Dressler Syndrome - A delayed complication of Myocardial Infarction. (QF_FR_077)

Dressler syndrome is a form of immune mediated pericarditis which occurs after damage to the heart muscles. The damage can result from a heart attack, heart surgery or a serious injury. It usually develops weeks to months after myocardial infarction. Symptoms of Dressler syndrome include chest pain, fever and shortness of breath. 
We present a case of 87-year-old man who presented to emergency with complaint of central chest pain radiating to left shoulder. His troponin levels were raised, and ECG showed changes of non-ST elevation MI. Diagnostic coronary angiogram revealed moderate stenosis along LAD at first diagonal bifurcation and severe ostial D1 stenosis. OCT to LAD showed suspicion of LAD plaque rupture. Patient was managed conservatively and an outpatient cardiac MR examination was planned. 

Diagnostic Techniques and Their Most Important Findings:

Cardiac MR was planned 6 weeks after the initial presentation of myocardial infarction. It was done on viability and adenosine stress perfusion protocol. 
Left ventricle appeared normal in size. Hypokinetic mid to apical anterior segments noted with overall left ventricular ejection fraction of 55%. There is >50% thickness late gadolinium enhancement involving mid to apical anterior segments in keeping with LAD territory infarct (two segments non-viable). No mismatched perfusion defect on stress imaging to suggest inducible ischemia. 
In addition, there was mild pericardial thickening with rim of fluid and late gadolinium enhancement, as well as sub-epicardial basal to mid lateral wall enhancement. Pericardial enhancement given the clinical history is suggestive of Dressler syndrome. No findings to suggest constrictive pericarditis.

Learning Points from this Case:

Dressler syndrome is a clinical condition characterized by sterile pericarditis that develops after a known cardiac injury. It is now considered a rare phenomenon with the evolution of reperfusion procedures.  It is believed that it develops via activation of the immune system in response to myocardial damage leading to pericarditis.
The case we presented was planned to have a Cardiac MR as an outpatient follow up after acute MI and was done 6 weeks post MI to evaluate the viability and any post MI complications. The pericardial enhancement in this context is quite confirmatory of Dressler syndrome.
The clinical course is usually benign. Conservative management helps including NSAIDs. It is very less likely to progress to tamponade or rupture but if happens need urgent surgical attention.