Dressler syndrome is a delayed immune-mediated or secondary pericarditis developing weeks to months after a myocardial infarction characterized by pleuritic chest pain, low-grade fever, and pericarditis. It is also called post-myocardial infarction syndrome.
Earlier the Dressler syndrome was quite common but the incidence has decreased owing to better reperfusion.
Dressler syndrome is now considered under the group postpericardiotomy syndrome which is a febrile illness secondary to an inflammatory reaction involving the pleura and pericardium.
As the name suggests, the peripericardiotomy syndrome is more common in patients who have undergone surgery that involves opening the pericardium.
Other presentations are following myocardial infarction (Dressler syndrome) and after percutaneous procedures such as coronary stent implantation, epicardial pacemaker leads and transvenous pacemaker leads, and following traumatic heart injury [blunt trauma, stab wounds, and heart puncture].
Post-pericardiotomy syndrome has been observed even after radiofrequency ablation and pulmonary vein isolation.
A classical Dressler syndrome or post-myocardial infarction syndrome usually occurs 2-5 weeks after the initial event but it can be delayed for as long as three months.
Dressler’s syndrome was first described in 1956. It is named after cardiologist William Dressler who described it.
Dressler syndrome is more likely to recur if there is a previous history of the syndrome. It seems more likely to occur after a large infarct.
The etiology is not well understood. Several possible suggested mechanisms include local inflammation, autoimmune response and latent viruses. There is a consensus that Dressler syndrome is most likely immune-mediated.
Though it is most commonly seen after transmural infarction, however, it may also be seen in milder forms of myocardial infarction too.
Clinical Presentation of Dressler Syndrome
Patients typically present from one week to few months after large myocardial infarction.
Typical symptoms include pleuritic chest pain and fever. The pain is often in the left shoulder, often pleuritic, and worse on lying down. There may be malaise, fever, and dyspnoea.
A pericardial friction rub may be heard [murmurs by auscultation]. The typical sound of pericarditis is described as the sound of boots walking over fresh snow.
Rarely, it may cause cardiac tamponade or acute pneumonitis.
- A further episode of angina or myocardial infarction
- Pulmonary embolism.
- CBC will show leukocytosis, sometimes with eosinophilia
- Elevated ESR.
- Heart autoantibodies on serology
- ECG may show ST elevation without reciprocal ST depression [typical of pericardial effusion]
- Echocardiography – pericardial effusion.
An x-ray may reveal nonspecific cardiac enlargement
- Pericardial effusion of varying size
- Thinning of the infarcted region
- Previous stents if a present
ECG-gated MR (cardiac MR or CMR) is the imaging modality of choice. It shows intense late post-gadolinium enhancement of entire pericardium and regional thinning and akinesis of the infarcted myocardium.
The clinical course is most often benign. Conservative management includes NSAIDs, steroids and colchicines.
Aspirin is the choice among NSAIDs and can be given in large doses.
Other NSAIDs may be used, especially if there are severe and recurrent symptoms.
Steroids can be used when severity requires pericardiocentesis, and when an infection has been excluded.
In resistant or recurrent cases, colchicine may be useful.
Significant pericardial effusion can necessitate relieving the constriction on the heart.
Cardiac tamponade and free wall rupture require urgent surgery.
- pleurisy and pleural effusion.
- cardiac tamponade.
- Constrictive pericarditis.
- Wessman DE, Stafford CM. The postcardiac injury syndrome: case report and review of the literature. South Med J. 2006 Mar
- Luckie M, Jenkins NP, Davidson NC, et al. Dressler’s syndrome following pulmonary vein isolation for atrial fibrillation. Acute Card Care. 200810(4):234-5.
- Steadman CD, Khoo J, Kovac J, et al. Dressler’s syndrome demonstrated by late gadolinium enhancement cardiovascular J Cardiovasc Magn Reson. 2009 Jul 2311(1):23.
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