Pericarditis refers to inflammation of the lining of the heart known as the pericardium.
Inflammation of the pericardium can be acute or chronic:
Acute pericarditis is the most common pericardial disease. Although true incidence is difficult to quantify, acute pericarditis is estimated to be present in 1% of adults who present with ST elevation changes on an ECG to accident & emergency. In developed countries, acute pericarditis is most commonly secondary to a viral aetiology.
There are several terms used in the description of pericarditis and associated disorders:
The serous pericardium is a double layered membrane that surrounds the heart.
The pericardium is composed of a tough, outer fibrous layer and an inner, serous layer. The combined thickness of these layers is 1-2mm. The fibrous pericardium is a tough sac, which completely surround the heart but remains unattached.
The serous pericardium is composed of two membranes that line the heart. These are the parietal and visceral pericardium. Between these two membranes is a small volume of fluid.
The pericardium has three main physiological functions:
In developed countries, the majority of cases are due to a transient viral infection.
In most cases of acute pericarditis, the pericardial sac is acutely inflamed with infiltration of immune cells secondary to an acute infection or as manifestation of a systemic disease.
The aetiology of acute pericarditis is numerous:
Due to the usually benign disease course associated with a viral infection, an in-depth search for an underlying aetiology is not necessary in most cases. The need for inpatient admission and further investigations is guided by the likelihood of an underlying disorder on initial assessment and the presence of prognostic risk factors (discussed below).
This is a specific autoimmune form of acute pericarditis that occurs 2-3 weeks following a myocardial infarction.
Unlike the immediate post-myocardial infarction pericarditis due to direct inflammation from transmural infarction, Dressler’s syndrome is thought to be an autoimmune reaction to myocardial antigens post infarction.
These are factors associated with a worse prognosis and warrant search for an underlying aetiology and inpatient admission.
As discussed, the majority of cases are due to a viral infection and a relatively benign course. However, in the presence of major of minor risk factors, patients require inpatient admission and search for an underlying aetiology.
Major risk factors:
Minor risk factors:
The cardinal feature of acute pericarditis is chest pain.
Diagnosis is usually based on a typical history, characteristic ECG findings and exclusion of other causes.
Formal diagnosis of acute pericarditis is based on finding two of the following four features:
NOTE: based on 2015 European Society of Cardiology guidelines on pericardial disease
Patients with suspected acute pericarditis require formal assessment, blood tests, ECG, CXR and echocardiogram.
Selective blood tests may be completed based on suspected aetiology. These include cultures, virology, autoimmune screen or tuberculosis work-up.
The characteristic ECG findings are widespread saddle-shaped ST elevation with PR depression.
Most cases show ST elevation in both limb and chest leads. May be difficult to distinguish from myocardial infarction or benign repolarisation. T wave changes and q waves rarely seen in acute pericarditis, which would favour myocardial infarction. Reciprocal ST depression sometimes seen in aVR and V1 as shown in ECG above.
Useful to exclude an alternative diagnosis in any patient presenting with chest pain. In addition, helps exclude pneumonia if raised inflammatory markers. May show enlarged cardiac shadow if significant pericardial effusion.
In acute pericarditis, typically normal. Essential in patients with suspected pericardial effusion as helps to quantify amount and assess for any haemodynamic compromise of cardiac function.
Useful if concern regarding myocardial infarction or myocardial involvement. Able to look for any regional wall motion abnormalities that represent focal areas of myocardial dysfunction due to myocarditis or ischaemia.
Cardiac MRI and CT may be needed in specific cases. Cardiac MRI is useful for the assessment of myocardial involvement. CT is useful at assessment of surrounding pulmonary and pleural structures that may suggest a specific underlying cause (e.g. tuberculosis).
The mainstay of treatment for acute pericarditis is the use of NSAIDs, aspirin or colchicine.
In cases of idiopathic/viral acute pericarditis, the treatment involves NSAIDs/Aspirin +/- colchicine.
Specific causes of acute pericarditis should be treated according to the underlying disease. Medications above may be used in addition to definitive treatment.
Patients without major/minor risk factors or a suspected underlying aetiology can be managed as outpatients. Important to advise on restriction of physical activity until symptoms resolve or diagnostic tests (e.g. CRP/ECG) improve. In athletes, further minimal restriction of physical activity advised for three months.
The majority of patients with acute pericarditis make a good recovery.
In idiopathic/viral pericarditis, around 15-30% of patients without treatment will develop recurrent disease. Incessant (pericarditis for 4-6 weeks) and recurrent (repeated acute episodes) pericarditis can be problematic.
Rare, but serious, complications of acute pericarditis include cardiac tamponade and chronic pericarditis.
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