexes, bigeminy and ventricular tachycardia (VT) that did not respond to cardioversion and anti-arrhythmic therapy. It was not clear to us that such extreme ventricular irritability may have been caused by a large pericardial effusion and had not been reported. The rapid resolution of arrhythmias following drainage of the pericardial fluid has led us to believe that ventricular arrhythmia is yet another form of presentation of pericardial tamponade.

  Case Report Top

A 58-year-old male presented with 2 hour duration of sudden-onset palpitations and breathlessness. He did not complain of chest discomfort and any localized or radiating pain to the shoulders. On arrival in the emergency room, the vital parameters showed a heart rate of 190 beats/min, blood pressure of 90/60 mmHg, respiratory rate of 24/min, and body temperature of 38.4°C. There was no pleuro-pericardial friction rub on auscultation. Electrocardiogram demonstrated monomorphic VT with right bundle branch block [Figure 1]a. Echocardiography showed a large pericardial effusion, with early cardiac tamponade features [Figure 2]a, [Figure 2]b, [Figure 2]c, [Figure 2]d. Additional findings were regional wall motion abnormalities of the inferoposterior wall with mild left ventricular dysfunction (ejection fraction – 45%). He had a posterior wall ST-segment myocardial infarction (MI), which was not thrombolysed for which he had percutaneous transluminal coronary angioplasty 2 weeks earlier. Before the start of the procedure, anticoagulation in the form of unfractionated heparin was given (100 units/kg). Post procedure, as there was no demonstrable thrombus, he did not receive any anticoagulation as per our institutional routine. He did not require the implantation of temporary pacing lead.
Figure 1: (a) Electrocardiogram done in the emergency room demonstrated monomorphic wide QRS tachycardia of right bundle branch block morphology. (b) Upon cardioversion and administration of anti-arrhythmic medications, multiple episodes of short runs of nonsustained ventricular tachycardia, triplets and couplets were recorded. (c) Cardiac monitor showing restoration of normal sinus rhythm in the catheterization laboratory following pericardiocentesis. (d) Post pericardiocentesis, electrocardiography showed normal sinus rhythm, QS pattern in leads II, III, and aVF, and early R/S transition in leads V1–3

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Figure 2: (a-d) Echocardiography in short axis at the level of the mid ventricles (panel a), parasternal (panel b), subcostal (panel c), and modified four-chamber (panel d) views demonstrating large pericardial effusion

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Direct current cardioversions (220 and 300 J), intravenous magnesium sulphate and lignocaine did not convert to regular sinus rhythm, and several short runs of VT were observed [Figure 1]b.

Pericardiocentesis was performed through a subxiphisternal approach as we did not find any other cause for the intractable arrhythmia, and 450 ml of hemorrhagic pericardial fluid was removed. Normal sinus rhythm was restored during the procedure after the initial drainage of 50 ml [Figure 1]c and [Figure 1]d. Postprocedure chest X-ray revealed mild cardiomegaly without signs of pleural involvement [Figure 3]. His laboratory parameters, including serum electrolytes, were normal except for mild elevation of serum creatinine secondary to prolonged hypotension, which normalized with hydration for 24 h.
Figure 3: After emergency pericardiocentesis, the chest X-ray showing mild cardiomegaly with enhanced bronchovascular markings, and bilateral costo-phrenic angles appeared clear. Also, the pigtail catheter inserted into the pericardial space via subxiphisternal approach is seen along the cardiac silhouette

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Pericardial fluid was exudative with a plenty of red blood cells (hemorrhagic). It was tested negative for malignancy, tuberculosis, or other infectious diseases. The patient was discharged following observation with advice of dual antiplatelet agents, beta-blocker, oral amiodarone, angiotensin-converting enzyme inhibitor, and high-dose statin. He did not receive any form of steroids during or after hospitalization. During 1 year of follow-up, the patient had no recurrence of symptoms.

  Discussion Top

In 1956, William Dressler provided the original description of the condition after his study of ten patients who were admitted to the Maimonides Hospital. “In 10 cases of post MI, there accompanied by a febrile complication that causes idiopathic pleuritis and/or pneumonitis, idiopathic pericarditis. In eight instances, pericardial friction rub was detected. In two cases, roentgenological evidence of pericardial effusion has been found. In seven cases pleural effusion occurred. A unusual temperature curve was correlated with the symptoms of pericarditis, which was associated with prolonged periods of low-grade fever and between elevated fever peaks there were chest pain flare-ups. In 7 of the 10 instances, leucocytosis, an occasional finding with counts as high as 35,000 cells per cubic millimetre, was present.”

It is a type of post-infarction pericarditis, an immune-inflammatory condition characterized by prolonged or persistent pleuritic chest pain, pulmonary infiltration, fever, higher erythrocyte sedimentation rate, and/or pericardial friction rub. This syndrome typically occurs 2–11 weeks after the infarction although it is recognized sometimes within the first week.[1],[2]

Patients with acute coronary syndrome who experience high elevations of their myocardial necrosis markers, particularly without reperfusion therapy (as in our case), are at higher risk of developing it. Recently, changing practices with easy access to faster reperfusion therapies, such as rapid thrombolysis with fibrin-specific fibrinolytic agents and primary percutaneous interventions, have reduced the size of the infarction, contributing to the shorter exposure to infarcted myocardial antigens to the immune system, minimizing the incidence of Dressler 's syndrome.[3]

Dressler also noticed that patients with recent MI had not been regularly screened for x-rays. When there is a small amount of effusion that can not be identified by chest X-rays and “heart enlargement” which suggests significant pericardial effusion can only be confirmed through serial roengentological studies.[1] He reported pericardial friction rub in approximately 13.8%–29% of cases. When postinfarction pericarditis was diagnosed on the basis of a friction rub alone, the average incidence of this disorder among patients without lytic therapy was 14%.[2] It was absent in our case as there was a large pericardial effusion, which prevented friction between the pericardium layers. In addition, in his series, only seven patients had evidence of pleural effusion on chest X-ray.

Choudhary and Mohanty reported the association between pericardial effusion and VT in their patient, who developed intractable VT following surgical replacement of the mitral valve. Cardioversion and antiarrhythmic drugs did not help, but pericardiocentesis, as in our case, aborted high-grade ventricular arrhythmias and, could revert it to normal sinus rhythm.[4] Kathrotia and Hindupur reported a case of purulent pericarditis which presented as atrial fibrillation with fast ventricular rate, which responded to pericardial drainage and anti-arrhythmic therapy.[5]

No reported case describing a secondary association of VT to post-MI-pericardial effusion, Dressler's syndrome, is identified in literature. We have therefore defined a new terminology as “electrical tamponade,” which describes the development of any persistent arrhythmia secondary to pericardial tamponade that responds only to pericardial drainage.

  Conclusion Top

This case highlights the significance of a thorough clinical assessment of patients those who present with palpitations following recent MI. Although rare, Dressler syndrome should be considered especially in patients with pericardial effusion in the differential diagnosis of post-acute coronary syndrome pericardial effusion. This is particularly relevant in developing countries, where many patients do not undergo reperfusion therapy because of difficulties in accessing the public health system. The literature had not previously described pericardial effusion and its relationship to ventricular arrhythmias.

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.


We thank Mr. Naveen Rao and Mr. Srinivas Rao for his technical assistance.

Financial support and sponsorship


Conflicts of interest

There are no conflict of interest.

  References Top

Dressler W. A post-myocardial infarction syndrome; preliminary report of a complication resembling idiopathic, recurrent, benign pericarditis. J Am Med Assoc 1956;160:1379-83.  Back to cited text no. 1
Simon K, Oliva PB, Hammill SC, Talano JV. Effect of definition on incidence of postinfarction pericarditis: Is it time to redefine postinfarction pericarditis? Circulation 1995;91:1611-2.  Back to cited text no. 2
Leib A, Foris L, Nguyen T, Khaddour K. Dressler Syndrome. StatPearls Publishing; 2020. Available from: https://www.ncbi.nlm.nih.gov/books/NBK441988/. [Last updated on 2020 Apr 05].  Back to cited text no. 3
Chowdhry V, Mohanty BB. Pericardial effusion causing ventricular arrhythmias: Atypical presentation. Ann Card Anaesth 2012;15:319-20.  Back to cited text no. 4
[PUBMED]  [Full text]  
Kathrotia A, Hindupur MR. Massive purulent pericardial effusion presenting as atrial fibrillation with rapid rate: Case report and review of the literature. Am J Case Rep 2014;15:504-7.  Back to cited text no. 5


  [Figure 1], [Figure 2], [Figure 3]


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