Pericarditis: Causes, Pathophysiology, Symptoms, Diagnosis, Management and Prevention

Pericarditis: Causes, Pathophysiology, Clinical Manifestations, Diagnosis and Management

~Introduction

Pericarditis refers to inflammation of the pericardium, the double-layered fibroserous sac surrounding the heart. The pericardium serves important physiological functions — it stabilizes the heart within the thoracic cavity, prevents excessive cardiac dilation, and acts as a barrier against infection and malignancy. However, when inflamed, it can cause chest pain, pericardial effusion, and, in severe cases, lead to cardiac tamponade or constrictive pericarditis.

Pericarditis is a relatively common cardiovascular disorder that may occur as an isolated condition or as part of systemic diseases. It can be acute, recurrent, or chronic, with causes ranging from viral infections to autoimmune diseases and malignancies. Understanding its clinical presentation, diagnostic approach, and management strategies is essential for timely and effective treatment.

~Anatomy and Physiology of the Pericardium

The pericardium consists of two layers:

1. Fibrous pericardium: A tough, inelastic outer layer that anchors the heart to surrounding structures such as the diaphragm and great vessels.

2. Serous pericardium: Divided into two sublayers:

   • Parietal layer (lining the inner surface of the fibrous pericardium)

   • Visceral layer (epicardium) (adhering directly to the heart)

Between these layers lies the pericardial cavity, containing 15–50 mL of lubricating fluid that reduces friction during cardiac movements.

Inflammation of this structure disrupts normal fluid balance and tissue integrity, leading to pain, effusion, and in some cases, hemodynamic compromise.

~Classification of Pericarditis

Pericarditis can be classified based on duration, etiology, or pathological features.

1. Based on Duration

• Acute Pericarditis: Lasts less than 6 weeks; most common type.

• Subacute Pericarditis: Persists between 6 weeks and 6 months.

• Chronic Pericarditis: Lasts longer than 6 months, often leading to constrictive pericarditis.

2. Based on Etiology

• Infectious Pericarditis: Caused by viruses, bacteria, fungi, or parasites.

• Non-infectious Pericarditis: Due to autoimmune diseases, trauma, metabolic disorders, or neoplasms.

3. Based on Pathological Findings

• Fibrinous (Dry) Pericarditis

• Serous Pericarditis

• Purulent (Suppurative) Pericarditis

• Hemorrhagic Pericarditis

• Caseous (Tuberculous) Pericarditis

~Etiology (Causes of Pericarditis)

The causes of pericarditis are diverse, and in many cases, the exact origin remains idiopathic. The main categories include:

1. Infectious Causes

• Viral: Most common cause; includes Coxsackievirus B, Echovirus, Adenovirus, Hepatitis B and C, HIV, and Influenza.

• Bacterial: Staphylococcus aureus, Streptococcus pneumoniae, Neisseria meningitidis, Mycobacterium tuberculosis (particularly in developing countries).

• Fungal: Candida, Histoplasma, Aspergillus (seen in immunocompromised individuals).

• Parasitic: Rare; includes Entamoeba histolytica, Toxoplasma gondii.

2. Non-Infectious Causes

• Autoimmune/Inflammatory Diseases: Systemic lupus erythematosus (SLE), rheumatoid arthritis, scleroderma, dermatomyositis, and vasculitis.

• Post-myocardial infarction:

  • Early pericarditis (within 24–48 hours)

  • Dressler’s syndrome (autoimmune, 2–6 weeks post-MI)

• Neoplastic: Secondary to metastases from lung, breast, or lymphomas; rarely primary pericardial tumors.

• Uremia: Seen in advanced chronic kidney disease.

• Trauma or Surgery: Post-cardiac surgery (post-pericardiotomy syndrome) or penetrating injury.

• Radiation-induced: After mediastinal irradiation for malignancies.

• Drug-induced: Certain medications like hydralazine, procainamide, and isoniazid can provoke pericardial inflammation.

In clinical practice, viral and idiopathic pericarditis constitute the majority of acute cases.

~Pathophysiology

The pathogenesis of pericarditis involves inflammation of the pericardial layers with subsequent changes in vascular permeability and fluid accumulation.

• Acute Inflammation: Leads to fibrin deposition and leukocyte infiltration, producing friction between the layers (fibrinous pericarditis).

• Pericardial Effusion: Increased capillary permeability causes fluid to collect in the pericardial space, varying in amount and composition (serous, purulent, or hemorrhagic).

• Tamponade: If effusion accumulates rapidly or extensively, it may compress the heart, impairing diastolic filling and reducing cardiac output.

• Chronic Inflammation: May result in fibrosis and calcification, restricting heart expansion — the hallmark of constrictive pericarditis.

~Clinical Manifestations

The hallmark of acute pericarditis is chest pain, but clinical presentation may vary based on the underlying cause and stage of disease.

1. Symptoms

• Chest pain: Sharp, pleuritic pain localized retrosternally or to the left chest, radiating to the neck, shoulder, or trapezius ridge. Pain worsens with inspiration or lying flat and improves when sitting forward.

• Fever: Low to moderate, often with malaise and fatigue.

• Dyspnea: Due to pain, anxiety, or large effusion.

• Cough or palpitations: Occasionally present.

2. Signs

• Pericardial friction rub: A characteristic, scratchy, triphasic sound best heard at the left lower sternal border when the patient leans forward.

• Tachycardia: Common due to pain or fever.

• Signs of pericardial effusion: Muffled heart sounds, distended neck veins, hypotension (Beck’s triad) suggest cardiac tamponade.

• Pulsus paradoxus: Exaggerated fall in systolic blood pressure during inspiration in tamponade.

3. In Chronic or Constrictive Pericarditis

• Fatigue and exercise intolerance

• Elevated jugular venous pressure

• Hepatomegaly, ascites, peripheral edema

• Kussmaul’s sign: Paradoxical rise in jugular venous pressure during inspiration

~Complications

1. Pericardial Effusion: Accumulation of excess fluid, which may be serous, hemorrhagic, or purulent.

2. Cardiac Tamponade: Life-threatening compression of the heart due to rapid effusion; leads to hypotension, muffled heart sounds, and jugular venous distension.

3. Constrictive Pericarditis: Fibrosis and calcification causing rigid pericardium and impaired ventricular filling.

4. Chronic Recurrent Pericarditis: Reappearance of symptoms after apparent recovery.

~Diagnosis

Diagnosis is primarily clinical, supported by electrocardiography, imaging, and laboratory findings.

1. Clinical Criteria (ESC 2015 Guidelines)

Acute pericarditis is diagnosed when two or more of the following are present:

1. Characteristic chest pain

2. Pericardial friction rub

3. ECG changes typical of pericarditis

4. New or worsening pericardial effusion

2. Electrocardiogram (ECG)

Classically shows diffuse, concave ST-segment elevation and PR-segment depression across multiple leads. These changes occur in four stages:

1. ST elevation and PR depression

2. ST normalization

3. T wave inversion

4. ECG normalization

3. Echocardiography

• Detects pericardial effusion, tamponade, or thickened pericardium.

• Important for monitoring effusion progression.

4. Laboratory Tests

• Elevated ESR, CRP, and leukocytosis indicating inflammation.

• Elevated cardiac enzymes (Troponin I, CK-MB) in myopericarditis.

• Blood cultures to identify infectious etiology.

• ANA and rheumatoid factor in suspected autoimmune causes.

• Renal function tests for uremic pericarditis.

5. Imaging Studies

• Chest X-ray: May show an enlarged, “water-bottle”-shaped cardiac silhouette in large effusions.

• CT or MRI: Useful for detecting pericardial thickening, calcification, or loculated effusions.

~Differential Diagnosis

Conditions that mimic pericarditis include:

• Acute myocardial infarction

• Pulmonary embolism

• Pleuritis

• Pneumonia

• Aortic dissection

ECG changes and the positional nature of pain help differentiate pericarditis from myocardial infarction.

~Management

The main objectives in treating pericarditis are pain relief, inflammation control, and management of underlying cause or complications.

1. General Measures

• Rest until symptoms and inflammation resolve.

• Avoid strenuous activity for several weeks to prevent recurrence.

2. Pharmacologic Therapy

• Nonsteroidal Anti-inflammatory Drugs (NSAIDs):
  First-line treatment for idiopathic or viral pericarditis.

  • Ibuprofen 600–800 mg every 6–8 hours

  • Aspirin 750–1000 mg every 8 hours

  • Continue for 1–2 weeks, followed by gradual tapering.

• Colchicine:
  Reduces recurrence rates when used with NSAIDs.

  • 0.5–1 mg daily for 3 months (acute) or 6 months (recurrent).

• Corticosteroids:
  Reserved for autoimmune, uremic, or refractory cases.

  • Prednisone 0.25–0.5 mg/kg/day, tapered slowly.

• Antibiotics:
  For bacterial pericarditis, guided by culture results. Drainage may be necessary in purulent cases.

• Antitubercular therapy:
  For confirmed or suspected tuberculous pericarditis.

3. Drainage Procedures

• Pericardiocentesis: Indicated in cardiac tamponade or large effusion.

• Pericardial window or pericardiectomy: For recurrent effusions or constrictive pericarditis.

4. Treatment of Specific Causes

• Post-MI (Dressler’s Syndrome): NSAIDs and colchicine.

• Uremic Pericarditis: Dialysis optimization.

• Malignant Pericarditis: Chemotherapy, radiotherapy, or pericardial drainage.

~Prognosis

The prognosis of pericarditis depends on the underlying cause and presence of complications.

• Idiopathic or viral pericarditis: Excellent prognosis; most recover completely within weeks.

• Bacterial or tuberculous pericarditis: More serious, often leading to constrictive changes if untreated.

• Recurrent pericarditis: Occurs in up to 20–30% of idiopathic cases.

Prompt diagnosis and adequate treatment generally result in full recovery without sequelae.

~Prevention

1. Prompt treatment of infections (especially respiratory and tuberculosis).

2. Careful use of drugs known to cause pericardial inflammation.

3. Regular monitoring in patients receiving radiation or with autoimmune diseases.

4. Secondary prevention with colchicine in recurrent cases.

~Recent Advances

• Cardiac MRI provides high-resolution imaging for early detection of inflammation and fibrosis.

• Novel anti-inflammatory drugs (e.g., anakinra, rilonacept) targeting interleukin-1 pathways show promise in refractory cases.

• Biomarker research (high-sensitivity CRP and troponin) aids in risk stratification.

These advancements are improving outcomes and reducing recurrence rates in patients with pericarditis.

~Conclusion

Pericarditis is a clinically significant inflammatory disorder of the pericardium, presenting primarily with chest pain and potential complications like effusion and constriction. Early recognition through characteristic clinical features, ECG, and echocardiography is vital for effective management.

Most cases are benign and respond well to anti-inflammatory therapy; however, bacterial, tuberculous, or malignant pericarditis can lead to serious complications if untreated. Ongoing research and new biologic therapies continue to enhance treatment outcomes, emphasizing the importance of individualized, evidence-based care.