Table 3.
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Severe chronic systemic venous congestion associated with low cardiac output, including jugular venous distension, hypotension with a low pulse pressure, abdominal distension, oedema, and muscle wasting |
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Can be normal, or reveal low QRS voltage, generalised T wave inversion/flattening, LA abnormalities, atrial fibrillation, atrioventricular block, intraventricular conduction defects, or rarely pseudoinfarction pattern |
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Pericardial calcifications, pleural effusions |
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Pericardial thickening and calcifications* as well as the indirect signs of constriction:
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Restricted filling of both ventricles with respiratory variation >25% over the AV valves‡¶ |
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Measurement of the pericardial thickness |
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Measurements of the pericardial fibrosis and thickening |
Cardiac catheterisation: | “Dip and plateau” or “square route” sign in the pressure curve of the right and/or left ventricle |
Equalisation of pressures in the range of 5 mmHg or less§ | |
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The reduction of RV and LV size and increase of RA and LA size |
During diastole a rapid early filling with stop of further enlargement (“dip-plateau”) | |
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In all patients over 35 years and in patients with a history of mediastinal irradiation, regardless of the age. |
*Thickening of the pericardium is not always equal to constrictive physiology.
†Diagnosis is difficult in atrial fibrillation. Hepatic diastolic vein flow reversal in expirium is observed even when the flow velocity pattern is inconclusive.
‡Patients with increased atrial pressures or mixed constriction and restriction demonstrate <25% respiratory changes. A provocation test with head-up tilting or sitting position with decrease of preload may unmask the constrictive pericarditis.
§In the early stage or in the occult form, these signs may not be present and the rapid infusion of 1–2 litres of normal saline may be necessary to establish the diagnosis. Constrictive haemodynamics may be masked or complicated by valvar and coronary artery disease.
¶In chronic obstructive lung disease mitral in-flow velocity will decrease nearly 100% during inspiration and increase during expiration. The mitral E velocity is highest at the end of expiration (in constrictive pericarditis mitral E velocity is highest immediately after start of expiration). In addition, superior vena cava flow increases with inspiration in chronic obstructive lung disease, whereas it does not change significantly with respiration in constrictive pericarditis.
LA, left atrium; LV, left ventricle; MRI, magnetic resonance imaging; RA, right atrium; RV, right ventricle, TOE, transoesophageal echocardiography.