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Constrictive pericarditis is the result of a chronic inflammation of the pericardium. Chronic constrictive pericarditis is still a rare disease but is being recognized more frequently. It is characterized by fibrous thickening and calcification of pericardium that impairs diastolic filling, reduced cardiac output, and ultimately leads to diastolic heart failure. Clinically, chronic constrictive pericarditis is characterized by dyspnea during exercise, symptoms of right heart failure. Pericardiectomy with complete decortication is the treatment of choice for constrictive pericarditis.
Department of Cardiovascular Surgery, Ministry of Health Adana City Hospital, Adana, Turkey
*Address all correspondence to: dronrubenli@gmail.com
1. Introduction
Normal pericardium consists of an outer sac or fibrous- parietal- pericardium and an inner double-layered sac called the serous -visseral- pericardium.The layers of serous pericardium include the visseral layer or epicardium,which covers the heart and proximal great vessels. The fibrous parietal pericardium, which contains collagen and elastin fiber and is normally ≤2 mm thick. The visseral pericardium is composed of a single layer of mesothelial cells with accompanying collagen and elastin,which adheres to the epicardium. The visceral and parietal layers are separated by the pericardial cavity, which in healthy people contains up to 50 mL of physiological pericardial serous fluid. The pericardium serves a variety of functions. In addition to its mechanical effects on the heart (limiting distention, promoting chamber – coupling interaction, maintaining cardiac geometry, enabling fictionless movement, hemodynamic effect on the atria and ventricles myocardial and serving as a barrier to infection), the pericardium has immunologic, vasomotor, paracrine, and fibrinolytic activities. However, due to the close proximity to the myocardium, alternations in pericardial elasticity thickness, and volume of pericardial fluid can cause compromise of cardiac filling resulting in pericardial constriction or tamponade.
Constrictive pericarditis occurs with severe fibrotic and cicatricial thickening of the pericardium, loss of elasticity, calcification, and adhesions in the pericardial cavity. Diastolic heart failure occurs as the pericardium, which has lost its elasticity, suppresses cardiac diastole filling. (Hypodiastolia Syndrome).
In conclusion, chronic constrictive pericarditis is one of the causes of diastolic right heart failure. Making that diagnosis may be difficult, as constrictive pericarditis may mimic other disorders. However, constrictive pericarditis is a pericardial disease process characterized by the development of right heart failure secondary to pericardial induced impaired diastolic filling, despite preserved right and left ventricular myocardial function. Since it has different pathophysiology, etiology and treatment from other causes of diastolic right heart failure, its definitive diagnosis is mandatory.
Constructive pericarditis, which has been described as “Pericardial adhesion”, “Chronic pericardial adhesion”, has also been named as callous, calcified or ossified pericardium, “Concertio cordis cum pericarditis”, as a result of knowledge, experience and observations on this subject. This clinical syndrome is also known as “Pick’s disease” [1]. In 1669 Lower described the clinical effect of the constrictive pericardium on the diastole of the heart in detail [2]. Based on the autopsy findings of a 30-year-old woman with pericardial adhesion in 1669, Lower stated that the pericardium, which should have been thin/translucent, was thickened, opaque and hardened (callous), which would limit the movements of the heart. J. Mayow, in 1674, described a pericardial adhesion as “as if the heart was surrounded by cartilage and stuck to the front”, and reported that this condition prevented blood return to the ventricle [3]. T. Bonet, in 1679, said that pericardial adhesion was the cause of palpitation and used the term (cordis tremor) [4]. R. De Vieussens mentioned the effect of pericardial adhesions on cardiac functions in two cases in 1679 and 1715, and stated that the adhesions were of inflammatory origin, not congenital [5]. A. von Haller described pericardial calcification in 1755 based on autopsy findings [6]. G. B. Morgagni described pericardial adhesions and calcifications in 7 cases in 1761 and gave information about the physiopathology and clinic of constructive pericarditis [7]. In 1823, R. T. H. Laénec detected calcification between the pericardial leaves in the autopsy of a 65-year-old patient with exertional dyspnea but no orthopnea, with cyanotic lips [1]. N. Chevers explained diastolic dysfunction in constructive pericarditis and its clinical picture for the first time in 1842 [8]. Wilks explained constructive pericarditis in detail in 1870 [9]. A. Kusmaul reported in 1874 that venous filling in the inspiratory increased in constrictive pericarditis (Kusmaul’s sign) [10]. J. M. Charcat reported constructive pericarditis due to rheumatoid arthritis in 1891 [11]. F. Pick mentioned “pseudo cirrhosis” (Pick’s disease) resulting from right heart failure in 1896 [12]. G. Daniel and S. Puder drew attention to the relationship between hemopericardium and constrictive pericarditis in 1932 [13]. T. H. Sellors in 1946 [14] and P. While in 1951 indicated tuberculosis as the primary cause of constructive pericarditis [15]. W.G. Bigelow et al. in 1956 [16], H. B. Schumaker Jr. and Rose [17] in 1960, and Fitzpatrick et al. [18] in 1962 reported that radical pericardiectomy was the only method to prevent recurrence of pericardial constructions. C.A. Bush et al. reported that constrictive pericarditis can disrupt hemodynamics even without adherence to the epicardium [19] E. Weil predicted the excision of the thickened fibrous pericardium in constructive pericarditis in 1895, and E. Delorme also showed on cadavers that pericardial decortication could be applied in 1898 [20, 21]. E. Rehn performed experimental pericardiectomy in 1913, performed pericardiectomy in 4 cases of constrictive pericarditis in humans in 1920, and reported that this was the treatment method of choice [22]. It was predicted by C. S. Beck that this type of intervention could be performed in 1901 [23] and helped in the development of the pericardiectomy technique from 1930 [24]. C. S. Beck reported in 1937 as a result of his experimental studies that the removal of the thickened pericardium provided hemodynamic improvement [25].
The prevalence of constrictive pericarditis is not known for certain, but it is a rare disease. In a prospective study of 500 patients followed for a media of 6 years after an episode of acute pericarditis and the rate of development of chronic constrictive pericarditis is 1.8% [26]. The incidence of constrictive pericarditis in patients with idiopathic or viral pericarditis is lower when compared to other etiologies such as rheumatic disease, connective tissue disease, pericardial injury syndrome,malignancy or bacterial infection. In patients undergoing open heart surgery, the incidence of symptomatic chronic constrictive is similarly low (0.2%–2.4%) [27, 28].
Histologically, constrictive pericarditis typically demonstrates fluctuating pericardial edema, inflammation and fibrin deposition similar to acute pericarditis, rather than the pericardial fibrosis and calcification more commonly seen in chronic pericardial constriction. This results in pericardial thickening in both situations leading to a loss of elasticity of the the pericardium and ultimately constrictive physiology. Although the constrictive, inelastic pericardium is typically fibrotic, calcific and thick, it is seen that the pericardium is of normal thickness at a rate of 18% in constrictive pericarditis [29].
All of the causes in the etiology of acute pericarditis can become chronic and lead to constriction (Table 1) [30]. However, pericarditis caused by some etiological agents, especially tuberculosis, tends to become more chronic. Tuberculosis from these etiological agents; In regions such as China, Iran, and South Africa, it is the dominant cause of constrictive pericarditis with a rate of 22.2–91% [31, 32, 33]. A South African institution reported 121 cases of constrictive pericarditis over 22 years (1990–2012) and of these, tuberculosis was confirmed as the cause in 29.8% of cases and suspected in an additional 61.2% of cases. However, tuberculosis was historically the most common cause for constrictive pericarditis in North America; a report from 1962 cited tuberculosis as the cause of 48% of cases of constrictive pericarditis. And at the present time, in developed countries (North America and Europe), constrictive pericarditis due to tuberculosis is very low (less than 5.6%). In these regions, idiopathic or previous cardiac surgery, radiotherapy to the thorax, human immunodeficiency virüs and AIDS old acute pericarditis are more common in the etiology of constrictive pericarditis [34, 35, 36, 37, 38]. It is known that there is a relationship between hemopericardium and constructive pericarditis [39, 40]. Radiation-induced “late pericarditis”. Constructive pericarditis requiring pericardiectomy develops in 20% of cases [41, 42]. Constructive pericarditis occurs an average of 23 months after cardiac surgery [39, 40].
Causes of constrictive pericarditis (AIDS: acquıred immunodeficiency syndome; HIV: Human immunodeficency virus).
Recent studies show that changes in gene expression could be directly associated with inflamation and the subsequent formation of fibrosis [43], the key pathological process underlying the constrictive pericarditis. Furthermore, an array of changes in non-coding RNAs, including micro RNAs (miRNAs), long non-coding RNAs(IncRNAs) and circular RNAs(circRNAs) were belived to play a critical role in the relevant molecular signaling pathways and biological processes leading to fibrosis.Nevertheless, how these molecular substrates mediate the constrictive pericarditis is still poorly understood. High-throughput sequencing and bioinformatics analysis have been widely exploited to identify specific genes associated with various diseases [44]. These interesting findings promoted researchers to explore if there are abnormally expressed genes and sigaling pathways involved in the inflammation and fibrosis processes of Constrictive pericarditis. Molecular biological experiments are neede to further delineate the roles of these circRNAs identified in Constrictive pericarditis [45].
In constrictive pericarditis, the pericardium leaves are stuck together and the thickness may be 5–6 mm, sometimes more than 1 cm. Focal or diffuse calcification is seen in 50% of cases. Calcification can sometimes envelop the entire pericardium. The heart in this state is called the “armored heart”. In constrictive pericarditis, the basis of the pathophysiological event is the obstruction of the diastolic filling of the right heart and venous return. As a result, cardiac output decreases, venous pressure rises and systemic arterial pressure decreases. The pathological process often extended to the myocardium. In this case, myocardial contractility is impaired (systolic dysfunction). In constrictive pericarditis, in contrast to the symptoms in cardiac tamponade, blood and plasma administration does not increase cardiac output. With decreased cardiac output, liver and kidney perfusion decrease. Salt and water retention increases. Increased blood volume and increased venous pressure do not increase cardiac output. Venous pressure elevation causes congestive symptoms and signs. In constrictive pericarditis, although the left ventricular ejection fraction is normal, stroke volume and cardiac output are decreased. As a result, exercise dyspnea occurred. Because cardiac volume is limited due to constriction, cardiac filling and output vary depending on respiration. The right ventricle will not dilate even though venous return is increased in the inspiration. Rarely, right ventricular volume may be increased by a shift (shift) of the ventricular septum towards the left ventricle. This will reduce left ventricular filling and output.
The hemodynamic changes and symptoms of constrictive pericarditis are shown in Table 1. In chronic constrictive pericarditis, patients may have retrosternal pain and palpitations. In constrictive pericarditis, fatigue and exertional dyspnea develop due to low cardiac output. However, signs of pulmonary congestion (orthopnea, paroxysmal nocturnal dyspnea) are not seen. There may be syncope attacks caused by exertion as a result of the cardiac output not meeting the adequate perfusion. Although exertional dyspnea and peripheral edema are common symptoms in most patients, peripheral edema is scarce [31, 32, 37]. Initially, abdominal discomfort, tenderness, pain, and then ascites occur due to passive hepatic congestion (Pick’s disease-Pseudocirrhosis) (Table 2).
Haemodynamic Effects
Dynamic Changes in Right and Left Heart Filling with Respiration Elevation and Equalization of Cardiac Filling Pressures İncreased Venous Pressure Decreased Cardiac Output
Symptoms vary depending on the stage of the disease.
The main finding is jugular venous distension. This finding may not be seen in mild constrictive pericarditis and hypovolemic patients [46].
Inflate the patient’s face and abdomen.
Systemic arterial pressure is within normal limits or low.
The pulse pressure range is reduced.
Contrary to normal, the elevated venous pressure increases further with inspiration. (Kusmaull sign) [47].
Diastolic beat can be noticed with palpation. (Diastolic shock).
By listening, the heart is usually quiet and S1 and S2 are soft. A high-frequency early diastolic snap sound may be heard along the left edge of the sternum. (Pericardial knock). This early diastolic additional sound occurs as a result of abrupt cessation of ventricular filling [48, 49]. This is a sign of the sudden decrease in the “y” wave in central venous pressure and the response of ventricular filling.
Peripheral pulse may be paradoxical. (Pulsus Paradoxus).
Pulsus Paradoxus: Pulsus paradoxus described by Kusmaul in 1872; It is a decrease in systolic arterial pressure by more than 10 mmHg as a result of the pooling of the blood expelled from the right ventricle in the lung bed in the inspiration [10]. In summary; It is the exaggerated form of a normal physiological event [50, 51]. Venous return limitation caused by pericardial restriction causes a decrease in systolic arterial pressure of more than 10 mm Hg in inspiration [51, 52, 53]. This event is the dynamic between the pericardium and the heart. Explains the clinical findings that occur because the relationship affects the intracardiac volume/pressure relationship at every stage of the cardiac cycle.
Constrictive pericarditis is not immediately diagnosed with standard tests. The reasons why diagnosis is difficult is because it shows symptoms similar to heart failure or lung/liver disease. Constrictive pericarditis should be considered in the presence of unexplained heart failure, pleural effusion, jugular venous distension, liver disease, edema. In addition to these findings, if there is a history of cardiac surgery, chest radiotherapy/pericarditis, the diagnosis of constrictive pericarditis is correct. Constrictive pericarditis is most often confused with restrictive cardiomyopathy, which has similar findings.
Diagnostic methods initially include ECG, Chest radiograph, laboratory findings and echocardiogram.
Electrocardiography: The ECG is nonspecific. Low-voltage QRS, nonspecific changes in the ST segment, widening/inversion of the T wave are seen in approximately 25% of patients. The P wave may be narrow and bifid. Atrial fibrillation was detected in approximately 30% of them [32, 37, 38, 54].
9.2 Chest radiography
Findings on chest X-ray are nonspecific, but cardiomegaly due to pleural effusion, pulmonary vascular congestion, or pericardial effusion is seen. Pericardial calcification is seen on chest X-ray in 27% of constrictive pericarditis cases.
9.3 Laboratory assessment
The plasma brain natriuretic peptide (BNP) level can be used for diagnosis. BNP is a determinant of ventricular dysfunction and wall tension. Elevation is typical in many forms of heart failure and cardiomyopathy. In constrictive pericarditis, BNP elevation is less than in cardiomyopathy. Hepatic function tests are abnormal due to congestion.
9.4 Echocardiogram
While echocardiography is performed to rule out heart failure, left ventricular, right ventricular dysfunction, and valve dysfunction, it is very important to distinguish between constrictive pericarditis and restrictive cardiomyopathy, which is most confused (Table 3). In echocardiography performed specifically for constructive pericarditis; movement-shift of the ventricular septum towards the left ventricle, as an indicator of increased vena cava inferior pressure; Enlargement of the hepatic veins and inferior vena cava is seen. Pericardial thickening, calcification is seen.
Clinical signs
Constrictive pericarditis
Restrictive cardiomyopathy
Heart size Jugular venous pressure symptom of vomiting systolic murmur S3 Galop** Systemic Disease Thorax radiography heart shadow Pericardial calcification ECG P mitral Atrial fibrillation message defect T wave Q wave Echocardiography pericardium Calcification Septal movement CT/MRI
Normal M view* There is Rare There is Tuberculosis Normal 50% have it There is There are 33% Rare Inversion frequent ---------------- Thick Pericardial Normal Thick pericardium
Often enlarged M view There is There is Except for amyloid Amyloid,Sarcoidosis Normal/slightly enlarged. Rare Rare Stylish Stylish Inversion frequent Pseudo MI pattern is common --------------- myocardial weakened normal pericardium
Table 3.
Clinical and examination findings in the differential diagnosis of constrictive pericarditis and restrictive cardiomyopathy (* due to significant x and y descents, **pericardial knock).
Left shift of the ventricular septum in relation to respiration (shift): A decrease in left-sided cardiac filling during inspiration causes the ventricular septum to shift to the left. This increases right ventricular filling. In contrast, two-dimensional and M-mode echocardiography shows the septum shifting to the right in the expiration. Sliding movement in the ventricular septum is very important in relation to respiration in constrictive pericarditis, and its sensitivity is 93%.
Change in mitral inflow velocity in relation to respiration: A decrease in cardiac filling of the left side during inspiration is an indication of a decrease in mitral early inflow velocity [55, 56, 57].
Reversal of hepatic vein flow in relation to respiration: During late diastole in expiration, right-sided cardiac filling decreases as a sign of hepatic vein flow reversal. Reverse hepatic vein diastolic flow during expiration is 88% specific for constrictive pericardium [56].
Computed Tomography (CT): Measurement is made for pericardial thickening and calcification in cardiac CT of the heart (Figure 1). Pericardial thickening is detected at a rate of 72% and pericardial calcification at a rate of 35% in CT [29]. In addition, defect in the ventricle contour is detected due to pathology-disease in the pericardium in CT [58].
Figure 1.
Computed tomography view of calcific pericardium in constrictive pericarditis.
Cardiac Magnetic Resonance Imaging (CMRI): Provides information on cardiac anatomy including pericardial thickness, calcification and pericardial effusion, such as CMRI, cardiac CT [58, 59].
Delayel gadolinium enhancement (DGE): Granulation tissue and chronic inflammation in the DGE of the pericardium are associated with increased fibroblast proliferation and neovascularization [60]. DGE of the pericardium shows the presence of inflamation, which is a part of the constrictive process, and highlights medical therapy, which is an early -stage option in the treatment [61].
Invasive Haemodynamics evaluation: Hemodynamic catheterization is necessary when non-invasive evaluation methods for CP are inadequate. Especially if the central venous pressure is less than the expected value (less than about 15 mmHg), the sensitivity of the evaluation with catheterization is high [62].
Right and left ventricular diastolic filling pressures close to equivalent, and CVP and intracardiac pressures increased.
When the right atrial pressure is observed, deep “y” wave descent and right ventricular pressure “dip and plateau or square root” sign are observed. Both signs occur with decreased pericardial compliance and rapid-early diastolic filling of the right ventricle.
The atrial pressure curve shows high “a” and high “v” waves and prominent “x” and “y” descents (“M” and “W” appearance) (Figure 2).
Due to high venous pressure, ventricular filling is rapid in early diastole. The result is a deep fall in early diastole followed by a spike (“tip”) and a high diastolic plateau in ventricular pressure curves. This typical finding is called “square root sign” because it resembles the “ deep and plateau” and the square root () sign (Figure 3).
Right ventricular systolic pressure is less than 50% mmHg.
Right ventricular end diastolic pressure is less than 1/3 of right ventricular systolic pressure.
Figure 2.
High “a” and “v” waves, deep and slow “x” and “y” descents (M view) in right atrial pressure curve for constrictive pericarditis.
Figure 3.
“Deep” and plateau (square root, indicated by a red elliptical circle) sign in the right ventricular pressure curve for constrictive pericarditis.
When the gradient between pulmonary capillary wedge pressure and intrathoracic and left ventricular diastolic pressure develops, a difference of ≥5 mmHg between the expiration and inspirum has been reported as 81% specificity and 93% sensitivity for the diagnosis of constrictive pericarditis (Figure 4) [63].
Figure 4.
Simplified diagnostic algorithm for the diagnosis and treatment of symptomatic constrictive pericarditis.
10.1 Biopsy and surgical exploration
There may be cases where the diagnosis remains uncertain even after extensive evaluation with hemodynamic catheterization, imaging modalities, and echocardiography. Surgical exploration is sometimes recommended in these cases. Endomyocardial biopsy may be a suitable option before surgical exploration [64] (Table 4).
Catheter Finding
Constrictive pericarditis
Restrictive cardiomyopathy
In intracardiac pressures change with breathing Diastolic pressures left atrial pressure right atrial pressure “√¯” (“square root”) appearance (“deep and plateau”) in the right ventricular pressure curve RVEDP / LVESP LVEDP -RVEDP Pulmonary Hypertension
No Same Equal to RA pressure > 15 mmHg There is > 1/3 < 6 mmHg Light
There is LV/RV It is 10–20 mmHg higher than the RA pressure. < 15 mmHg Disappears with treatment < 1/3 > 6 mmHg Intermediate or advanced
Table 4.
Catheterization findings in constrictive pericarditis and restrictive cardiomyopathy.
10.2 Treatment
10.2.1 Transient constrictive pericarditis
In some cases of Constrictive Pericarditis, it resolves spontaneously or with anti-inflammatory therapy. In a study conducted at the Mayo Clinic, 17% of Constrictive Pericarditis cases healed spontaneously without the need for surgery [65]. 67% of these cases were temporary Constrictive Pericarditis with effusion. Transient Constrictive Pericarditis most commonly occurs after cardiac surgery. It is also accepted that it may be idiopathic or have infection, trauma or malignancy. Most patients who respond to steroid or non-steroidal anti-inflammatory drug therapy are most likely seen in pericarditis with high serum inflammatory marker levels and high DGE in cardiac MRI [61, 66]. In patients with subacute and distinct pericardial inflamation is reasonable to try 2–3 months of anti-inflammatory therapy [67]. The typical regimen of medical treatment consists of a non-steroidal anti-inflammatory drug with Colchicine or an oral steroid. However, more work needs to be done.
2) Chronic Constrictive Pericarditis: In most of the cases, constrictive pericarditis is chronic and progressive. Diuretic therapy is strictly palliative. The defined and accepted treatment is surgical total pericardiectomy (Pericardial decortication) [67]. Pericardiectomy is an elective surgery. Left anterior thoracotomy is performed by bilateral thoracotomy or median sternotomy. Decortication should be performed on the left and right ventricles, covering the anterolateral and diaphragmatic surfaces, from the phrenic nerve to the other phrenic nerve (if necessary, extending to the posterior of the left phrenic nerve). In this procedure, as much pericardium as possible should be removed (removal) to cover the diaphragmatic and posterolateral pericardium [68]. Pericardial stripping is started from the anterior aspect of the left ventricle and is performed towards the apex. The pericardium over the right ventricle and right atrium is then resected. If the pericardium on the right atrium and right ventricle is liberated first, pulmonary edema will develop as right ventricular output increases and left ventricular pressure continues. Although there are those who suggest that stripping the pericardium on the vena cava and right atrium is unnecessary, the majority recommends that pericardiectomy be performed in these regions as well. Most of the arrhythmias that occur during surgery are due to small infarcts in the coronary vessels. These arrhythmias are controlled with 0.1% lidocaine HCL. Although peeling of the pericardium over the atrium and vena cava is hemodynamically beneficial, the risk is high. To reduce the risk. A cardiopulmonary bypass can be used [69]. Careful care is required in the early postoperative period. Arterial and central venous pressure are monitored. Myocardial insufficiency due to chronic construction does not return to normal immediately after the operation. Low dopamine infusion is started for those with ventricular irritability. Existing hepatomegaly, ascites, edema continue for a few more months. Appropriate diuretics and protein loss are replaced.
11. Prognosis after pericardiectomy
Depending on the prognosis etiology, it is seen that the patient’s condition worsens after pericardiectomy in advanced stages of NYHA functional classification, elderly patient, impaired renal function, pulmonary hypertension, decreased Ejection fraction, increased Child Pugh liver disease [35, 37, 70]. Care should be taken not to injure the phrenic nerves during the pericardiectomy procedure. The mortality rate after pericardiectomy is 5–15%, and the most common cause is low cardiac output. The main cause of postoperative low cardiac output is myocardial atrophy caused by chronic constriction; myocardial fibrosis found in cases secondary to mediastinal radiation. After incomplete pericardiectomy, recurrent constrictive pericarditis is associated with an increased risk and reduced survival rate [71]. In the publications of several large volume centers, the mortality rate for surgical pericardiectomy has been reported as 6%–7.1% [34, 35, 36, 37]. Long-term survival after pericardiectomy varies greatly depending on etiology and patient character, not age and gender [37]. For example; The cure rate of patients with idiopathic constrictive pericarditis is ≥80% in 5–7 years [34, 35, 36]. The long-term recovery rate after surgery is >80% in asymptomatic or mildly symptomatic patients [37]. On the other hand, it has been reported that the outcome after pericardiectomy is very poor in patients with constrictive pericarditis due to chest radiotherapy. The recovery rate in these is 0% - 30% for 5–10 years [34, 35, 36, 37].
12. Conclusion
Constrictive Pericarditis; It is a disorder of cardiac filling caused by a diseased, inelastic pericardium that restricts cardiac chamber expansion. Key pathophysiologic feature include dissociation of intrathoracic and intracardiac pressures and and enhanced ventricular interaction. It is a form of diastolic heart failure with different pathophysiology and treatment. It often requires special study as it resembles other forms of heart failure. It should be considered in all patients with unexplained right heart failure symptoms or signs,especially when the left ventricular ejection fraction is preserved.
Diagnosis remains challenging,and the most effective tools are designed to identify the unique pathophysiologic mechanism underlying constrictive pericarditis: dissociation of intrathoracic and intracardiac pressures and enhanced ventricular interaction. Echocardiography is very important in the diagnosis of Constrictive Pericarditis. Methods of cross-sectional imaging are as essential as hemodynamic catheterization in confirming the diagnosis. Cardiac MRI is necessary to provide information about the character of the pericardial tissue, while DGE is necessary to show the presence of significant inflammation in the pericardium and to determine medical therapy(with antiinflamatory).
Complete surgical pericardiectomy has been accepted as the only definitive treatment for patients with chronic constrictive pericarditis.
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