Constrictive pericarditis

• Constrictive pericarditis is a form of diastolic heart failure in which the pericardium has become a rigid, scarred or calcified shell that prevents the heart from filling.
• The underlying problem is not weak muscle; it is a noncompliant pericardium. Early diastolic filling is rapid, then abruptly stops against the shell.
• It declares itself with high venous pressure (raised jugular venous pressure, oedema, ascites), a rapid Y descent on the jugular tracing, and sometimes a pericardial knock in early diastole. Kussmaul sign (jugular pressure rising with inspiration) may be present.
• Echocardiography is the first and often definitive test: ventricular septal shift with respiration, a medial mitral annular velocity that is paradoxically high (at least 9 cm/s on Mayo criteria), and expiratory diastolic flow reversal in the hepatic veins. ^[1]
• Unlike tamponade, diastolic filling is rapid early and the problem is chronic stiffness; unlike restrictive cardiomyopathy, the myocardium is healthy and the constriction is mechanically reversible, most often by radical pericardiectomy.

By the end of this page you should be able to:

1. Explain how a thick, inelastic pericardium converts normal respiration into ventricular interdependence and equalised filling pressures.
2. Recognise the clinical picture and distinguish Kussmaul sign from the pressure pattern of cardiac tamponade.
3. Interpret the key echocardiographic clues (septal shift, medial e' velocity, hepatic vein reversal, annulus reversus) and the catheter findings (dip-and-plateau, systolic area index).
4. Separate constrictive pericarditis from restrictive cardiomyopathy and from tamponade using physiology rather than memorised labels.
5. Choose between anti-inflammatory medical therapy and surgical pericardiectomy, and describe the operative aims and early postoperative care.
6. Plan investigation of an undiagnosed patient, including when a fluid challenge or exercise testing helps.

Constrictive pericarditis is one of three pericardial compressive syndromes, alongside cardiac tamponade and effusive-constrictive pericarditis. Classically two subcategories are distinguished.

• Transient (subacute, inflammatory) constrictive pericarditis: the constriction is driven by active pericardial inflammation and oedema. It may resolve spontaneously or with 3 to 6 months of anti-inflammatory therapy.
• Chronic constrictive pericarditis: the pericardium is fibrotic, often calcified, and irreversibly noncompliant. It usually needs radical surgical pericardiectomy.
• Effusive-constrictive pericarditis: a pericardial effusion and constrictive physiology co-exist. Drainage of the effusion leaves persistent constriction; it lies on a continuum between pure tamponade and chronic constriction.

The distinction between inflammatory and chronic disease is the single most important decision in management, because it determines whether the patient receives tablets or an operation.

The whole clinical picture follows from two facts: the pericardium can no longer stretch, and it no longer transmits the pressure swings of breathing to the heart.

Normal pericardium. The normal pericardial sac has a shallow pressure-volume curve at low volumes and steepens abruptly once its reserve volume is reached. Breathing changes intrathoracic pressure by about 5 to 10 mm Hg, and a compliant pericardium lets those swings reach the cardiac chambers. The right ventricle fills more in inspiration while the left side is shielded because the pulmonary veins are inside the chest; the free wall of the right ventricle simply bulges outward and the interventricular septum barely moves. ^[1]

Loss of compliance. In constrictive pericarditis the fibrous pericardium has become a hard casing. It does not stretch, and it stops transferring respiratory pressure changes to the heart, so the cardiac chambers are isolated from the thorax. Filling pressures throughout the heart become almost equal, and rapid early diastolic filling is brought to an abrupt halt by the inelastic wall, producing the dip-and-plateau (square root) pressure pattern on catheter tracings. ^[1]

Ventricular interdependence. Because the total space is fixed, every gain in volume by one ventricle is lost by the other.

• In inspiration, intrathoracic pressure falls. The extrathoracic (superior and inferior) vena cavae still deliver blood to the right atrium, helped by rising abdominal pressure, but the pulmonary veins (intrathoracic) deliver less to the left side. The right ventricle fills more, the septum bows left into the left ventricle, and left-sided output falls. Kussmaul sign can appear: the jugular venous pressure rises paradoxically during inspiration because venous return to the right atrium meets the rigid shell. ^[1][2]
• In expiration the reverse occurs: left-sided filling rises, the septum bows right, and hepatic venous blood is pushed backwards, producing expiratory diastolic flow reversal in the hepatic veins. ^[1]

This opposite respiratory behaviour of the two ventricles is the hallmark of constriction and is what makes the diagnosis secure.

Why it feels like heart failure. Diastole is shortened and filling is limited, so cardiac output is low, particularly on exertion. The heart is trapped, so even modest volume loads raise filling pressures sharply and produce pulmonary congestion when left-sided dynamics are stressed, and systemic venous congestion (oedema, ascites, hepatomegaly) the rest of the time.

Grossly the pericardium is thickened, opaque and often adherent; it can be leathery and heavily calcified (sometimes spectacularly, producing the classic shell on chest imaging). Calcification is most marked along the atrioventricular and interventricular grooves. Microscopically there is fibrous thickening, organisation of fibrin, hyalinisation and calcium deposition. In the inflammatory form the pericardium is hyperaemic, coated with fibrin or shaggy exudate, with granulation tissue and oedema rather than dense scar; whether the two layers have been obliterated determines whether the process is reversible. The pericardial cavity may contain fluid in effusive-constrictive disease, or be completely obliterated in chronic disease.

Causes are heterogeneous and geographically patterned.

• In developed countries the most common cause is idiopathic, followed by post-cardiac surgery (especially valvular or coronary) and prior mediastinal radiotherapy. Other causes include viral or bacterial infection, connective tissue disease, uraemia, post-myocardial infarction effusion and malignancy. ^[3]
• Where tuberculosis is endemic, tuberculosis is the most common cause of constrictive pericarditis, often in association with HIV infection; in sub-Saharan Africa tuberculous pericarditis remains a major cause of heart failure. ^[2]
• Radiation-associated disease deserves special caution: the myocardium is often also damaged, so the physiology is frequently mixed (constriction plus restriction) and outcomes after surgery are poorer. ^[4]
• Other recognised causes include purulent pericarditis, haemopericardium, trauma, mesothelioma and other primary tumours, and metabolic or autoimmune disease.

There is no reliable way to predict from the size or appearance of the pericardium whether a given inflammatory episode will heal or scar, which is why reassessment rather than assumption is required.

Pericardial diseases are common but constriction is not. In the 2024 international position statement, acute pericarditis has an incidence of about 32.4 ± 3.5 cases per 100,000 population per year in an Italian region, pericarditis is responsible for about 0.1% of all hospital admissions and about 5% of emergency department admissions for chest pain, men aged 16 to 65 years are at higher risk (relative risk 2.02) than women, and recurrences affect about 30% of patients after a first episode and up to 50% after a first recurrence, with an estimated 40,000 patients with recurrent pericarditis in the United States. ^[2] Recurrent or incompletely treated pericarditis is one route to constriction, through organisation and scarring. Average pericardial fluid volume in health is about 25 mL (up to 50 mL). ^[2]

The patient usually presents with symptoms of heart failure, not chest pain.

• Exertional breathlessness and reduced exercise tolerance, often out of proportion to apparent cardiac function; dyspnoea on lying flat can appear late because venous pressure is already high.
• Peripheral oedema, abdominal swelling or fullness from ascites (which can be large enough to mimic liver disease and is a classic source of diagnostic delay).
• Fatigue and cachexia from chronic low output.
• Chest discomfort is less common than in acute pericarditis, though a prior episode of pericarditis may be recalled.
• Systemic features (fever, weight loss) suggest an active inflammatory or tuberculous cause rather than burnt-out chronic constriction.

The venous pressure is the key to the examination.

• Raised jugular venous pressure that is often very high, with prominent X and Y descents: a rapid X plus a rapid, steep Y descent giving a characteristic W-shaped waveform. The Y descent is rapid because blood empties quickly into the relaxed ventricle in early diastole before being abruptly stopped by the shell.
• Kussmaul sign: paradoxical rise (or failure to fall) of the jugular venous pressure during inspiration. It is a sign of constrictive pericarditis and severe right heart dysfunction; it is not specific on its own.
• Pericardial knock: a short, sharp, high-pitched early diastolic sound, heard shortly after the second heart sound, often mistaken for a third heart sound. It corresponds to the abrupt halt in ventricular filling and to the nadir of the Y descent. It is one of the most useful physical signs when present.
• Pulsus paradoxus is not expected (it belongs to tamponade), and when severe right-sided congestion dominates the picture a small-volume, rapid pulse may be seen.
• A diastolic rumble can mimic mitral stenosis if a heavily calcified pericardium restricts flow, and signs of tricuspid regurgitation and right heart failure are common.
• Hepatomegaly, sometimes with a pulsatile liver from tricuspid regurgitation, ascites and peripheral oedema, and often a pleural effusion.
• Findings vary with posture and volume status, so examine the patient both sitting and after a fluid challenge where appropriate.

The two great traps are cardiac tamponade and restrictive cardiomyopathy; the third is heart failure from other causes with high venous pressure.

Constrictive pericarditis and tamponade share elevated venous and filling pressures and respiratory variation of transvalvular flow, but in tamponade filling is limited throughout diastole and the pericardial sac still transmits respiratory pressure swings, whereas in constriction early filling is exaggerated and the heart is isolated from the thorax. ^[1] Pressure equalisation after pericardiocentesis (fall in right atrial pressure by at least 10 mm Hg or by more than 50%) separates pure tamponade from effusive-constrictive disease, where the right atrial pressure stays high and constriction is revealed. ^[2]

Differentiating constriction from restriction is the harder problem. Restrictive cardiomyopathy (for example cardiac amyloidosis) also shows rapid early filling and a square root sign, with high and equalised pressures, but the disease is in the myocardium. ^[1] Discriminating clues favouring constriction are annulus reversus (medial mitral e' greater than lateral), a medial mitral e' velocity of at least 9 cm/s on Mayo criteria (or greater than 8 cm/s in the 2024 position statement), annulus paradoxus (E/e' falls as wedge pressure rises), a right atrial to pulmonary capillary wedge pressure ratio of at least 0.77, and pericardial calcification. Clues favouring restriction are a low medial e' velocity, a raised E/e' ratio, absence of annulus reversus, and evidence of infiltrative disease. When doubt remains, the right atrial to wedge pressure ratio of 0.77 or greater suggests predominant constriction with better survival after pericardiectomy, whereas a ratio below 0.77 suggests mixed or myocardial disease. ^{[1] [2]}

Echocardiography is the initial test and is often sufficient to establish the diagnosis and to proceed to surgery. ^[1] The examination is technical and requires long (10 beat or more) clips with a respirometer. Report these features:

• Ventricular septal shift with respiration (the septum moves left on inspiration), shown by extended 2-D or M-mode clips. This is the most direct demonstration of ventricular interdependence.
• Diastolic septal bounce or shudder, from the timing difference between right and left early filling. It supports constriction but is not specific.
• Mitral inflow: restrictive pattern (E greater than A, E/A greater than 0.8) with respiratory variation of 25% or greater in mitral E velocity; absence of variation does not exclude the diagnosis when filling pressures are very high. ^[1]
• Tricuspid inflow: respiratory variation of greater than 40% in tricuspid E velocity. This is physiological to some degree in everyone and is not a diagnostic criterion on its own. ^[1]
• Medial (septal) mitral annulus e' velocity: at least 9 cm/s on Mayo criteria (greater than 8 cm/s in the 2024 position statement), paradoxically increased; this is one of the best predictors and rises further with higher filling pressure.
• Annulus reversus: medial mitral e' greater than lateral, because the lateral free wall is tethered to the stiff shell.
• Annulus paradoxus: E/e' falls as wedge pressure rises, the opposite of myocardial disease.
• Hepatic vein: expiratory diastolic flow reversal with a reversal to forward velocity ratio of at least 0.79 on Mayo criteria (at least 0.8 in the 2024 position statement); hepatic venous flow reversals are highly specific. ^[1][2]
• Inferior vena cava: dilated with less than 50% collapse. ^[3]
• Superior vena cava: loss of the normal inspiratory increase in systolic flow, opposite to the exaggerated variation seen in lung disease.
• Pericardial thickness when visible.

When resting studies are equivocal, exercise echocardiography exaggerates the same findings: septal motion, medial e' velocity and hepatic reversals all become more prominent, while cardiac output augmentation is limited. ^[1]

• Cardiac computed tomography is the best test for pericardial calcification and thickness, and for preoperative planning (relationship of the sternum to the heart and great vessels). Calcium is a marker of chronicity and supports constriction. ^[3]
• Cardiac magnetic resonance (CMR) can show early inspiratory septal shift on free-breathing cine sequences, pericardial thickening (greater than 3 mm), wall tethering and conical deformity, and, crucially, pericardial inflammation on T2-weighted short tau inversion recovery and late gadolinium enhancement. CMR is the best test for separating an inflammatory, reversible constrictor from a burnt-out fibrotic one, and for assessing myocardial involvement. ^[3]
• Invasive haemodynamic catheterisation remains important when non-invasive tests are inconclusive or there is mixed myocardial disease. Simultaneous right and left ventricular pressure recording shows:
  • rapid X and Y descents on the right atrial tracing with a W configuration; the Y descent nadir corresponds to the pericardial knock;
  • the dip-and-plateau (square root sign) in ventricular diastolic pressures, from rapid filling brought to an abrupt halt;
  • discordant respiratory change in left and right systolic pressures, the systolic area index decreasing in the left and increasing in the right with inspiration;
  • the right atrial to pulmonary capillary wedge pressure ratio (at least 0.77 suggests predominant constriction; below 0.77 suggests mixed disease). ^[1]
  • In early or treated (diuresed, hypovolaemic) disease the findings may be absent; an exercise test or a rapid fluid challenge can bring them out. ^[1]
• Coronary angiography or CT coronary assessment when surgery is planned, particularly in older patients, because concomitant coronary disease is common; catheter manipulation in the heart carries a small risk of dislodging an intracardiac thrombus, although thrombus is less relevant here than in myxoma.
• Pericardial biopsy is rarely needed; tissue diagnosis is reserved for suspected tuberculosis or malignancy.

A restrictive filling pattern with high E velocities does not by itself mean constriction: it is found in restriction and in severe diastolic dysfunction too. The diagnosis rests on the combination of high venous pressure, the characteristic clinical signs, and imaging that proves ventricular interdependence. No single isolated finding is diagnostic; a constellation in the right clinical context is required. ^[3]

Normal ranges quoted in this section (mitral variation 25% or greater, tricuspid variation greater than 40%, medial e' at least 9 cm/s, hepatic reversal ratio 0.79 or greater, RA to wedge ratio 0.77 or greater) come from the open-access hemodynamics review and the 2024 international position statement, which quote slightly different cut-offs for the same phenomena. ^[1][2]

There is no single scoring system for constrictive pericarditis. The working approach used in current consensus documents is:

1. Clinical syndrome of heart failure with high venous pressure and preserved ejection fraction.
2. Echocardiographic demonstration of constriction (septal shift, medial e' elevation, hepatic reversals, annulus reversus).
3. Corroboration by CT (calcification, thickness) or CMR (inflammation, tethering) when the echo is not clear.
4. Invasive haemodynamics when doubt remains, especially with mixed myocardial disease.
5. Tissue characterisation and inflammatory markers to separate transient from chronic disease.

Transient versus chronic disease is the functional staging: active inflammation (raised CRP or ESR, pericardial late gadolinium enhancement or oedema on CMR) points to a medically reversible form; a burnt-out, calcified shell points to surgery. Repeat imaging after 3 to 6 months of therapy decides whether pericardiectomy is still required. ^[3][4]

• Diuretics relieve congestion (oedema, ascites, raised venous pressure) but are palliative; they do not change the course of a rigid pericardium and should not delay definitive treatment once fibrosis predominates. ^[2][4]
• Salt restriction and careful fluid management; weight monitoring.
• Treat the cause: antituberculous therapy where tuberculosis is the cause (with corticosteroids in some regimens to enhance improvement), treatment of renal or thyroid disease, and oncological treatment where relevant. ^[3]
• Heart failure medications such as angiotensin pathway blockers, beta blockers and mineralocorticoid antagonists may help congestion but evidence is limited; goal-directed therapy is implemented pragmatically. ^[3]

If there is active pericardial inflammation (transient constriction), the first-line treatment is anti-inflammatory, for 3 to 6 months. ^[3][4]

• Colchicine (with or without a non-steroidal anti-inflammatory drug when not contraindicated) is the standard anti-inflammatory basis; the 2025 ACC statement recommends combination anti-inflammatory therapy for acute pericarditis, and the same agents are extrapolated to inflammatory constriction. ^[3][4]
• Corticosteroids are considered where inflammation is significant, as in tuberculous or refractory disease; systemic corticosteroids tapered over time have been used in tuberculous constriction in some regimens, though institutional practice varies.
• Interleukin-1 inhibitors (anakinra, rilonacept) may be considered in selected inflammatory cases refractory to first-line agents. ^[4]
• Reassess at 8 to 12 weeks with echocardiography and serial C-reactive protein measurements; tapering only begins once symptoms resolve and the marker normalises. ^[3][4]
• Failure to improve after appropriate medical therapy is a prompt for surgical referral without further delay. ^[4]

(Note: specific milligram doses for colchicine and steroids in this condition are not given here beyond what the cited documents state; follow the local formulary and the 2025 consensus recommendations.)

Radical (complete) pericardiectomy is the definitive treatment for chronic or medically refractory constriction and should be performed at an experienced high-volume centre. ^[3][4][5]

• Indication: persistent symptoms with objective constriction in chronic fibrotic or calcified disease, or failure of medical therapy in the inflammatory form.
• Approach: via median sternotomy, with the aim of removing all restricting pericardium (anterior phrenic-to-phrenic, plus diaphragmatic and posterior pericardium behind the left atrium between the pulmonary veins and along the inferior vena cava), leaving no confluent bands or rings that could perpetuate constriction.
• Cardiopulmonary bypass is used selectively or liberally in contemporary practice: it provides haemodynamic stability, allows more complete and safer resection, and enables concomitant coronary or valve surgery. Its use generally reflects anatomical complexity rather than added risk. ^[4]
• Posterior and diaphragmatic pericardium must not be left in place, because residual rings can produce recurrent constriction.
• Partial (anterior only) pericardiectomy is not recommended in contemporary practice, given superior outcomes with complete resection. ^[3]

Abrupt removal of the shell can cause acute volume overload and myocardial stunning. Care centres on gentle filling, close monitoring of filling pressures and pulmonary artery pressures, low-dose inotropic support when output is persistently low, atrial pacing if needed, and careful fluid administration. Early complications include atrial arrhythmias, vasoplegia (particularly with advanced hepatic disease) and adrenal insufficiency after long-term steroids. ^[4]

The 2025 European Society of Cardiology guidelines on myocarditis and pericarditis recommend pericardiectomy as the definitive treatment for chronic constrictive pericarditis or disease refractory to anti-inflammatory therapy, preferably complete resection at experienced high-volume centres. ^[4][5] The 2025 American College of Cardiology expert consensus statement similarly emphasises early referral for radical pericardiectomy in chronic constriction with heart failure, noting that medical therapy may relieve congestion but does not alter disease progression. ^[3][4] There are no randomised controlled trials defining surgical timing, which is reflected in the honest uncertainty of the source documents. ^[4]

• Untreated constriction progresses to cirrhosis, renal impairment and cachexia from chronic low output, and can cause sudden deterioration with acute pulmonary oedema when a volume load is imposed.
• Mixed constrictive-restrictive physiology is common in radiation-associated and advanced disease and limits surgical benefit. ^[4]
• Postoperative low cardiac output when the myocardium has been deconditioned by chronic underfilling.
• Atrial fibrillation from chronic atrial stretch.
• Recurrence or residual constriction after incomplete (partial) pericardiectomy.
• Iatrogenic injury to coronary arteries, phrenic nerve or myocardium at operation.
• Peri-operative bleeding and infection, and acute right ventricular distension after sudden relief of constriction.

Prognosis depends mainly on the substrate: chronicity, myocardial involvement and end-organ dysfunction, rather than on the technical operation itself. ^[4] Idiopathic inflammatory forms do well; cures can be achieved with medical therapy. Chronic calcific disease treated with radical pericardiectomy at experienced centres shows meaningful functional improvement. Radiation-associated mixed disease and advanced hepatic or renal impairment carry worse outcomes. The medial mitral e' velocity carries prognostic value: higher (less myocardial involvement) means better survival after pericardiectomy, while low values indicate mixed disease. ^[1] Overall, with appropriate selection and early referral, most patients with pure chronic constriction improve substantially after radical pericardiectomy.

There is no population screening. The best prevention is prompt, adequate treatment of acute pericarditis (anti-inflammatory therapy with colchicine for 3 months after a first episode and at least 6 months after a recurrence, plus exercise restriction until markers normalise) to prevent the chronic scarring that leads to constriction. ^[3] Early referral and assessment of pericardial inflammation at 8 to 12 weeks prevents progression. Close follow-up of inflammatory disease with imaging identifies the transient form before it is assumed to be chronic. ^[4]

• Children: constriction in children is uncommon and usually post-surgical or post-infectious, including tuberculosis. Outcomes after pericardiectomy in paediatric series are generally good when disease is pure constriction.
• Pregnancy: constriction complicates pregnancy management because fluid shifts and volume loads are poorly tolerated; decisions about timing of pericardiectomy versus medical management require a multidisciplinary team. The source documents do not provide specific pregnancy algorithms for constriction beyond general pericardial disease principles.
• Older adults: coronary and valve disease are commonly associated; preoperative coronary assessment is needed.
• Immunocompromised patients (including HIV): tuberculosis is a major cause in endemic regions; antituberculous therapy is central.
• Radiation-induced disease: mixed physiology warrants particular caution in counselling about expected benefit from surgery. ^[4]

• Echocardiography is the decisive test: in a patient with unexplained ascites, high venous pressure and preserved systolic function, look for interventricular septal shift with a simple free-breathing 2-D clip, together with mitral inflow and a dilated inferior vena cava. This is feasible on basic machines without tissue Doppler in a pinch, and can be extended with careful offline review. ^[1]
• Where CT, CMR or invasive catheterisation are not available, the clinical and echo picture, plus a trial of diuresis and observation of response, is usually enough to make a decision; a fluid challenge can bring out latent constriction.
• Tuberculosis should be actively sought and treated in endemic regions.
• Pericardiectomy requires cardiopulmonary bypass and an experienced team; where not available locally, refer early to a cardiac surgery centre, because delay leads to cirrhosis and irreversible myocardial change.
• Diuretics, salt restriction, nutritional support and cause-directed therapy remain the backbone while referral is arranged.

• Constrictive pericarditis is diastolic heart failure from a rigid, noncompliant pericardium, with preserved systolic function and very high filling pressures.
• The pericardium stops transmitting respiratory pressure changes; ventricular interdependence produces opposite respiratory behaviours of the left and right ventricles (septal shift, hepatic flow reversal, Kussmaul sign).
• Kussmaul sign, a pericardial knock, a rapid Y descent and ascites are classic clinical clues; the knock corresponds to the nadir of the Y descent.
• Echocardiography is first-line and often definitive: septal shift, medial e' at least 9 cm/s, hepatic expiratory diastolic flow reversal (ratio at least 0.79), annulus reversus and a dilated inferior vena cava.
• Cardiac tamponade differs in physiology (impaired filling throughout diastole, pulsus paradoxus, chamber collapse) and equalises then releases pressure on pericardiocentesis; constrictive pericarditis does not.
• Restrictive cardiomyopathy (for example amyloidosis) also shows rapid early filling but has a low medial e', no annulus reversus and evidence of myocardial disease; the right atrial to wedge ratio of 0.77 or greater favours constriction.
• CT shows calcification and thickness; CMR shows inflammation and tethering and best distinguishes transient from chronic disease.
• Management is dictated by inflammatory versus chronic disease: 3 to 6 months of anti-inflammatory therapy for the inflammatory form, reassessed at 8 to 12 weeks; radical pericardiectomy for chronic or refractory disease.
• Diuretics relieve congestion but do not fix the shell; medical heart failure therapy is an adjunct.
• Radical pericardiectomy with complete resection, on bypass as needed, at a high-volume centre offers the best outcome; partial resection is not recommended.
• Tuberculosis is the commonest cause where it is endemic; idiopathic, post-surgical and post-radiation causes predominate in developed countries, and radiation-associated mixed disease does worse after surgery.
• Early referral matters: prolonged congestion leads to cirrhosis, renal impairment and irreversible myocardial change.

• Acute pericarditis and recurrent pericarditis
• Cardiac tamponade and pericardial effusion
• Restrictive cardiomyopathy, including cardiac amyloidosis
• Echocardiography and multimodality cardiac imaging
• Pericardiectomy and postoperative critical care
• Tuberculous pericarditis in endemic regions