Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3715_Библиотеки_им_академика_М_И_Перельмана

The venous pole of the heart is embraced by a single continuous line of reection, but only the lower third of the superior caval vein is surrounded by the visceral pericardium, while upper two-thirds are extrapericardial.

The transverse pericardial sinus is a “narrow horseshoe tunnel” with walls consist­ing of visceral epicardial mesothelium that embraces the posterior surface of the aortopulmonary vascular pedicle forming the anterior wall and the surface of the anterosuperior part of the left atrium, and the superior caval vein forms the posterior wall of transverse pericardial sinus. The oor of the transverse sinus is formed by the roof of the left atrium. The transverse pericardial sinus has direct communica­tions with other pericardial sinuses and recesses (Figs. 1.2 and 1.3) [79, 121,

These are the cavities situated between the respective superior and inferior pulmo­nary veins. Milhiet proposed the terminology in 1956 and Vesely described in 1986 [94, 126]. Their shape changes based on their depth and base, which is the distance between the atrial ending of two pulmonary veins. These recesses may be absent, when there is a common pulmonary vein. It is directly related to carina and esopha­gus posteriorly. The shape of oblique sinus may vary from a square to triangular or an inverted shape based on the depth and symmetry of right and left pulmonary venous recesses (Figs.1.2 and 1.3) [17, 104, 105].

Pericardiophrenic and musculophrenic branches of the right and left internal mam­mary artery and descending thoracic aorta provide approximately 80% of the arte­rial supply to the pericardium. Small mediastinal branches originating from the descending thoracic aorta or esophageal or bronchial branches supply the posterior aspect of the pericardium. Branches from superior phrenic and intercostal arteries supply the pericardium inferiorly..

There are two layers of pericardial lymphatic vessels around the parietal pericar­dium and also within the fat and loose areolar tissue [62]. The anterior sternocostal part of the diaphragm drains laterally towards the phrenic nerves into the diaphrag­matic or superior phrenic nodes or at the prepericardial nodes located at the pericardio- diaphragmatic junction. Inferolateral portion of the pericardium drains into the lateral pericardial nodes, superior portion drains into the tracheobronchial or paratracheal lymph nodes. The posterior pericardium drains into the superior and inferior tracheobronchial lymph nodes. The diaphragmatic pericardium drains via short channels to the lymph nodes at the right border of the caval foramen. Overall, most of the lymphatic drainage of the pericardium is to the right lymphatic and thoracic ducts. Lymphangiogenesis, i.e. the formation of neolymphatic vessels is benecial in delaying atherosclerotic plaque formation [62, 71, 110].

The pericardium is well innervated. Pain from the brous layer of pericardium and parietal pericardium is mainly mediated by somatic afferents of the left and right phrenic nerves. Pain from the visceral layer of serous pericardium is transmitted along visceral afferent bres that travel through sympathetic nerves arising from the cervical, upper thoracic and stellate ganglia and traveling to cardiac and aortic plex­uses. The pericardium is also innervated by left recurrent laryngeal nerve and vagal bres via the esophageal plexus.

(primarily type 1 and type 3 collagen) interspersed with scant elastin bres. It is the orientation and abundance of the collagen bres responsible for the viscoelastic mechanical properties of the pericardium, like stress relaxation, hysteresis and creep. The external bundles tend to have a weaved organization, whereas the brous tissue bundles present subjacent to the mesothelium are arranged cephalocaudally, allowing pericardial brosa to have some distensibility. The brosa contain small vessels which penetrate in an oblique plane and extend for approximately 8μm (Figs.1.4a–d and 1.5). Interestingly, bovine pericardium possess only thick brous layer and no elastic tissue(Fig. 1.4c, d) [78, 80, 125].

In response to an acute injury, the pericardial inammation is characterised by uid exudation due to increased vascular permeability, desquamation of mesothelial cells, brin and/or inammatory cells [91]. Inammatory aggregates and brin strands form a layer of granulation tissue, broblastic proliferation and neovascular­ization and on cardiac magnetic resonance imaging presents as pericardial late gad­olinium enhancement [131].

Although, following pericardiectomy or in instances of congenital agenesis of peri­cardium, no adverse consequences have been noted, the pericardium indeed serves important functions.

Investigators have demonstrated that mechanoreceptors, chemoreceptors, and neu­roreceptors present in pericardium alter blood pressure and heart rate in response to distension of ventricles, constituents of pericardial uid, and pulmonary ination respectively. These different reexes provide “pericardial servo mechanisms” thus modulating mechanical properties of pericardium [19, 115].

114, 115, 124, 129]

Investigators have demonstrated epicardial fat as a cardiovascular risk marker asso­ciated with various cardiovascular risk factors, namely, age, obesity, diabetes and hypertension [10]. Its molecular and biochemical properties are different from

pericardial fat located outside parietal pericardium also known as mediastinal, para­cardial or intrathoracic fat. Epicardial fat is nourished from the coronary arteries while pericardiophrenic artery supplies pericardial fat. The functions of epicardial fat include regulation and local distribution of vascular ow; mechanical and inam­matory protection of coronary arteries and myocardium; acts as an immune barrier and provides fatty acids for myocardium during high demand; and exerts thermo­genic effects. It helps in metabolism of glucose-insulin and triglyceride, acts as source of anti-inammatory and proinammatory cytokines, and low-grade chronic inammation. Epicardial fat may accelerate process of atherosclerosis by enhancing smooth muscle cell proliferation, endothelial dysfunction, plaque instability and increased oxidative stress [10, 58, 96, 114, 115, 124, 129].

Diaphragmatic and pericardiosternal ligaments act by preventing excessive torsion and limiting displacement of pericardium and its contents within the thorax and neutralize the effects change of body position and respiration [87]. These attach­ments also contribute to the compliance of pericardial pressure volume relation [65].

Pericardial imaging modalities provide information on morphological features of pericardium and cardiac structures and cardiac functional assessment secondary to pericardial involvement, particularly cardiac lling. Although cardiac magnetic resonance in conjunction with computed tomography imaging are the preferred modalities for demonstration of pericardial morphology and pericardial sinuses and recesses, cardiac magnetic resonance alone can substantially aid in assessment of pericardial morphology and functional assessments [11–16].