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

Pericarditis

~Introduction

Pericarditis is an inflammatory condition of the pericardium—the thin, double-layered sac that surrounds the heart. It can occur as an isolated disease or as part of a systemic illness. Pericarditis is one of the most common causes of acute chest pain encountered in clinical practice, second only to myocardial infarction. Although most cases are mild and self-limiting, certain forms of pericarditis can lead to serious complications such as cardiac tamponade and constrictive pericarditis, making early recognition essential.

The pericardium consists of a visceral layer (epicardium) adhered to the heart and a parietal layer, between which lies the pericardial space containing 15–50 mL of lubricating fluid. Inflammation of this sac leads to characteristic symptoms, clinical signs, and diagnostic features.

~Anatomy and Physiology of the Pericardium

Structure

• Visceral pericardium: Inner layer directly covering the myocardium.

• Parietal pericardium: Fibrous external layer.

• Pericardial cavity: Small fluid-filled space to reduce friction.

Functions

• Mechanical protection of the heart

• Maintaining optimal cardiac position

• Preventing acute cardiac dilation

• Reducing friction during cardiac movement

• Acting as a barrier to infection

~Types of Pericarditis

Pericarditis is classified based on its duration, underlying pathology, and clinical presentation:

1. Acute Pericarditis – lasting <6 weeks

2. Subacute Pericarditis – 6 weeks to 6 months

3. Chronic Pericarditis – >6 months

4. Recurrent Pericarditis – relapse after initial resolution

Pathological Types

• Fibrinous (Dry) Pericarditis

• Serous Pericarditis

• Purulent (Bacterial) Pericarditis

• Hemorrhagic Pericarditis

• Caseous (Tuberculous) Pericarditis

• Constrictive Pericarditis

~Etiology

Pericarditis has a wide range of causes, though in many Western countries a large proportion is idiopathic (presumed viral).

1. Infectious Causes

Viral

• Coxsackievirus B (most common)

• Echovirus

• Influenza virus

• HIV

• Cytomegalovirus (CMV)

Bacterial

• Staphylococcus

• Streptococcus

• Neisseria meningitidis

• TB (Mycobacterium tuberculosis) → common in developing countries

Fungal

• Histoplasma

• Candida (in immunocompromised patients)

2. Non-Infectious Causes

Autoimmune & Systemic Diseases

• Systemic lupus erythematosus (SLE)

• Rheumatoid arthritis

• Scleroderma

• Post-MI (Dressler’s syndrome)

• Post-pericardiotomy syndrome

Metabolic

• Uremia (chronic kidney disease)

• Hypothyroidism (rare)

Neoplastic

• Lung cancer

• Breast cancer

• Lymphoma

• Leukemia

Trauma

• Penetrating or blunt chest trauma

• Iatrogenic (catheters, pacemaker insertion)

Drugs

• Isoniazid

• Hydralazine

• Procainamide

• Chemotherapy agents (doxorubicin, cyclophosphamide)

~Pathophysiology

Inflammation of the pericardium leads to:

• Edema and infiltration of inflammatory cells

• Increased production of pericardial fluid

• Fibrin deposition (in fibrinous type)

• Formation of adhesions or thickening in chronic forms

Excessive accumulation of fluid can increase pericardial pressure, impairing ventricular filling and leading to cardiac tamponade—a life-threatening emergency.

Repeated inflammation may cause fibrosis and calcification, resulting in constrictive pericarditis, where the heart is encased in a rigid shell limiting diastolic filling.

~Clinical Features

Symptoms

1. Chest Pain (most common)

   • Sharp, stabbing, pleuritic in nature

   • Worse with inspiration, coughing, or lying down

   • Improved by sitting up and leaning forward

   • May mimic myocardial infarction but differs in position and behavior

2. Fever

3. Dyspnea
   – Mainly due to pain or effusion

4. Palpitations
   – If arrhythmias occur

5. Fatigue and malaise

Signs

• Pericardial friction rub: High-pitched, scratchy sound heard best at left lower sternal border; pathognomonic.

• Tachycardia

• Reduced heart sounds (if effusion present)

• Signs of tamponade:

  • Hypotension

  • Jugular venous distension

  • Pulsus paradoxus

  • Weak, muffled heart sounds

~Complications of Pericarditis

1. Pericardial Effusion

Accumulation of fluid in the pericardial space.

2. Cardiac Tamponade

Life-threatening compression of the heart causing obstruction of venous return and reduced cardiac output.

3. Constrictive Pericarditis

Thickened, calcified pericardium restricting heart function.

4. Chronic or Recurrent Pericarditis

Relapses occurring months or years after initial recovery.

~Diagnosis

Diagnosis of pericarditis is made clinically with supportive laboratory and imaging findings.

Diagnostic Criteria

At least two of the following:

1. Characteristic chest pain

2. Pericardial friction rub

3. ECG changes typical of pericarditis

4. Pericardial effusion on imaging

Investigations

1. ECG Findings

Typical stages:

• Stage I: Widespread ST elevation with PR segment depression

• Stage II: ST segments normalize

• Stage III: T-wave inversion

• Stage IV: EKG returns to normal

ECG helps differentiate pericarditis from myocardial infarction.

2. Laboratory Tests

• Elevated ESR, CRP

• Leukocytosis

• Cardiac biomarkers: Mild troponin rise in myopericarditis

• Renal function tests (uremic pericarditis)

• Autoimmune markers (ANA, RF if suspected)

3. Imaging

Echocardiography

• First-line imaging

• Detects pericardial effusion, tamponade physiology

CT Scan

• Shows pericardial thickening, calcification

• Useful for suspected neoplastic pericarditis

MRI

• Excellent for detecting inflammation and fibrosis

• Differentiates constrictive vs. restrictive cardiomyopathy

4. Pericardiocentesis

Indicated in:

• Large effusion

• Cardiac tamponade

• Suspected infection or malignancy

Fluid analysis includes cell count, cultures, cytology, and biochemical markers.

~Management

Management depends on the cause and severity.

1. General Treatment for Acute Pericarditis

A. NSAIDs (First-line)

• Ibuprofen: 600–800 mg every 6–8 hours

• Aspirin (especially post-MI): 650–1000 mg every 6 hours

Given for 1–2 weeks with gradual tapering.

B. Colchicine

Improves symptoms and reduces recurrence.

• Dose: 0.5–1 mg/day for 3 months

C. Corticosteroids

Used only when:

• NSAIDs/colchicine contraindicated

• Autoimmune causes

• Uremic or refractory pericarditis

Risk of recurrence is higher with steroids, so used cautiously.

2. Treatment Based on Specific Causes

Viral Pericarditis

• NSAIDs + Colchicine

• Rest and reassurance

Bacterial Pericarditis

• Intravenous antibiotics

• Pericardial drainage (often required)

Tuberculous Pericarditis

• Anti-TB therapy for 6–12 months

• Steroids may help reduce inflammation

Uremic Pericarditis

• Urgent dialysis

• NSAIDs generally avoided due to kidney dysfunction

Neoplastic Pericarditis

• Treat underlying cancer

• Pericardial window or pericardiectomy if effusion recurs

3. Management of Complications

A. Pericardial Effusion

• Small, asymptomatic: Observe

• Large or symptomatic: Pericardiocentesis

B. Cardiac Tamponade

Medical Emergency

• Immediate pericardiocentesis

• IV fluids to maintain preload

• Avoid positive-pressure ventilation if possible

C. Constrictive Pericarditis

• Diuretics for symptom relief

• Pericardiectomy is the definitive treatment

~Prognosis

The prognosis of pericarditis varies:

Acute idiopathic or viral pericarditis

• Excellent recovery with treatment

• Low mortality

Bacterial or purulent pericarditis

• High mortality if untreated

• Requires aggressive intervention

Tuberculous pericarditis

• Risk of constriction

• Good outcomes with therapy if detected early

Recurrent pericarditis

• Occurs in ~30% of patients

• Colchicine reduces recurrence risk significantly

Constrictive pericarditis

• Requires surgery

• Early intervention leads to good functional recovery

~Prevention

While it is impossible to prevent all forms of pericarditis, certain measures help reduce risk:

• Early treatment of viral infections

• Prompt management of tuberculosis

• Tight control of autoimmune diseases

• Regular dialysis in patients with end-stage renal disease

• Careful use of pericardiotomy and invasive cardiac procedures

• Minimizing unnecessary immunosuppression

~Conclusion

Pericarditis is a clinically significant condition with diverse causes and presentations. Acute pericarditis often presents with sharp chest pain and a characteristic friction rub, and is usually manageable with NSAIDs and colchicine. However, certain forms—especially bacterial, tuberculous, and autoimmune—can be more severe and may lead to life-threatening complications such as cardiac tamponade or chronic constrictive pericarditis.

Appropriate evaluation using ECG, biomarkers, and imaging is crucial for accurate diagnosis. Management depends on the underlying cause and ranges from anti-inflammatory medications to urgent pericardial drainage and even pericardiectomy in advanced cases.

Recognizing pericarditis promptly and initiating timely treatment helps prevent progression, reduce recurrence, and ensure excellent outcomes in most patients.

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.