Pericarditis implies inflammation of the pericardium – a thin fibro-elastic sac that encases your heart. It can be acute, subacute, recurrent, or chronic pericarditis. A diagnosis of pericarditis takes a toll on the intervening clinician because of the various more sinister mimics. It is for this reason that a clinician always consults with a cardiologist before they start treatment. Complications, though rare, may include pericardial effusion, cardiac tamponade, and constrictive pericarditis. Despite an excellent outcome, recovery from the disease takes weeks or months: so, patience and compliance from the patient, attendants, as well as, health care providers are paramount to achieving complete remission. Viruses are notably the most encountered culprits; however, tuberculosis pericarditis remains a disease of public importance in low- and middle-income countries. Today, we go all-in on the nitty-gritty surrounding pericarditis and how to go about it. We also emphasize the need to consult with a specialist before you commit to treating the disease.
The pericardium has two layers – visceral and parietal membranes, in between which is a serous fluid that is about 15 to 50 millilitres. The fluid lubricates the heart as the sac encases it to hold it within the thoracic cavity (chest walls). Pericarditis is the inflammation of this sac. Inflammation may cause scarring and thickening resulting in constriction (constrictive pericarditis). The process may also follow a myocardial injury like following a heart attack.
Besides constriction, fluid may accumulate around the heart – a pericardial effusion. It may compromise heart function leading to cardiac tamponade. It is noteworthy that such fluid may be haemorrhagic (bloody), serous (serum-like, amber yellow), or purulent (pus-like). Also, the compromise in heart functioning doesn’t necessarily depend on how much fluid accumulates but the accumulation rate.
Pericarditis can either be due to an infectious or non-infectious cause.
Infectious causes: viruses are the most notable culprits – parvovirus B19, coxsackieviruses A and B, adenoviruses, HIV, CMV, EBV, and influenza. Tuberculosis tops the bacterial causes of pericarditis. Others include streptococcus, staphylococcus, pneumococcus, meningococcus, and Coxiella burnetii. People with low immunity are prone to fungal infections or parasites like toxoplasma.
Cancer from distant sites (metastases), systemic lupus erythematosus, rheumatoid arthritis: Bechet’s disease, uraemia, and myxoedema, as well as trauma, are the non-infectious causes. In a few instances, certain drugs have been implicated: such as hydralazine, procainamide, isoniazid, ipilimumab, nivolumab, and some monoclonal antibodies. Sarcoidosis and amyloidosis are other critical diseases that may be associated with pericarditis. However, for about 90%, we cannot delineate the culprit – so we call it idiopathic pericarditis.
Acute pericarditis affects more men than women between 20 and 50 years. It is a frequent cause of chest pain. It is imperative not to mistake it for angina, pleurisy, or pneumonia.
Lasting less than six weeks, it is acute pericarditis. More than six weeks but less than three months, that’s subacute pericarditis. Anything more than three months falls under chronic pericarditis. It is recurrent pericarditis if you develop similar symptoms after complete remission 4 to 6 weeks later.
Classically, chest pain is retrosternal (behind the breast bone), sharp, and severe: worsens with deep breathing (pleuritic): and improves with sitting and leaning forward (positional). It may radiate to the shoulder and neck. You may have a fever in case of infectious causes and palpitations. With constrictive pericarditis, a compromise in function results in leg and belly (abdominal) oedema. Shortness of breath may also be present.
Do watch out for unintentional weight loss in case of tuberculosis and malignancies. Unlike stable angina, chest pain in pericarditis neither worsens by exertion nor emotion. But varied presentations may occur. Be on the lookout.
As with most heart diseases, auscultation of the chest is paramount. In acute pericarditis, we pick up a left parasternal pericardial friction. We describe it as a rasping, scratchy triphasic sound. The sounds correspond to the pericardial rubbing, which occurs in atrial and ventricular systole and early ventricular diastole. When present, it confirms acute pericarditis but, its absence doesn’t rule out the disease.
We often do basic and specific tests to aid us in delineating diagnosis. They include complete blood count, c-reactive protein, erythrocyte sedimentation rate, and basic metabolic panel: liver function tests, electrocardiography, echocardiography, cardiac enzymes, chest X-ray, with or without cardiac MRI. We may require more investigations in case of autoimmune diseases like lupus and rheumatoid arthritis.
A chest x-ray may delineate the heart size: the cardiac silhouette to ascertain the possibility of fluid around the heart – pericardial effusion. Electrocardiography will show signs of inflammation: echocardiography may show fluid collection around the pericardium.
We cannot ascertain the cause of pericarditis in 90% of the scenarios; however, the aim remains to identify the cause and manage pain. Nonsteroidal anti-inflammatory drugs (NSAIDs) are the gold standard for pain management. Colchicine treats and prevents recurrences. For cases like TB pericarditis, prednisone will reduce the risk of pericardial scarring. When fluid accumulates beyond a certain level, we will drain it through a procedure we call pericardiocentesis. It will prevent cardiac tamponade.
Rarely, pericarditis will need surgery to give the heart an extra space to function – pericardiectomy.
All that said, the prognosis after acute pericarditis is excellent; however, recovery takes weeks or months. It is imperative that you judiciously take your medications and comply. Call your clinician if your symptoms worsen. Do not exercise until you get a clearance from your primary doctor.