Dressler syndrome I24.1

The Dressler syndrome was first described in 1956 by William Dressler (1890-1969) (Bendjelid 2004).

A Dressler syndrome is a special form of pericarditis, a so-called late pericarditis, which occurs about 1 - 6 weeks after an acute myocardial infarction (Herold 2018).

The Dressler syndrome is associated with the following diseases:

• Currently after acute myocardial infarction
• in the context of a pulmonary embolism with considerable right ventricular strain (Erdmann 2009)

In the past, Dressler's syndrome was found in about 3 % - 4 % of patients with acute myocardial infarction. Nowadays it occurs only rarely. In his 2004 article " Is Dressler Syndrome Dead?", Bendjelid sees the reason for this on the one hand in the effective reperfusion therapies such as thrombolysis, coronary balloon angioplasty (PTCA) and stent implantation, but also in the immunomodulatory effect of the drugs such as beta-blockers, statins, angiotensin converting enzyme inhibitors (ACE inhibitors).

The etiology is not completely clear. Since antimyocardial antibodies are detectable in patients with Dressler syndrome, it is assumed that autoimmunological factors play a role. In another hypothesis, the cause is thought to be bleeding in the pericardial space caused by anticoagulants, which were previously used therapeutically more frequently in myocardial infarction (Erdmann 2009). Foris (2019) considers primarily an injury of mesothelial cells in the pericardium in combination with blood in the pericardial space to be responsible for the immunological reaction, which results in deposits of immune complexes in the pericardium. He describes the following predisposing factors:

• younger age
• Virus infections (adenoviruses, Coxsackie B viruses, human cytomegaloviruses etc.; virus titres are elevated in these patients, but no viruses are detectable in the pericardium or effusion fluid)
• greater myocardial damage during e.g. operations
• Pericarditis in the medical history
• Currently undergoing prednisone therapy
• Blood type B neg.
• Anesthesia with Halothane

• Fever
• Lassitude
• Chest Pain
• Breath-dependent thoracic pain (with involvement of the pleura)
• occasionally also dyspnoea, arthralgia or pulsus paradoxus (Foris 2019)

Echocardiography: Echocardiography is the standard procedure in the diagnosis of Dressler's disease. Echocardiography often reveals a pericardial effusion, the size, location, and hemodynamics of which can be readily assessed by echocardiography (see also pericardial tamponade).

In addition, myocardial dysfunction is found in the infarct area and general dysfunction due to any pericardial constriction.

Computed tomography / magnetic resonance imaging: The echo-free space behind the heart and, in the case of large effusions, also in front of the heart can be better assessed in computed tomography or magnetic resonance imaging than with the help of echocardiography (Herold 2018). Due to the different density values, it is also possible to differentiate between hemorrhagic and serous pericardial effusions with this type of examination (Maisch 2008).

Histologically, Dressler's syndrome shows an unspecific reaction of the pericardium with fibrin deposits (Erdmann 2009).

Laboratory

• Anti-SMA antibodies often detectable (Herold 2018)
• CRP increased
• Leucocytosis
• BSG increase

Auscultation

• occasionally pericardial drift
• Damping (with simultaneous pericardial effusion) (Erdmann 2009)
• Occasional heart rhythm disturbances (Kaiser 2002)
• Tachycardia (Foris 2019)

ECG

The ECG shows changes that are difficult to interpret due to the repolarization disorders caused by acute myocardial infarction (Erdmann 2009). Foris (2019) describes a global ST segment elevation and low voltage in the presence of larger effusions.

Pleuropneumonia (Erdmann 2009).

Re-infarction; to be distinguished from Dressler syndrome by differential diagnosis:

• after nitro administration the pain symptoms do not improve
• the ECG lacks evidence of newly occurring Q-waves
• no CK-MB reaction can be detected (Erdmann 2009)

The following complications can occur in the context of Dressler syndrome:

• Pleuritis
• Pleural effusion
• recurrent pericardial effusion

Oral anticoagulants should be avoided at all costs if Dressler's syndrome is proven, otherwise the risk of hemorrhagic pericarditis is significantly increased (Erdmann 2009).

In case of pain it is recommended to administer ASS or NSAID (e.g. Diclofenac 2-4 x 50 mg / d with appropriate stomach protection.

If no improvement can be achieved under these conditions, an attempt should be made to treat with corticosteroids (e.g. prednisolone 1 mg / kg bw/d for 2-3 weeks, followed by creeping out with a constantly reduced dose.

In rare cases, pericardial windowing may be necessary in recurrent pericardial effusion (Erdmann 2009).

The prognosis for the Dressler syndrome as a whole is good, but relapses are not rare. They are usually observed up to one year after the first event (Foris 2019).

Foris (2019) recommends that patients who have to undergo heart surgery and who are younger, have blood group B neg. or have a history of pericarditis or have been treated with a corticosteroid, should consider the possibility of Dressler's syndrome in the event of p. o. complaints.

1. Bentjelid K et al (2004) Is Dressler Syndrome Dead? chest Journal (126) Elsevier SienceDirect 1680-1682
2. Erdmann E (2009) Clinical Cardiology: Diseases of the heart, the circulation and the vessels near the heart. Springer publishing house S 342
3. Foris L A et al (2019) Dressler syndrome. StatPearls Publishing LLC. PubMed PMID: 28723017
4. Herold G et al (2018) Internal Medicine Herold Verlag SS 235, 255
5. Kaiser H et al (2002) Cortisone therapy: Corticoids in clinic and practice. Georg Thieme publishing house S 256
6. Maisch B et al (2008) New possibilities for the diagnosis and therapy of pericarditis. The internist 49: 18-25