Acute pericarditis with transient constriction: surgical impetus must be contained

BACKGROUND

Constrictive pericarditis is typically a chronic and progressive condition characterised by pericardial thickening and calcification commonly representing a late sequela of pericarditis. This condition classically presents with debilitating chronic right heart failure and surgical pericardiectomy remains the treatment of choice.1 In spite of this, the development of constrictive physiology has also been described in the acute phase of pericarditis.2^–5 In most patients with acute pericarditis, complete and spontaneous resolution is the rule but, in some of them, recovery may be preceded by signs of pericardial constriction with overt heart failure.

CASE PRESENTATION

A 29-year-old man, previously healthy, presented to the emergency department complaining of a sharp, stabbing, chest pain aggravated on deep inspiration. This symptom had appeared 15 days prior to admission, was associated with daily fever and loss of 10% of his total body weight. On examination he was tachypnoeic, the heart rate was 90 beats/min and the blood pressure was 110/70 mmHg. Thoracic auscultation revealed a pericardial rub and, except for this, the physical examination was unremarkable. Electrocardiogram showed diffuse non-specific repolarisation abnormalities and chest roentgenogram revealed an enlarged cardiac silhouette. A diagnosis of acute pericarditis was established and treatment with a non-steroidal anti-inflammatory drug was initiated.

At admission, echocardiography disclosed increased pericardial thickness and a small circumferential pericardial effusion, without signs of diastolic restriction. The laboratory data were obtained and no specific cause was apparent after assessment. The Mantoux test, antinuclear antibodies and viral serologies, including HIV, hepatitis and cytomegalovirus tests, were negative. Laboratory tests revealed haemoglobin 10.0 g/dL; leucocyte count 6.5×10³/mm³; platelets 622×10³/mm³; normal thyroid function; c-reactive protein (CRP) 137 mg/L.

Despite adequate treatment, the patient remained symptomatic, with fever, and his condition deteriorated: dyspnoea, leg swelling, painful hepatomegaly, jugular venous distension and pulsus paradoxus were noted. Nuclear MR was performed and revealed thickened pericardium (8 mm) at the left ventricular lateral wall and discrete pericardial effusion (fig 1). Cine cardiac evaluation in the short, long axis and four chambers views revealed early diastolic flattening of the interventricular septum and biventricular restriction.

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Figure 1

Four-chamber view using Triple-IR spin-echo revealing pericardium thickening more evident in the left ventricular lateral wall (white arrows). Additionally, moderate pericardial effusion located in the right ventricular free wall (black arrows). Stain: black and white.

A pericardial biopsy was performed 9 days after admission with drainage of 10 mL of pericardial fluid. The biopsy showed non-specific pericarditis without granulomas. Neither acid-fast bacilli nor fungi were detected on special staining. Cultures were negative. PCR reaction for Mycobacterium tuberculosis was negative. Treatment with prednisone (1 mg/kg/day) was begun and, because of overt signs of restriction, a pericardiectomy was scheduled.

OUTCOME AND FOLLOW-UP

Before the intervention, clinical signs of pericardial constriction gradually resolved. The patient had complete remission of symptoms within 2 weeks, without surgical procedure, and was discharged from hospital. Eight weeks after beginning treatment, a follow-up scan (fig 2) did not show pericardial thickening or diastolic restriction. The dose of prednisone was gradually tapered with addition of colchicine to the treatment regime, with very good clinical response. After 2 months of corticoid removal, the patient remained stable without symptom relapse and inflammatory markers remained in the normal range.

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Figure 2

Follow-up image did not show pericardial thickening or effusion. Stain: black and white.

DISCUSSION

Transient cardiac constriction complicating acute pericarditis was first reported by Sagristà-Sauleda et al in 1987.2 They described 16 patients from a series of 177 with effusive acute idiopathic pericarditis in whom features of constriction were detected in the acute phase. After a mean period of 2.7 months, the features of constriction spontaneously subsided. In another series of 36 patients with diagnosis of transient constrictive pericarditis, viral and idiopathic pericarditis were the most common causes described.3 A transient form of constrictive pericarditis has also been described in the setting of purulent bacterial pericarditis4 and chemotherapy.5

The severity of haemodynamic repercussion due to restriction may sometimes prevent the adoption of an expectant treatment, as initially occurred with our patient. Fortunately, soon after he was scheduled for surgical treatment, our patient’s signs and symptoms related to pericardial constriction started to relieve and surgical treatment was obviated.