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Iran Red Crescent Med J. 2015 November; 18(11):e28697.
doi: 10.5812/ircmj.28697.
Published online 2015 August 10.
Case Report
Dressler Syndrome: A Case Report
Thiago Andrade Macedo,1,* Roberto Nery Dantas Junior,2 Pedro Gabriel Melo de Barros e Silva,1 and
Marcio Campos Sampaio3
1
Cardiology Division, Heart Institute (InCor), Medical School of University of Sao Paulo (FMUSP), Sao Paulo, Brazil
Cardiovascular MRI and CT Division, Heart Institute (InCor), Medical School, University of Sao Paulo (FMUSP), Sao Paulo, Brazil
Cardiovascular MRI and CT Division, Institute Dante Pazzanese of Cardiology (IDPC), Sao Paulo, Brazil
2
3
*
Corresponding author: Thiago Andrade Macedo, Cardiology Division, Heart Institute (InCor), Av Dr Eneas Carvalho de Aguiar, 44, Zip Code: 05403-904, Sao Paulo, Brazil. Tel:
+55-1135677586, Fax: +55-1126615948, E-mail: [email protected]
Received 2015 March 29; Revised 2015 June 13; Accepted 2015 July 14.
Abstract
Introduction: Dressler Syndrome should be considered in the differential diagnosis of chest pain, especially in patients who are in
a late stage of the evolution of the ischemic process.
Case Presentation: A 46-year-old male was admitted to the emergency department due to pleuritic chest pain. Two weeks before
this admission, he presented with a typical angina episode, likely an ST segment elevation myocardial infarction (STEMI), and did
not receive reperfusion therapy or any medical care. The patient’s electrocardiogram showed diffuse ST segment elevation and PR
segment depression, and his blood tests showed positive myocardial necrosis markers. A coronary angiography showed a proximal
occlusion (not recanalized) of the circumflex artery. There was a late gadolinium enhancement area seen through cardiac magnetic
resonance imaging (CMR), suggestive of recent transmural infarction, pericardial injury, and pleural effusion (inflammatory).
Conclusions: These findings strongly suggest the diagnosis of delayed post-infarction pericarditis, or Dressler Syndrome, a rare
disease in the age of reperfusion therapy. Although rare, it is a syndrome that must be considered in the differential diagnosis of
chest pain.
Keywords: Chest Pain, Myocardial Infarction, Pericarditis, Dressler Syndrome
1. Introduction
Dressler syndrome (DS) was first described by William
Dressler in 1956, after observing the late period development of an acute myocardial infarction (1). It is an
immuno-inflammatory disease similar to others that occur after myocardial injury, such as post-pericardiectomy
syndrome and post-traumatic pericarditis (2). After myocardial infarction (MI), injuries to the cardiac myocytes
expose myocardial antigens to the immune system, stimulating immune complex formation. This immune system
activation triggers a systemic immune-inflammatory response that may involve other organs, such as the pleura,
due to immune cross-reactions (3). The symptoms tend to
occur 2 - 3 weeks after MI, and may include pleuritic chest
pain and fever. A direct relationship between systemic
inflammation and myocardial ischemia has been demonstrated by several authors (2, 3).
2. Case Presentation
A 46-year-old male with hypertension and diabetes had
a 30-minute long episode of strong oppressive chest pain
during physical exertion, radiating to the jaw, but did
not seek medical care. Two weeks later, the patient came
to the emergency department of the heart institute (InCor) at the University of Sao Paulo, Brazil, in January of
2015, reporting pain of a different pattern: severe constrictive chest pain lasting one hour that worsened with
deep inspiration and while in a supine position. The physical examination demonstrated a blood pressure of 140/85
mmHg (semi-automatic digital sphygmomanometer, Omron 705CP, calibrated), tachycardia (105 bpm), temperature of 99.5°F, and no jugular venous distension. A pericardial friction sound was easily audible at the lower left
sternal border. Moreover, the electrocardiogram (EKG Machine, Philips PageWriter Trim III, calibrated) showed diffuse ST-segment elevation with a depression of the PR segment, mainly in DII (Figure 1), highly suggestive of pericarditis. Chest radiography showed a cardiac area in the
upper normal limit, and mild right pleural effusion. The
results of the laboratory blood tests were as follows: glucose = 307 mg/dl, CKMB = 5.8 ng/mL (normal = < 4 ng/mL),
troponin I = 18 ng/mL (normal = < 1.0 ng/mL), Hb = 15.2 g/l,
WBC = 8,600/µL (no predominance of younger lineages),
Copyright © 2015, Iranian Red Crescent Medical Journal. This is an open-access article distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0
International License (http://creativecommons.org/licenses/by-nc/4.0/) which permits copy and redistribute the material just in noncommercial usages, provided the
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Macedo TA et al.
Table 1. Patient’s Characteristics
Variables
Results
Age in years
46
Gender
Male
Symptoms
Chest pain worsening with deep inspiration
Pulse rate, bpm
105
Blood pressure, mmHg
140/85
Cardiac auscultation
Pericardial friction easily audible
WBC, µL
8,600
CKMB, ng/mL
5.8
Troponin I, ng/mL
18
ECG
Diffuse ST-segment elevation and depression of
the PR segment
X-ray radiography
Cardiac area in the upper normal limit
LVEF
0.34
CMR
Pericardial injury and pleural effusion
(inflammatory)
Abbreviations: CMR, cardiac magnetic resonance imaging; ECG, electrocardiogram; LVEF, left ventricle ejection fraction; WBC, white blood cell.
and platelets = 162,000. The lipid profile was normal, the
myocardial necrosis markers decreased progressively during an in-hospital stay, and the echocardiogram (GE Vivid
7) demonstrated inferolateral hypokinesia, with a left ventricle ejection fraction (LVEF) of 0.55, without pericardial
effusion. The clinical characteristics are described in Table
1.
The coronary angiography revealed proximal occlusion of the circumflex artery, without other stenosis, and
an angioplasty attempt was unsuccessful due to the impossibility of overcoming the obstruction. Cardiac magnetic resonance imaging (CMR) was performed to analyze
the pericardium, and to better characterize the extent of
the ischemia. A transmural inferolateral late gadolinium
enhancement was found, suggestive of fibrosis due to myocardial infarction (MI) (Figure 2A), with an underlying
area of no-reflow (microvascular obstruction, indicating a
recent injury), inferior akinesia (LVEF = 0.34), pericardial
injury (a small area of epicardial scarring in the left lateral
wall), and mild right pleural effusion (Figure 2B). A semiautomatic quantification of fibrosis determined a 7.6 g myocardial scar (8% of the total myocardial volume) by that
time (3 standard deviations and full width at half maximum, Circle CVI Software, version 4.2.1).
The clinical features of the patient’s chest pain (different from the initial pain two weeks before), and the highly
suggestive electrocardiogram and CMR findings suggest
late post MI pericarditis or Dressler Syndrome. The patient
2
received full anti-ischemic drug treatment, in addition to
aspirin at an anti-inflammatory dose of 2 g/day, and exhibited improvement in his chest pain. He was then discharged on the fourth day of hospitalization.
3. Discussion
A young patient (46-year-old) with hypertension and
diabetes was admitted to the emergency department complaining of chest pain. The presence of constrictive chest
pain in a patient with coronary artery disease risk factors
initially suggested acute myocardial ischemia. However,
the worsening of the chest pain upon deep breathing and
while in a supine position, in addition to a clear pericardial friction sound, could also indicate pericarditis. In the
clinical history, the patient had an initial complaint of typical angina two weeks previously, followed by the actual
pleuritic chest pain which led him to our emergency department. The electrocardiogram, demonstrating diffuse
ST-segment elevation and depression of the PR, was highly
suggestive of pericarditis. In some cases, PR segment depression can occur even in the absence of ST-segment elevation, and may appear as the initial manifestation of acute
pericarditis (4).
The elevation of the myocardial necrosis markers may
indicate coronary ischemia or the myopericardial pathological process known as myopericarditis. Patients with
acute coronary syndrome who develop great elevations
in their myocardial necrosis markers, especially without
reperfusion therapy (as in this case), are at a higher risk of
developing post-infarction pericarditis (5).
Interestingly, the markers collected upon admission
showed the typical kinetics of a subacute process of about
2 weeks: the CKMB was almost normal (5.8 ng/mL) and
the troponin, although still very high (18 ng/mL), was also
reducing progressively. The echocardiogram showed no
evidence of pericardial effusion, which is not mandatory
for the diagnosis of pericarditis. However, the evidence of
persistent chest pain, elevated myocardial necrosis blood
markers, and inferolateral hypokinesia without pericardial abnormalities, led to an early coronary angiography,
which detected a proximal occlusion of the circumflex
artery without the features of acute thrombosis. The suspicion of persistent ischemia motivated an attempt to perform angioplasty, which was not possible due to the inability to overcome the obstruction, reinforcing the hypothesis of a chronic or subacute injury to that coronary site.
The patient underwent a CMR to further determine the
ischemia burden, and for a better evaluation of the pericardium (6). Confirming the clinical hypothesis, the CMR
images showed inferolateral transmural necrosis (with
Iran Red Crescent Med J. 2015; 18(11):e28697.
Macedo TA et al.
Figure 1. Electrocardiogram Showing Diffuse ST Segment Elevation with Depression of the PR Segment, Mainly in DII
Figure 2. CMR images demonstrating: A, left ventricle inferolateral transmural fibrosis in white (arrow) and pericardial damage*; and B, late gadolinium enhancement
sequences (four chamber) with a small pleural effusion (arrow) (cine SSFP four chamber image); CMR: cardiac magnetic resonance imaging, SSFP: steady state free precession.
features of subacute evolution), subtle pericardial involvement (but with no effusion), and evident right pleural effusion, which is an inflammatory signal described in DS
Iran Red Crescent Med J. 2015; 18(11):e28697.
(Figure 2B). The patient’s history, laboratory, and imaging findings led to the hypothesis of an acute MI without
reperfusion therapy two weeks before his visit to the emer-
3
Macedo TA et al.
gency department, which was complicated by late pericarditis, strongly suggesting the possibility of DS. In the
case described, the immuno-inflammatory response was
suggested by the presence of pleural effusion, similar to
other descriptions of the clinical presentation of DS (7),
correctly evidenced by the CMR (Figure 2B).
There was an interval of two weeks between the typical angina (probably related to the MI) and the new chest
pain with characteristics of pericardial involvement. The
diagnosis of DS requires the occurrence of pericardial injury in the subacute post-MI period. In a study of 15 cases
with characteristics of DS, the clinical presentation of pleuritic pain occurred up to the 21st day after the MI in 66.7% of
the patients (8).
Before the era of reperfusion, DS occurred after about
1% - 5% of the reported MIs; however, the incidence of DS
has declined dramatically, either after the advent of fibrinolysis (9) or after the spread of percutaneous reperfusion
treatment. A prospective study of 201 patients with acute
MIs undergoing thrombolytic therapy did not detect the
onset of DS in any patient undergoing early reperfusion (5).
Based on this finding, it was postulated that the decrease
in the infarct size promoted by the early coronary reperfusion, and the shorter exposure of the immune system to
the myocardial antigens, promoted the virtual disappearance of this entity (10, 11).
This case highlights the importance of the clinical assessment of patients admitted with chest pain. Although
rare, Dressler Syndrome should be considered in the differential diagnosis of chest pain, especially in patients who
are in a late stage of the evolution of the ischemic process.
This becomes especially important in developing countries, where many patients receive no reperfusion therapy
due to difficulties in accessing the healthcare system.
Acknowledgments
The authors would like to thank Valeria Costa Hong for
her guidance in the organization of the references.
4
Footnote
Authors’ Contribution: Study concept and design: Thiago Andrade Macedo; acquisition of data: Roberto Nery
Dantas Junior; analysis and interpretation of data: Pedro
Gabriel Melo de Barros e Silva and Marcio Campos Sampaio; drafting of the manuscript: Thiago Andrade Macedo;
critical revision of the manuscript for important intellectual content: Thiago Andrade Macedo; administrative,
technical, and material support: Pedro Gabriel Melo de Barros e Silva and Marcio Campos Sampaio; study supervision:
Thiago Andrade Macedo.
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