--- title: Constrictive pericarditis description: What constrictive pericarditis is, why a thickened, stiff pericardium stops the heart from filling with blood, what causes it and what its signs are, how it is told apart from restrictive cardiomyopathy, and how it is treated. type: disease aliases: - armoured heart - pericardial constriction sources: - tier: guideline org: minzdrav-rf title: Перикардиты year: 2025 url: https://cr.minzdrav.gov.ru/view-cr/746_2 - tier: guideline org: esc title: 2025 ESC Guidelines for the management of myocarditis and pericarditis year: 2025 doi: 10.1093/eurheartj/ehaf192 url: https://doi.org/10.1093/eurheartj/ehaf192 - tier: reference org: msd-manuals title: Pericarditis year: 2026 url: https://www.msdmanuals.com/professional/cardiovascular-disorders/pericarditis/pericarditis - tier: reference org: msd-manuals title: Restrictive Cardiomyopathy year: 2026 url: https://www.msdmanuals.com/professional/cardiovascular-disorders/cardiomyopathies/restrictive-cardiomyopathy sources_checked: 2026-10-13 review: null --- Constrictive pericarditis is a late consequence of inflammation or another disease process in the pericardium, the sac around the heart: its layers thicken and calcify, and this stops the chambers of the heart from filling with blood normally during diastole. The pericardium becomes thick and stiff. It is also called "armoured heart". It is usually not an acute condition but a long-term complication of [pericarditis](../pericarditis/).

Normally the pericardium is a closed, slit-like cavity around the heart that holds a small amount of fluid. It lets the left and right ventricles fill with blood normally, without restriction.

In constrictive pericarditis the thickened, stiff pericardium markedly impairs ventricular filling, so the heart pumps out less blood with each beat. The scar tissue often contains calcium deposits, but calcification is not seen in everyone. The atria are enlarged, while the ventricles are not dilated and their pumping function is usually preserved.

## Why it happens Constriction can follow pericarditis of almost any cause. In countries with well-resourced healthcare it most often follows pericarditis with no known cause or viral pericarditis, heart surgery or radiotherapy; worldwide, the most common cause is tuberculous pericarditis. Some people never had acute pericarditis before. The risk depends on the cause of the inflammation: after acute pericarditis with no known cause, constriction develops in fewer than 1% of cases, and the risk is highest with bacterial pericarditis, especially purulent and tuberculous pericarditis. The disease develops slowly. At first it may cause no symptoms for months or even years; then problems appear, at first only during physical exertion. The cause is marked inflammatory, fibrotic thickening of the pericardium; sometimes the visceral and parietal layers adhere to each other or to the myocardium, the fibrotic tissue often contains calcium, and significant fluid accumulation is rare. The stiff pericardium impairs ventricular filling, reducing stroke volume and cardiac output; diastolic pressures in the ventricles, atria and venous beds become virtually the same. According to the Russian Ministry of Health guideline, the risk of constriction is under 1% after acute idiopathic pericarditis, 2–5% in autoimmune, autoinflammatory and paraneoplastic pericarditis, and 20–30% in bacterial pericarditis, especially purulent and tuberculous. Effusive or constrictive pericarditis occurs in 6–30% of patients after radiotherapy. The ESC describes three main constrictive syndromes: transient constriction, a reversible pattern of constriction following spontaneous recovery or anti-inflammatory therapy; effusive–constrictive pericarditis, defined by failure of the right atrial pressure to fall by 50% or to below 10 mm Hg after pericardiocentesis; and chronic constriction, persisting after 3–6 months. The Russian Ministry of Health guideline also describes transient and effusive–constrictive forms as rarer than classic chronic constrictive pericarditis. ## Symptoms The main signs come from blood backing up in the veins: swollen neck veins, an enlarged liver, fluid in the abdomen (ascites) that makes the abdomen swell, and swollen legs. According to the Russian Ministry of Health guideline, a feature of constrictive pericarditis is that ascites and an enlarged liver appear before leg swelling. People feel breathless, especially on exertion, and may be very tired. Heart rhythm problems are common, particularly [atrial fibrillation](../atrial-fibrillation/). The Russian Ministry of Health guideline lists signs of marked chronic systemic venous congestion caused by low cardiac output: jugular venous distension, arterial hypotension with a low pulse pressure, an increase in abdominal girth, peripheral oedema and muscle weakness. Chronically raised systemic and hepatic venous pressure can lead to liver scarring, called cardiac cirrhosis, and patients may first present for evaluation of cirrhosis; occasionally a pleural effusion develops. On examination the neck veins are distended and venous pressure rises during inspiration (Kussmaul sign), which is absent in [tamponade](../cardiac-tamponade/). An early diastolic sound, the pericardial knock, may be heard; it is caused by abrupt slowing of diastolic ventricular filling by the rigid pericardium. Unlike in tamponade, pulsus paradoxus occurs in no more than 33% of cases and is usually less severe. Ventricular systolic function (based on ejection fraction) is usually preserved. ## How it is diagnosed The doctor asks about symptoms, examines the patient, and arranges an [ECG](../../diagnostic/ecg/), a [heart ultrasound (echocardiogram)](../../diagnostic/echocardiography/) and blood tests. A CT scan shows calcium deposits in the pericardium, and a cardiac MRI scan shows whether it is inflamed. If these tests do not give an answer, the pressures inside the heart may be measured by cardiac catheterisation. It is important to tell constrictive pericarditis apart from [restrictive cardiomyopathy](../restrictive-cardiomyopathy/), because their symptoms are very similar. In restrictive cardiomyopathy the wall of the left ventricle itself becomes stiff, whereas in constrictive pericarditis it is the pericardium. The ESC recommends multimodality imaging in all patients with suspected constrictive pericarditis to make the diagnosis and assess pericardial thickening, calcifications and active inflammation (I C); cardiac catheterisation for haemodynamic assessment should be considered when multimodality imaging is inconclusive (IIa C). ECG changes are non-specific: QRS voltage is usually low and T waves are non-specifically abnormal. Pericardial calcification is often best seen on a lateral chest radiograph, but the finding is non-specific. On echocardiography, paradoxical motion of the interventricular septum in early diastole is characteristic; the Russian Ministry of Health guideline also lists pericardial thickening and atrial enlargement with normal ventricular configuration and preserved systolic function. CT shows pericardial thickening more precisely, while MRI gives more information on constrictive physiology; pericardial thickening over 4 mm with typical haemodynamic changes can confirm the diagnosis, but a normal pericardial thickness does not exclude it. At catheterisation, because ventricular filling is restricted, ventricular pressure tracings show a sudden dip followed by a plateau in early diastole (the "square root" sign). The Russian Ministry of Health guideline also lists equalisation of ventricular end-diastolic pressures. These signs also occur in restrictive cardiomyopathy, so on their own they do not distinguish the two. In contrast to constrictive pericarditis, ventricular interdependence and respiratory variation in intracardiac pressures are minimal in restrictive cardiomyopathy. During inspiration, mitral diastolic flow velocity usually falls by more than 25% in constrictive pericarditis but by less than 15% in restrictive cardiomyopathy; mitral annular tissue velocities (e'), especially at the septal location, increase in constriction and decrease in restrictive cardiomyopathy. When no pericardial thickening or fluid is seen, restrictive cardiomyopathy is favoured but not proved; rarely, a biopsy is needed to exclude it. ## How it is treated Treatment depends on the form of the disease, and the doctor chooses it. If constriction has been found recently, the person is stable and there are signs of pericardial inflammation, anti-inflammatory treatment lasting several months is tried first: it can stop the disease progressing and help avoid surgery. If the constriction persists, a pericardiectomy is performed, an operation to remove the thickened pericardium. It is the only way to relieve persistent constriction. Surgery should not be put off for long once the condition starts to worsen, otherwise changes in the organs may become irreversible. In chronic constriction, congestion and swelling are reduced by limiting salt and by water tablets (diuretics) prescribed by the doctor. Treatment of constrictive pericarditis is mainly surgical, but medical therapy helps in three ways: treating the cause (as in tuberculous pericarditis) slows further progression of constriction, anti-inflammatory treatment can prevent constriction, and symptomatic therapy is used in advanced cases. The ESC recommends anti-inflammatory therapy in haemodynamically stable patients with a transient or new diagnosis of constriction and concomitant evidence of pericardial inflammation, to prevent progression and avoid pericardiectomy; for transient constriction the ESC gives a 3–6-month course of empiric anti-inflammatory therapy. Pericardiectomy is recommended in permanent constriction if there is no active inflammation or anti-inflammatory treatment has not succeeded after 3–6 months (I C), and in chronic constriction or constriction persisting despite medical therapy, to improve symptoms and survival (I C). The Russian Ministry of Health guideline also recommends pericardiectomy for constrictive pericarditis. After surgery, intracardiac haemodynamics return to normal in 60% of patients. In patients with constriction and severe tricuspid regurgitation, the ESC recommends tricuspid valve repair (I C). Patients whose constriction is due to irradiation or a systemic rheumatic disease are more likely to have severe myocardial damage and may not benefit from pericardial resection. The risk of constriction is reduced by timely guideline-based treatment of acute and recurrent pericarditis and by complete drainage of infected pericardial effusions. In tuberculous pericarditis the ESC recommends standard antituberculosis multidrug treatment to prevent pericardial constriction. ## When to call an ambulance Constrictive pericarditis usually develops slowly, as a long-term complication of pericarditis. But in the effusive–constrictive form there can be a lot of fluid in the pericardium, sometimes needing treatment as for [cardiac tamponade](../cardiac-tamponade/). Call your local emergency number (112 in the EU, 911 in the US and Canada, 999 in the UK) if bouts of sudden severe weakness, dizziness, fainting or rapidly worsening breathlessness appear: these are signs that tamponade may be developing. If breathlessness, swelling or the size of the abdomen gradually increase, do not put off seeing a doctor: once signs of decompensation appear, surgery should not be delayed for long. As with any heart condition, call an ambulance for fainting, chest pain or severe shortness of breath: this is the site's general safety rule, repeated at the bottom of every page.