*Onur Benli*

### **Abstract**

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.

**Keywords:** pericardium, constrictive, pericarditis, pericardiectomy, decortication

### **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.

### **2. History**

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].
