Pericarditis is inflammation of the pericardium, the two-layered sac surrounding the heart. The pericardium normally provides mechanical protection, helps maintain the heart's position and permits relatively frictionless cardiac movement through a small quantity of lubricating fluid between its layers. Inflammation can cause the layers to rub against one another, producing characteristic chest pain, and can increase pericardial fluid accumulation. Pericarditis may be acute, recurrent, incessant or chronic depending on its duration and clinical course. It differs anatomically from myocarditis and endocarditis because the principal inflammatory process is located in the pericardial sac rather than cardiac muscle or the inner cardiac lining.
Causes of Pericarditis are diverse. Viral infections are frequently implicated, although the exact pathogen is not always established. Other causes include bacterial or fungal infection, autoimmune and inflammatory diseases, malignancy, kidney failure, tuberculosis in relevant epidemiological settings, trauma, cardiac injury and certain medications. Pericarditis can also occur after myocardial infarction or cardiac surgery. In some cases it is classified as idiopathic when no specific cause is identified despite appropriate evaluation. Determining the cause matters because treatment and prognosis differ substantially between uncomplicated inflammatory pericarditis and conditions such as purulent bacterial infection, malignancy or tuberculosis.
The classic symptom is sharp or stabbing chest pain that may worsen with deep inspiration, coughing or lying flat and may improve when sitting upright or leaning forward. These characteristics reflect the movement of inflamed pericardial surfaces. A pericardial friction rub may sometimes be heard on examination, although it can be transient. Fever and inflammatory symptoms can accompany infection or systemic inflammation. Because chest pain has many potentially dangerous causes, characteristic features cannot safely establish the diagnosis by themselves, and acute coronary syndrome, pulmonary embolism, aortic disease and other emergencies may need to be excluded.
Diagnostic assessment commonly incorporates an electrocardiogram, inflammatory markers, cardiac biomarkers, echocardiography and clinical examination. Acute pericarditis can produce characteristic widespread ST-segment and PR-segment changes on an electrocardiogram, although patterns vary and are not diagnostic in isolation. Troponin can be elevated when inflammation extends into cardiac muscle, in which case the condition may be described as myopericarditis or perimyocarditis depending on the predominant involvement. Echocardiography can identify pericardial effusion and assess whether the accumulated fluid is impairing cardiac filling.
Pericardial effusion is an accumulation of excess fluid in the pericardial space and can accompany Pericarditis. A small effusion may have little physiological effect, but rapidly accumulating or large effusions can compress the heart. Cardiac tamponade occurs when pericardial pressure becomes sufficiently high to impair cardiac chamber filling and reduce effective cardiac output. This is a medical emergency and can cause hypotension, tachycardia, raised venous pressure and other signs of circulatory compromise. The speed of fluid accumulation is important because a rapidly developing effusion can cause tamponade with a smaller volume than a slowly accumulating effusion.
Treatment depends on the underlying cause and severity. For uncomplicated acute inflammatory pericarditis, anti-inflammatory treatment is commonly used, often with colchicine to reduce symptoms and recurrence risk when clinically appropriate. Aspirin or another non-steroidal anti-inflammatory drug may be selected according to the circumstances, contraindications and underlying cause. Corticosteroids can be useful in selected situations but are not routinely preferred when effective alternatives exist because they can increase recurrence risk in some settings. Bacterial, tuberculous or malignant causes require disease-specific treatment rather than simply treating inflammation.
Recurrent Pericarditis is a recognised complication and can occur after an initial episode has resolved. Recurrences may reflect persistent inflammation, immune mechanisms or inadequate control of the original process. Colchicine has an important role in reducing recurrence in appropriately selected patients. Chronic inflammation can occasionally lead to constrictive pericarditis, in which the pericardium becomes thickened, scarred or less compliant and restricts cardiac filling. Constrictive disease can produce systemic venous congestion and heart-failure-like symptoms and may require advanced imaging, haemodynamic assessment or surgical pericardiectomy in selected severe cases.
A common misconception is that all Pericarditis is harmless because many uncomplicated cases resolve well. The condition can occasionally cause tamponade, recurrent inflammation, constrictive physiology or myocardial involvement, and chest pain requires appropriate assessment because several life-threatening diseases have similar symptoms. Another misconception is that pericardial effusion automatically means tamponade; effusion describes fluid accumulation, whereas tamponade describes haemodynamic impairment caused by pressure. Correct diagnosis therefore depends on clinical context, imaging, electrocardiographic findings and assessment for complications rather than the presence of chest pain alone.
