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CHRONIC PERICARDITIS

Article written and reviewed by Dr Luca Moretti

Chronic pericarditis is a persistent inflammation of the pericardium, characterized by a prolonged course of more than 3 months, which may be associated with chronic pericardial effusion or progress to constrictive pericarditis. Unlike acute pericarditis, the chronic form presents with an insidious and often asymptomatic course, with progressive pericardial thickening and changes in cardiac dynamics.

Chronic Pericardial Effusion

Chronic pericardial effusion is characterized by a slow and persistent accumulation of fluid in the pericardial sac. In many cases, it is idiopathic, but it can also be secondary to underlying pathological conditions. The main causes include:

• Neoplasms (primary pericardial tumors or metastases from lung, breast, leukemia, and lymphomas).
• Infections (tuberculosis, bacterial or fungal infections).
• Autoimmune diseases (systemic lupus erythematosus, rheumatoid arthritis, scleroderma, Sjögren's syndrome).
• Chronic renal failure (uremic pericarditis with accumulation of uremic toxins).
• Metabolic disorders (myxedema due to severe hypothyroidism, marked hypercholesterolemia).
• Thoracic trauma or cardiac surgery.

The progression of effusion is slow and allows a certain adaptation of the pericardium. If the fluid accumulates gradually, the pericardium can distend without causing significant hemodynamic effects, and the patient may remain asymptomatic. However, in large effusions (>500 mL), ventricular filling may be compromised, resulting in exertional dyspnea, asthenia, and signs of venous congestion.

The composition of pericardial fluid varies depending on the cause:

• Idiopathic: straw-colored fluid, specific gravity 1010-1015, proteins 5-6 g/dL.
• Neoplastic: hemorrhagic, rich in atypical cells and tumor markers.
• Tuberculous: serous exudate with high protein and lymphocyte content.
• Uremic: transudate poor in cells and proteins.
• Myxedematous: dense fluid, rich in mucopolysaccharides.

Diagnosis is based on echocardiography, which allows assessment of the quantity and characteristics of the fluid. In cases of large effusion or suspicion of neoplastic/inflammatory etiology, pericardiocentesis is indicated with biochemical, cytological, and microbiological analysis of the fluid.

Constrictive Pericarditis

Chronic constrictive pericarditis is a condition in which the pericardium, following persistent inflammation, undergoes progressive fibrosis and calcification, resulting in rigid compression of the heart and limitation of ventricular filling. It is a late complication of pericarditis, with a slow clinical evolution that can remain unrecognized for years.

Etiology

The main causes of constrictive pericarditis include:

• Infectious pericarditis (bacterial, viral, tuberculous).
• Neoplasms (pericardial metastases, mesothelioma).
• Thoracic radiotherapy (post-radiation pericardial fibrosis).
• Cardiac surgery (post-pericardiotomy pericarditis).
• Autoimmune diseases (SLE, rheumatoid arthritis, scleroderma).
• Thoracic trauma with chronic hemopericardium.

Pathophysiology

The pericardium progressively thickens and becomes rigid, preventing normal ventricular filling. Unlike cardiac tamponade, where elevated pericardial pressure impairs filling throughout diastole, in constrictive pericarditis the block occurs only in late diastole, with increased end-diastolic pressure and reduced ventricular compliance. This alteration leads to increased systemic resistance, compensatory tachycardia, and progressive right heart failure.

Clinical Features

The main symptoms include:

• Exertional dyspnea, progressive with fatigue.
• Signs of venous congestion (ascites, peripheral edema, hepatomegaly).
• Kussmaul's sign (absence of jugular venous pressure reduction during inspiration).
• Pulsus paradoxus (decrease in arterial pressure during deep inspiration).
• Non-palpable apical impulse and, sometimes, systolic retraction of the precordium.

Diagnosis

• ECG: low voltage, diffuse T wave changes, atrial fibrillation in 30% of cases.
• Chest X-ray: shows pericardial calcifications in 25-50% of cases.
• Doppler echocardiography: reveals pericardial thickening, "septal bounce" (abnormal interventricular septal motion), and abnormal respiratory variations in mitral and tricuspid inflow.
• Cardiac CT or MRI: confirms pericardial fibrosis and calcification.

Treatment

In mild cases, clinical monitoring is adopted. Medical therapy is indicated to control congestion (diuretics) and arrhythmias (digoxin). The only definitive treatment is pericardiectomy, indicated in patients with refractory symptoms. However, the procedure carries a high operative risk (mortality 5–15%).

References
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