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Media
Powerpoint slides on Dressler's syndrome Images of Dressler's syndrome Photos of Dressler's syndrome Podcasts & MP3s on Dressler's syndrome Videos on Dressler's syndrome
Evidence Based Medicine
Cochrane Collaboration on Dressler's syndrome Bandolier on Dressler's syndrome TRIP on Dressler's syndrome
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Definitions of Dressler's syndrome
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Healthcare Provider Resources
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VisualWikitext

Revision as of 00:34, 1 January 2020

For patient information click here

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Abdelrahman Ibrahim Abushouk, MD [2]; Mohammed A. Sbeih, M.D.[3]; Cafer Zorkun, M.D., Ph.D. [4]; Nabeel Ahmed, M.B.B.S

Synonyms and keywords: Postmyocardial infarction syndrome; PMIS; Post-cardiac injury syndrome

Overview

Dressler's syndrome or post myocardial infarction syndrome is a form of pericarditis that occurs in the setting of injury to the heart as a result of myocardial infarction. Dressler's syndrome typically occurs 2 to 10 weeks after myocardial infarction. This differentiates Dressler's syndrome from the much more common post myocardial infarction pericarditis which occurs between days 2 and 4 after myocardial infarction.

Historical Perspective

Dressler's syndrome was first characterized by William Dressler in 1956.
It should not be confused with the Dressler's syndrome of hemoglobinuria, named after Lucas Dressler who characterized it in 1854.^[1]^[2]^[3]

Classification

There is no established system for the classification of Dressler's syndrome.

Pathophysiology

Although the exact cause remains unknown, Dressler's syndrome is believed to result from an autoimmune inflammatory reaction to myocardial neo-antigens, as well as injury to the mesothelial pericardial cells.
It usually occurs within weeks or months of the infarction due to antimyocardial antibodies; this begins with myocardial injury that releases cardiac antigens and stimulates antibody formation.
The immune complexes that are generated as anti-actin and actomycin antibodies deposit onto the pericardium and causes inflammation.
The autoimmune response and syndrome may also develop secondary to pulmonary embolism.^[4]

Gross Pathology

Image courtesy of Professor Peter Anderson, DVM PhD. Published with permission © PEIR, University of Alabama at Birmingham, Department of Pathology^[5]

Causes

The common causes of Dressler's syndrome include:

Surgeries associated with myocardial damage as
- Coronary artery bypass grafting and
- Aortic valve replacement.
Myocardial infarction
Pulmonary embolism

Differentiating Dressler's Syndrome from other Diseases

Dressler's syndrome typically occurs 2 to 10 weeks after a myocardial infarction has occurred.^[6]^[7] This differentiates Dressler's syndrome from

Post myocardial infarction pericarditis that occurs in 17,000 to 25,000 in every 100,000 cases of acute myocardial infarction between days 2 and 4 after the myocardial infarction.

Pulmonary embolism, another identifiable cause of pleuritic (and non-pleuritic) chest pain in people who have been hospitalized and/or undergone surgical procedures within the preceding weeks.

Further, Dressler's syndrome should be differentiated from:

Congestive Heart Failure
Influenza
Acute anemia with or without gastrointestinal bleeding
Uremia

Epidemiology and Demographics

Incidence: In the setting of myocardial infarction, Dressler's syndrome occurs in about 3 to 4% of MI cases.^[8]
Dressler's syndrome was more commonly seen in the era prior to reperfusion, but its incidence has markedly decreased in the reperfusion era, presumably because of smaller infarct sizes.^[9]
Age: Dressler's syndrome occurs more often in younger age groups.
Gender: There is no gender predilection for Dressler's syndrome.
Race: There is no racial predilection for Dressler's syndrome.
Mortality rate: The mortality rate can reach up to 60% in hospital setting.

Risk Factors

The risk of Dressler's syndrome increases with the size of the infarction.
Further, a former episode of Dressler's syndrome increases the risk of relapse upon recurrent MI.
Epidemiological studies showed a higher risk ratio of Dressler's syndrome with:

- Cardiac surgeries associated with greater myocardial damage as aortic valve replacement.
- Younger age
- Prior treatment with prednisone
- B -ve blood type
- Halothane anesthesia
- Viral infections that have been associated with Dressler's syndrome (based on the seasonal variations in incidence and elevated blood levels of viral components in Dressler's Syndrome patients) include:

Screening

There is insufficient evidence to recommend routine screening for Dressler's syndrome.

Natural History, Complications, and Prognosis

Pericardial effusion may result from the accumulation of fluids as a result of inflammation in the pericardial sac.
Cardiac tamponade can occur if the accumulation of fluids in the pericardium is large enough and rapid enough.Classic findings of tamponade include Beck's triad:
- Low blood pressure
- Distended neck veins (JVD)
- Muffled/distant heart tones
Constrictive pericarditis can occur if there is a chronic inflammatory response

Diagnosis

Diagnostic Study of Choice

2017 Revised ESC Guidelines for the Management of ST-Elevation Myocardial Infarction (DO NOT EDIT)

Diagnostic criteria do not differ from those for acute pericarditis including two of the following criteria: (i) pleuritic chest pain (85–90% of cases); (ii) pericardial friction rub (<_33% of cases); (iii) ECG changes (<_60% of cases), with new widespread ST-segment elevation, usually mild and progressive, or PR depression in the acute phase; and (iv) pericardial effusion (<_60% of cases and generally mild).

History and Symptoms

The syndrome consists of a persistent low-grade fever, and chest pain which is usually pleuritic in nature.The symptoms tend to occur after a few weeks or even months after myocardial infarction and tend to subside in a few days.

Physical Examination

Pericardial friction rub: This characteristic sign may disappear secondary to either improvement in or worsening of accumulation of pericardial fluid
Tachycardia
Pulsus paradoxus (>10 mmHg decrease in blood pressure with inspiration and decreased pulse amplitude on the radial artery).
Signs of pneumonitis (e.g., a cough, decreased oxygen saturation, fever).
Minimal respiratory symptoms to significant respiratory distress with large pleural effusions.

Laboratory Findings

Blood cultures should be obtained early in the workup of DS as this will help differentiate between an inflammatory versus an infectious cause of the patient’s condition. In the case of true DS, blood cultures should be negative.

Laboratory studies that may help point toward a diagnosis of DS include an elevated white blood cell count (with a leftward shift) and elevated acute phase reactants (e.g., erythrocyte sedimentation rate and C-reactive protein). Additionally, there may be a high titer of anti-heart antibodies present in serology.

If it is possible, pericardial fluid (e.g., through a pericardial drain) should be examined for cell count, differential, cultures, Gram stain, cytology, total protein, and triglyceride levels

Electrocardiogram

An electrocardiograph (ECG) may demonstrate

ST segment elevation
T-wave inversion (as with pericarditis).
PR depression
Variations in the amplitude or directionality of QRS from beat to beat and/or a low voltage QRS.

Widespread concave ST elevation and PR depression is present throughout the precordial (V2-6) and limb leads (I, II, aVL, aVF). Case Courtesy of Ed Burns ^[10]

X-ray

A chest x-ray will reveal flattening of the costophrenic angles and be employed if echocardiography is not available enlargement of the cardiac silhouette as a result of both pleural and pericardial effusions.^[11]

Echocardiography or Ultrasound

An echo will allow for evaluation of the pericardial fluid, if present, and help discern the exact cause of reduced cardiac output (i.e., determine whether truly DS or another condition such as congestive heart failure).
An echo will further allow for evaluation of ventricular contractility, in addition to assessment of the potential risk of cardiac tamponade (i.e., if cardiac chambers appear compressed by pericardial fluid). The more pericardial fluid that is accumulated, the easier it is to detect its presence by echocardiography.^[12]
Whilst definitive evaluation with formal echocardiogram is the gold standard, bedside cardiac ultrasound.

CT Scan

MRI

If it is difficult to assess the posterior pericardium with an echo, cardiac magnetic resonance imaging (MRI) may employed to determine whether there is an effusion present. In some instances, fluid collections become loculated.^[13]

Other Imaging Findings

There are no other imaging findings associated with Dressler's syndrome.

Other Diagnostic Studies

There are no other diagnostic studies associated with Dressler's syndrome.

Treatment

Medical Therapy

Dressler's syndrome is typically treated with high dose (up to 650 mg PO q 4 to 6 hours) enteric-coated aspirin. Acetaminophen can be added for pain management as this does not affect the coagulation system. Anticoagulants should be discontinued if the patient develops a pericardial effusion.^[14]