CHRONIC PERICARDITIS

Chronic pericarditis is a persistent inflammation of the pericardium, characterized by a prolonged course lasting more than 3 months. It may be associated with chronic pericardial effusion or evolve into constrictive pericarditis. Unlike acute pericarditis, the chronic form has an insidious course and is often asymptomatic, with progressive pericardial thickening and altered cardiac dynamics.

Chronic Pericardial Effusion

Chronic pericardial effusion is defined by the 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 and breast cancer, 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 due to toxin accumulation).
• Metabolic disorders (myxedema due to severe hypothyroidism, severe hypercholesterolemia).
• Thoracic trauma or cardiac surgery.

The progression of pericardial effusion is slow, allowing for pericardial adaptation. If fluid accumulates gradually, the pericardium can stretch without significant hemodynamic consequences, and the patient may remain asymptomatic. However, in large effusions (>500 mL), ventricular filling may be compromised, leading to exertional dyspnea, fatigue, and signs of venous congestion.

The composition of pericardial fluid varies depending on the underlying cause:

• Idiopathic: serous fluid, with a specific gravity of 1010-1015 and protein content of 5-6 g/dL.
• Neoplastic: hemorrhagic, rich in atypical cells and tumor markers.
• Tuberculous: serous exudate with high protein content and lymphocytes.
• Uremic: transudate with low cell and protein content.
• Myxedematous: dense fluid, rich in mucopolysaccharides.

Diagnosis is based on echocardiography, which allows assessment of the quantity and characteristics of the pericardial fluid. In cases of large effusion or suspected neoplastic/inflammatory etiology, pericardiocentesis is indicated for 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, leading to rigid compression of the heart and limiting ventricular filling. It is a late complication of pericarditis, with a slow clinical evolution that can remain undiagnosed 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 obstruction occurs only in the late diastolic phase, with increased end-diastolic pressure and reduced ventricular compliance. This alteration leads to increased systemic resistance, compensatory tachycardia, and progressive right heart failure.

Clinical Presentation

The main symptoms include:

• Exertional dyspnea, progressive with fatigue.
• Signs of venous congestion (ascites, peripheral edema, hepatomegaly).
• Kussmaul's sign (lack of jugular venous pressure reduction on inspiration).
• Pulsus paradoxus (decrease in blood pressure during deep inspiration).
• Impalpable apex beat and, sometimes, systolic retraction of the precordium.

Diagnosis

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

Treatment

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

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