Constrictive pericarditis
Terms
Chronic constrictive pericarditis involves irreversible thickening and fibrosis of the pericardium.
Transient constrictive pericarditis, caused by inflammation, may resolve on its own or with anti-inflammatory treatment in 3 to 6 months. In areas where tuberculosis is prevalent, it is the leading cause, while outside these regions, idiopathic causes are most common, followed by post-cardiac surgery and mediastinal radiation.
In this group, anti-inflammatory therapy should be initiated before considering pericardiectomy.
For tuberculous constrictive pericarditis, antituberculous therapy may resolve the constrictive pathophysiology, and corticosteroids may enhance clinical improvement.
Effusive constrictive pericarditis is a specific condition characterized by ongoing constrictive physiology even after the drainage of a pericardial effusion. Traditionally, this condition was diagnosed through invasive methods, particularly by observing that right atrial pressure (or pericardial pressure) does not decrease following pericardiocentesis. This phenomenon is typically associated with significant inflammation of the visceral pericardium.
The main hemodynamic features of constrictive pericarditis include the separation of intrathoracic and intracardiac pressures during respiration, which increases ventricular dependence and elevates diastolic filling pressures in both heart chambers. This results in a leftward shift of the interventricular septum during inspiration, a predominant E-wave mitral inflow pattern, elevated medial e’ tissue Doppler velocity, and a plethoric inferior vena cava. There is also late-diastolic flow with expiratory reversal in the hepatic veins.
Chest x-rays
Pericardial calcification was seen in a patient with end-stage kidney disease (ESKD) who also had uremic pericarditis.
Transthoracic echocardiography findings included
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Respirophasic ventricular dependence/septal shift
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E-wave predominant LV filling with respirophasic variation
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Dilated inferior vena cava with <50% collapse
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Hepatic vein end diastolic expiratory reversal flow velocity/forward flow velocy ≥ 0.8
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Preserved medial mitral annular e' velocity (>8 cm/s)
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Annulus reversus (medial>lateral e' mitral annula velocity)
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Loss of SVC systolic flow variation
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Respirophasic variation across mitral valve E-wave inflow velocities (>25% for mitral valve inflow velocity, >40% for tricuspid valve inflow velocity)
Diagnostic Algorithm and Validation of TTE Parameters for CP
Sens. | Spec. | PPV | NPV | |
|---|---|---|---|---|
1 | 94% | 73% | 93% | 77% |
2 | 81% | 91% | 97% | 58% |
3 | 71% | 79% | 93% | 45% |
4 | 73% | 66% | 86% | 42% |
1 and 2 | 80% | 96% | 99% | 58% |
1+2+4 | 67% | 99% | 100% | 50% |
Simultaneous RV and LV Hemodynamic Assessment in CP and RCM
End-diastolic filling pressures are elevated, indicating a "square root" sign.
During inspiration, the area of the right ventricular pressure curve increases while the area of the left ventricular pressure curve decreases.
End-diastolic filling pressures are elevated, indicating a "square root" sign.
In restrictive cardiomyopathy, left and right ventricular pressure tracings show no enhanced interdependence, with parallel changes in their pressure curves.
Cardiac tamponade VS Constrictive pericarditis VS Restrictive cardiomypathy
Cardiac tamponade
Physical examination
Tachycardia
Hypotension
Pulsus paradoxus
Increase JVP with prominent x andabsent y descent
Muffled heart sounds
ECG
Tachycardia
Low voltage amplitude
Electrical alternans
CXR
Increase cardiac silhouette
Echocardiography
Pericardial effusion
Cardiac chamber compression or collapse
Respirophasic ventricular interdependence by 2D and M-mode
Respirophasic variation in mitral and tricuspid inflow Doppler
Dilated inferior vena cava
Expiratory hepatic venousdiastolic flow reversals
Cardiac MR
Not be used for diagnosis of tamponade
Pericardial effusion
Cardiac chamber compression or collapse
Cardiac catheterization
Increase RA pressure with prominent x and attenuated y descent
Equalization of right and left ventricular diastolic pressures
Respirophasic ventricular interdependence and pulsus paradoxus
Intrathoracic-intracardiac dissociation
Treatment
Pericardiocentesis
Pericardial window
Constrictive Pericarditis
Physical examination
Increase JVP with prominent x and y descents
Kussmaul’s sign
Pericardial knock
Ascites
Peripheral edema
ECG
No pathognomonic features
Low voltage amplitude
Atrial fibrillation
CXR
Pericardial calcification seen in one-third of patients
Echocardiography
Respirophasic ventricular interdependence by 2D and M-mode
Respirophasic variation in mitral andtricuspid inflow Doppler
Increase Mitral annular e’ velocities
Annulus reversus (medial > lateral mitral annular e’ velocities)
Dilated inferior vena cava
Expiratory hepatic venous diastolic flow reversals
Cardiac MRI
Increase pericardial thickness
Respirophasic ventricular interdependence/septal shift on free breathing imaging sequences
Pericardial late gadolinium enhancement
Pericardial edema
Wall tethering, conical deformity of the ventricle
Cardiac catheterization
Increase RA pressure with rapid x and y descent and Kussmaul’s sign
Equalization of right and left ventriculardiastolic pressures with dip-and-plateau waveforms
Respirophasic ventricular interdependence and pulsus paradoxus
Intrathoracic-intracardiac dissociation
Distal coronary artery fixation on angiography
Treatment
Surgical radical pericardiectomy
Diuretics
Restrictive cardiomyopathy
Physical examination
Increase JVP with prominent y and attenuated x descents
Kussmaul’s sign
Third heart sound (S3)
Peripheral edema
ECG
No pathognomonic features
Atrial fibrillation
CXR
No pericardial calcification
Echocardiography
Atrial enlargement
Decrease mitral annular e’ velocities
Diastolic dysfunction
Elevated right ventricular systolic pressure
Dilated inferior vena cava
Inspiratory hepatic venous diastolic flow reversals
Increased left ventricular wall thickness
Cardiac MRI
Abnormal myocardial late gadolinium enhancement
Other abnormal myocardial sequences including abnormal nulling or T2 time
Normal pericardial thickness without peri-cardial late gadolinium enhancement
No ventricular interdependence on free-breathing sequences
Increased left ventricular wall thickness
Cardiac catheterization
Increase RA pressure with prominent y and attenuated x descents
Elevated right ventricular systolic pressure
No ventricular interdependence
No intrathoracic-intracardiac dissociation
Treatment
Goal directed medical therapy for heart failure and treat underlying etiology (eg, amyloidosis)
Reference
Wang, T, Klein, A, Cremer, P. et al. 2025 Concise Clinical Guidance: An ACC Expert Consensus Statement on the Diagnosis and Management of Pericarditis: A Report of the American College of Cardiology Solution Set Oversight Committee. JACC. 2025 Dec, 86 (25) 2691–2719. https://doi.org/10.1016/j.jacc.2025.05.023
Klein, A, Wang, T, Cremer, P. et al. Pericardial Diseases: International Position Statement on New Concepts and Advances in Multimodality Cardiac Imaging. J Am Coll Cardiol Img. 2024 Aug, 17 (8) 937–988. https://doi.org/10.1016/j.jcmg.2024.04.010