An ECG showing pericarditis. Note the ST elevation in multiple leads with slight reciprocal ST depression in aVR.
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Acute pericarditis is a type of pericarditis (an inflammation of the sac surrounding the heart, the pericardium) usually lasting < 6 weeks. It is by far the most common condition affecting the pericardium.
Symptoms and Signs
Chest pain is one of the common symptoms of acute pericarditis. It is usually of sudden onset, occurring in the anterior chest and may be pleuritic in nature --- that is, sharp and worsens with inspiration, due to concomitant pleural inflammation. The pain may be alleviated with sitting up and leaning forward while worsened with lying down, and also may radiate to the back, to one or both trapezius ridges. However, the pain can also be dull and steady, resembling the chest pain in an acute myocardial infarction. As with any chest pain, other causes must also be ruled out, such as GERD, pulmonary embolism, muscular pain, etc.
Pericardial rub is a very specific sign of acute pericarditis, meaning the presence of this sign invariably indicates presence of disease. However, absence of this sign does not rule out disease. This rub can be best heard by the diaphragm of the stethoscope at the left sternal border arising as a squeaky or scratching sound, resembling the sound of leather rubbing against each other. This sound should be distinguished from the sound of a murmur, which is similar but sounds more like a "swish" sound than a scratching sound. The pericardial rub is said to be generated from the friction generated by the two inflamed layers of the pericardium; however, even a large pericardial effusion does not necessarily present a rub. The rub is best heard during the maximal movement of the heart within the pericardial sac, namely, during atrial systole, ventricular systole, and the filling phase of early ventricular diastole.
Fever may be present since this is an inflammatory process.
One of the most feared complications of acute pericarditis is cardiac tamponade. Cardiac tamponade is accumulation of enough fluid in the pericardial space --- pericardial effusion --- to cause serious obstruction to the inflow of blood to the heart. This condition is fatal if not treated promptly. Another, longer term, complication is if pericarditis recurs over a longer period of time (normally more than 3 months), it can become constrictive pericarditis. Recent studies have shown this to be an uncommon complication. The definitive treatment for constrictive pericarditis is pericardial stripping, which is a surgical procedure where the entire pericardium is peeled away from the heart.
According to a recent article, the most common causes of acute pericarditis include:
- (35%) Neoplastic
- (23%) Autoimmune
- (21%) Viral - adenovirus, enterovirus, cytomegalovirus, influenza virus, hepatitis B virus, and herpes simplex virus, etc.
- (6%) Bacterial (other than tuberculosis)
- (6%) Uremia
- (4%) Tuberculosis
- (4%) Idiopathic
- (remaining) trauma, drugs, post-AMI, myocarditis, dissecting aortic aneurysm, radiation
- Acute and recurrent pericarditis
- Pericardial effusion without major hemodynamic compromise
- Cardiac tamponade
- Constrictive pericarditis
- Effusive-constrictive pericarditis
Acute pericarditis is characterised by the inflammation of the pericardial sac.
Molecular markers. Acute pericarditis is associated with a modest increase in serum creatine kinase MB (CK-MB) and cardiac troponin I (cTnI), both of which are also markers for myocardial injury. Therefore, it is imperative to also rule out acute myocardial infarction in the face of these biomarkers. The elevation of these substances is related to inflammation of the myocardium. Also, ST elevation on EKG (see below) is more common in those patients with a cTnI > 1.5 µg/L. Coronary angiography in those patients should indicate normal vascular perfusion. The elevation of these biomarkers are typically transient and should return to normal within a week. Persistence may indicated myopericarditis. Troponin levels increase in 35 - 50% of people with pericarditis.
Electrocardiogram (EKG). EKG changes in acute pericarditis mainly indicates inflammation of the epicardium (the layer directly surrounding the heart), since the fibrous pericardium is electrically inert. For example, in uremia, there is no inflammation in the epicardium, only fibrin deposition, and therefore the EKG in uremic pericarditis will be normal. Typical EKG changes in acute pericarditis includes
- stage 1 -- diffuse, positive, ST elevations with reciprocal ST depression in aVR and V1. Elevation of PR segment in aVR and depression of PR in other leads especially left heart V5, V6 leads indicates atrial injury.
- stage 2 -- normalization of ST and PR deviations
- stage 3 -- diffuse T wave inversions (may not be present in all patients)
- stage 4 -- EKG becomes normal OR T waves may be indefinitely inverted
Because the most common cause of ST elevation is an acute myocardial infarction, and since acute pericarditis can also be a short term complication after an acute myocardial infarction, steps must be taken to differentiate the two EKG readings.
Rarely, electrical alternans may be seen, depending on the size of the effusion.
Chest X-ray. Usually normal in acute pericarditis, but can reveal cardiomegaly (enlarged heart) if the pericardial effusion is more than 200 mL. Conversely, patients with unexplained new onset cardiomegaly should always be worked up for acute pericarditis.
Echocardiogram. Usually normal in acute pericarditis but can reveal pericardial effusion, the presence of which supports the diagnosis, although its absence does not exclude the diagnosis.
Patients with uncomplicated acute pericarditis can generally be treated and followed up in an outpatient clinic. However, those with high risk factors for developing complications (see above) will need to be admitted to an inpatient service, most likely an ICU setting. High risk patients include:
- subacute onset
- high fever (> 100.4 F/38 C) and leukocytosis
- development of cardiac tamponade
- large pericardial effusion (echo-free space > 20 mm) resistant to NSAID treatment
- history of oral anticoagulation therapy
- acute trauma
- failure to respond to seven days of NSAID treatment
- presence of moderate or severe cardiac tamponade
- diagnostic purpose for suspected purulent, tuberculosis, or neoplastic pericarditis
- persistent symptomatic pericardial effusion
NSAIDs in viral or idiopathic pericarditis. In patients with underlying causes other than viral, the specific etiology should be treated. With idiopathic or viral pericarditis, NSAID is the mainstay treatment. Goal of therapy is to reduce pain and inflammation. The course of the disease may not be affected. The preferred NSAID is ibuprofen because of rare side effects, better effect on coronary flow, and larger dose range. Depending on severity, dosing is between 300–800 mg every 6–8 hours for days or weeks as needed. An alternative protocol is aspirin 800 mg every 6–8 hours. Dose tapering of NSAIDs may be needed. In pericarditis following acute myocardial infarction, NSAIDs other than aspirin should be avoided since they can impair scar formation. As with all NSAID use, GI protection should be engaged. Failure to respond to NSAIDs within one week (indicated by persistence of fever, worsening of condition, new pericardial effusion, or continuing chest pain) likely indicates that a cause other than viral or idiopathic is in process.
Colchicine can be used alone or in conjunction with NSAIDs in prevention of recurrent pericarditis and treatment of recurrent pericarditis. For patients with a first episode of acute idiopathic or viral pericarditis, they should be treated with an NSAID plus colchicine 1–2 mg on first day followed by 0.5 daily or BID for three months. 
Corticosteroids are usually used in those cases that are clearly refractory to NSAIDs and colchicine and a specific cause has not been found. Systemic corticosteroids are usually reserved for those with autoimmune disease.
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