Dressler's syndrome

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mohammed A. Sbeih, M.D.[2] Phone:617-849-2629; Cafer Zorkun, M.D., Ph.D. [3]

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

It was first characterized by William Dressler in 1956. It should not be confused with the Dressler's syndrome of hemoglobinuria named for Lucas Dressler, who characterized it in 1854.

Pathophysiology

Dressler's syndrome is believed to result from an autoimmune inflammatory reaction to myocardial neo-antigens. 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 then deposit onto the pericardium and causes the inflammation . The autoimmune response and syndrome may also appear after pulmonary embolism.

Viruses that have been associated with Dressler Syndrome include

1. coxsackie B virus
2. Adenovirus
3. Cytomegalovirus

Gross Pathology Images

Images courtesy of Professor Peter Anderson DVM PhD and published with permission © PEIR, University of Alabama at Birmingham, Department of Pathology

• 

  Fibrinous pericarditis: Gross, external view of localized pericarditis over an acute infarction.

Causes

• Coronary artery bypass grafting
• Myocardial infarction (heart attack)
• Pulmonary embolism

Differentiating Dressler's syndrome from other Conditions

• Dressler's syndrome typically occurs 2 to 10 weeks after a myocardial infarction has occurred.
• This differentiates Dressler's syndrome from the much more common post myocardial infarction pericarditis that occurs in 17% to 25% of cases of acute myocardial infarction between days 2 and 4 after the myocardial infarction.
• Dressler's syndrome also needs to be differentiated from 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.
• Congestive Heart Failure
• Influenza
• Acute anemia with or without GI bleed
• Uremia

Epidemiology and Demographics

In the setting of myocardial infarction, Dressler's syndrome occurs in about 7% of cases. 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 .

Natural History, Complications, 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

Symptoms

The syndrome consists of a persistent low-grade fever, and chest pain which is usually pleuritic in nature.

• Malaise/generalized weakness
• Irritability
• Decreased appetite
• Dyspnea (with or without hypoxia)
• Palpitations/tachycardia
• Arthralgias

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

Cardiovascular Examination

• A pericardial friction rub, and /or a pericardial effusion is present.
• On physical examination, often tachycardic with a pericardial friction rub heard on auscultation. This characteristic pericardial friction rub may disappear.
•  This can be secondary to either improvement in or worsening of accumulation of pericardial fluid.
• Additionally, patients may present with pulsus paradoxus (greater than 10 mmHg decrease in blood pressure with inspiration, and decreased pulse amplitude palpated on the radial artery).
• Some patients with DS may exhibit signs of pneumonitis (e.g., a cough, decreased oxygen saturation, fever).
• The pulmonary component to symptoms can be minimal with no pulmonary complaints, ranging all the way to significant respiratory distress with large pulmonary effusions.

Laboratory Findings

Elevated ESR.

Imaging Findings

• 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.
• Whilst definitive evaluation with formal echocardiogram is the gold standard, bedside cardiac ultrasound.
• 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.
• 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.
• An electrocardiograph (ECG) initially demonstrate ST segment elevation and T-wave inversion, such as with pericarditis. Further inflammation of the myocardium will also result in ST segment elevations. Both electrical alternans (variation in amplitude or directionality of QRS from beat to beat) and/or a low voltage QRS.

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.

NSAIDs such as ibuprofen should be avoided in the peri-infarct period as they:

1. Increase the risk of reinfarction
2. Adversely impact left ventricular remodeling
3. Block the effectiveness of aspirin

Management of Pericarditis After STEMI (DO NOT EDIT)

Class I

"1. Aspirin is recommended for treatment of pericarditis after STEMI.(Level of Evidence: B)"

Class III (Harm)

"1. Glucocorticoids and nonsteroidal antiinflammatory drugs are potentially harmful for treatment of pericarditis after STEMI. (Level of Evidence: B)"

Class IIb

"1. Administration of acetaminophen, colchicine, or narcotic analgesics may be reasonable if aspirin, even in higher doses, is not effective. (Level of Evidence: B)"

Sources

• The 2004 ACC/AHA Guidelines for the Management of Patients With ST-Elevation Myocardial Infarction

• The 2007 Focused Update of the ACC/AHA 2004 Guidelines for the Management of Patients with ST-Elevation Myocardial Infarction

See also

• Pericarditis
• Postpericardiotomy syndrome
• Myocardial infarction
• Coronary artery bypass graft

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