Constrictive pericarditis is a condition characterized by chronic inflammation and fibrosis of the pericardium resulting in thickening (>4 mm, normal <2 mm) and stiffening; in this process the pericardium encases the heart like a restrictive shell and severely impairs diastolic filling. Incidence is low, but tuberculosis in developing countries and idiopathic/viral and post-cardiac surgery causes predominate in developed countries. Most patients present with chronic heart failure symptoms (peripheral edema, ascites, hepatomegaly, jugular venous distension). Clinical differentiation from restrictive cardiomyopathy is critically important because constrictive pericarditis is curable with surgery (pericardiectomy). On CT, pericardial thickening (>4 mm) and calcification (30-50%) are pathognomonic. On MRI, septal bounce (abnormal respiratory-synchronous motion of the interventricular septum) on cine sequences is characteristic. Late gadolinium enhancement (LGE) indicates active inflammation and carries prognostic significance for surgical timing.
Age Range
30-80
Peak Age
55
Gender
Equal
Prevalence
Uncommon
Constrictive pericarditis develops in the chronic phase of pericardial inflammation. The initial acute pericarditis (viral, tuberculosis, uremia, radiation, or post-surgical) organizes during healing, and fibrosis, collagen deposition, and sometimes calcification develop in the pericardial layers. The thickened and stiffened pericardium mechanically restricts diastolic cardiac expansion — early diastolic ventricular filling may be normal but filling abruptly stops when the elastic limit of the pericardium is reached (dip-plateau pattern or 'square root sign'). This restriction increases right and left ventricular interdependence: during inspiration, right ventricular filling increases while left ventricular filling decreases and the septum shifts leftward — this is seen as 'septal bounce' on MRI cine sequences. Pericardial calcification is the final stage of chronic inflammation — calcium-phosphate crystals accumulate in necrotic and fibrotic tissue through dystrophic calcification mechanism. It appears as high density (>400 HU) on CT because calcium (Z=20) provides high photoelectric absorption. Pericardial LGE reflects increased capillary permeability and expanded extracellular space in active granulation tissue — gadolinium accumulates in these areas and produces T1 shortening.
On cine MRI (especially real-time free-breathing SSFP sequence), abnormal bouncing motion of the interventricular septum synchronized with the respiratory cycle — leftward shift during inspiration, rightward during expiration. This finding is the pathognomonic indicator of constrictive pericarditis and directly reflects ventricular interdependence. It is the single finding with the highest diagnostic accuracy for differentiation from restrictive cardiomyopathy (sensitivity 90-95%, specificity 85-90%). In normal hearts, the septum shows minimal motion with respiration; in constrictive pericarditis, the rigid pericardium dramatically amplifies this motion because expansion of one ventricle can only occur at the expense of compression of the other.
On non-contrast CT, pericardial thickness measures >4 mm in constrictive pericarditis (normal <2 mm). Calcification is seen in 30-50% of cases and may be irregular, plaque-like, or diffuse band-like. Calcification is most commonly located on the anterior surface of the right ventricle and in the atrioventricular grooves. In tuberculosis-related cases, calcification may be more extensive, thick, and armor-like ('Panzerherz'). Associated findings: IVC and hepatic vein dilation, ascites, pleural effusion, hepatomegaly — these are CT indicators of chronic venous congestion.
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On CT, pericardial thickness measures ___ mm (normal <2 mm) with accompanying calcified plaques/diffuse calcification in the ___ region; consistent with constrictive pericarditis.
On contrast-enhanced CT, the normal conical shape of the ventricles is lost and tubular/cylindrical morphology is seen — the restrictive effect of the pericardium prevents ventricular expansion. Inferior vena cava and hepatic veins are markedly dilated (IVC diameter >28 mm) — a finding of chronic venous congestion. Hepatomegaly, perihepatic ascites, and splenic congestion (splenomegaly) may accompany. Pericardial thickening becomes more evident with contrast — mild pericardial enhancement may be seen in the presence of inflammation. However, in 'burned-out' (end-stage fibrotic) cases, pericardial enhancement may be minimal.
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On contrast-enhanced CT, ventricular cavities show tubular configuration, with markedly dilated IVC (diameter: ___ mm) and hepatic veins; consistent with chronic venous congestion due to constrictive pericarditis.
The most characteristic finding of constrictive pericarditis on cine SSFP MRI is septal bounce — an abnormal bouncing motion of the interventricular septum synchronized with the respiratory cycle. During inspiration, right ventricular filling increases and the septum shifts leftward; reverse motion occurs during expiration. This finding reflects ventricular interdependence and is the most valuable MRI finding for differentiation from restrictive cardiomyopathy (sensitivity 90-95%, specificity 85-90%). Concurrently, pericardial thickening (>4 mm), tubular ventricle morphology, atrial dilation, and pleural/pericardial effusion are evaluated. Real-time free-breathing cine sequences best demonstrate respiratory-related septal motion.
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On cine SSFP MRI, respiratory-synchronized interventricular septal bounce is observed, consistent with ventricular interdependence and constrictive pericarditis.
On T2-weighted images, pericardial thickening (>4 mm) is measured. Signal characteristics reflect disease stage: in active inflammation the pericardium is T2 hyperintense (edema, granulation tissue — increased free water content); in the chronic fibrotic stage the pericardium is T2 hypointense (collagen and fibrous tissue — short T2); calcified pericardium is hypointense on all sequences (very low proton density, no signal). This stage classification is critical for treatment approach — T2 hyperintense pericardium may respond to anti-inflammatory therapy, while fibrotic pericardium requires surgery. T2 dark-blood (turbo spin echo) sequence best demonstrates pericardial thickness and signal changes because flowing blood signal is suppressed.
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On T2-weighted images, the pericardium measures ___ mm in thickness, showing hyperintense/hypointense signal; this finding is consistent with active inflammatory/chronic fibrotic stage.
On late gadolinium enhancement (LGE) sequences, pericardial enhancement may be seen in constrictive pericarditis — this finding indicates active pericardial inflammation and the presence of vascularized granulation tissue. Cases with positive LGE have a higher likelihood of responding to anti-inflammatory therapy ('reversible constriction'). In LGE-negative cases, the pericardium is fibrotic/calcified and surgery is required. Pericardial LGE pattern may be diffuse or focal — diffuse pattern indicates widespread inflammation, focal pattern indicates partial activity. Whether myocardial LGE accompanies is important — myocardial LGE presence suggests myopericarditis or restrictive cardiomyopathy and may reduce surgical success rate.
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On LGE sequences, diffuse/focal late gadolinium enhancement is observed in the pericardium, suggesting active pericardial inflammation and potentially reversible constriction; myocardial LGE is not observed/is accompanying.
On T1-weighted images, thickened pericardium (>4 mm) is seen with low-to-intermediate signal intensity. Fibrotic pericardium shows hypointensity relative to myocardium, while active inflammation shows iso-to-mildly hyperintense signal. Calcified areas are markedly hypointense. The thin layer of pericardial fluid between pericardium and myocardium is reduced or absent in constrictive pericarditis — reflecting obliterated pericardial space fibrosis. Fat-suppressed T1 sequence clarifies the distinction between epicardial fat and pericardium and improves accuracy of thickness measurement.
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On T1-weighted images, the pericardium measures ___ mm in thickness, showing hypointense/isointense signal relative to myocardium.
Echocardiographic (US) findings suggesting constrictive pericarditis: pericardial thickening (echogenic thick pericardial line — though US thickness measurement is not as reliable as CT/MRI), septal bounce (septal motion synchronized with respiration on M-mode and 2D), increased early diastolic mitral annular velocity (e' ≥12 cm/s — 'annulus paradoxus'), hepatic vein expiratory flow reversal, and IVC dilation (>21 mm, collapsibility <50%). On Doppler, mitral inflow E/A >1.5 and pronounced respiratory variation (25%) are typical. These findings raise the initial suspicion for diagnosis and direct advanced imaging (CT/MRI).
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On echocardiography, pericardial thickening and respiratory-synchronized septal bounce are observed, accompanied by significant respiratory variation in mitral inflow (___%) and IVC dilation; consistent with constrictive pericarditis.
Criteria
Both pericardial effusion and constrictive physiology coexist. Hemodynamic findings do not improve after pericardiocentesis — intrapericardial pressure decreases but right atrial pressure remains elevated. Represents the transition phase from active inflammatory process to chronic constriction.
Distinct Features
CT/MRI shows pericardial effusion + thickened pericardium together. LGE-positive — active inflammation. Subtype with highest likelihood of response to anti-inflammatory therapy. Tuberculosis is the most common cause.
Criteria
Widespread, thick calcification in the pericardium — armor-like appearance. End-stage fibrotic-calcific phase. Usually tuberculosis-related. LGE-negative (no active inflammation). Surgical pericardiectomy mandatory.
Distinct Features
Best seen on CT — widespread high-density pericardium (>400 HU), usually dominant on the anterior surface of right ventricle. Signal void on all MRI sequences (no protons). Technically most difficult subtype for surgery — separating calcified pericardium from myocardium is challenging.
Criteria
Constrictive physiology present but completely resolves with anti-inflammatory therapy (colchicine, NSAID, steroid). Usually in subacute phase of acute pericarditis (15-20%). LGE-positive, T2 hyperintense — active inflammatory stage. Surgery not needed.
Distinct Features
MRI shows pericardial edema (T2 hyperintense) and prominent LGE — definitive indicator of active inflammation. No calcification on CT. Constrictive physiology resolves and pericardial thickness normalizes on reassessment after 2-3 months of anti-inflammatory therapy.
Criteria
Develops after mediastinal/thoracic radiotherapy (average latency 5-10 years). Hodgkin lymphoma, breast cancer radiotherapy are most common causes. Pericardial fibrosis + accompanying myocardial fibrosis (radiation cardiomyopathy), coronary artery disease, and valvular disease are common.
Distinct Features
Myocardial LGE accompanies (50%) — mixed (constrictive + restrictive) physiology. Surgical mortality is high (25-30% vs idiopathic 5-10%) because myocardium is also diseased. Evaluation of accompanying coronary and valvular disease is mandatory.
Distinguishing Feature
Pericardial effusion is a fluid collection without pericardial restriction — diastolic filling is not impaired unless tamponade develops. In constrictive pericarditis, thickened/calcified pericardium is present instead of fluid (except effusive-constrictive type). Effusion shows fluid density (0-25 HU) on CT, constrictive pericarditis shows soft tissue/calcification density.
Distinguishing Feature
In restrictive CMP, the pericardium is normal (<2 mm), pathology is in myocardium (amyloidosis, sarcoidosis, fibrosis). Septal bounce is ABSENT — septum shows minimal motion with respiration. Myocardial LGE is diffuse (subendocardial/diffuse). Tissue Doppler e' is low (<8 cm/s). In constrictive pericarditis, pericardium is thick (>4 mm), myocardium is normal, septal bounce is PRESENT, e' is preserved/increased (≥12 cm/s).
Distinguishing Feature
Pericardial mesothelioma shows nodular/irregular pericardial thickening (unlike diffuse homogeneous thickening of constrictive pericarditis). Hemorrhagic effusion is common. Enhancement is more intense and irregular. Calcification is common (30-50%) in constrictive pericarditis, rare in mesothelioma. Clinical: rapid progression and deterioration in mesothelioma, chronic stable course in constrictive pericarditis.
Distinguishing Feature
Tamponade is an acute condition presenting with massive pericardial effusion and hemodynamic instability. Increased intrapericardial pressure causes right chamber collapse. Constrictive pericarditis is a chronic condition — thickened/calcified pericardium instead of effusion, filling restriction instead of chamber collapse. Pericardiocentesis is curative in tamponade, pericardiectomy is needed in constrictive pericarditis.
Urgency
urgentManagement
surgicalBiopsy
Not NeededFollow-up
3-monthConstrictive pericarditis is a surgically curable cause of heart failure — correct diagnosis is life-saving. Treatment approach is determined by disease stage: in LGE-positive (active inflammation) cases, a 2-3 month anti-inflammatory therapy trial (colchicine 0.5 mg BID + ibuprofen or steroids) is attempted — complete resolution is achieved in 15-20% with transient constrictive pericarditis. In LGE-negative (fibrotic/calcified) cases or those unresponsive to medical therapy, surgical pericardiectomy is indicated (mortality 5-15%, depending on center experience). In radiation-induced cases, surgical mortality is higher (25-30%) because myocardial damage accompanies. In tuberculosis-related cases, anti-tuberculosis treatment is started concurrently. Postoperative follow-up: echocardiography + clinical evaluation at 3-month intervals, then annual follow-up after the first year. No biopsy indication — diagnosis is made by clinical + imaging findings.
Constrictive pericarditis is a rare but surgically curable cause of diastolic heart failure (pericardiectomy). Distinguishing it from restrictive cardiomyopathy is vital as treatment approaches are entirely different. CT calcification and MRI pericardial thickening with LGE are the gold standard for diagnosis. Early diagnosis and surgery yield good prognosis; delayed intervention may lead to myocardial atrophy and reduced surgical success.