It directly abuts the carina and the esophagus posteriorly. Three distinct layers can be defined in the parietal pericardium by microscopic exam: the serosa, the fibrosa, and an outer layer of epipericardial connective tissue. The serosa is the innermost surface of the pericardial sac and is formed by mesothelial cells [Figure 3]. The mesothelial cells are flat to cuboidal epithelial cells rich in microvilli which are important for the formation and reabsorption of pericardial fluid [Figure 5].
The fibrosa is composed of dense collagen bundles with interspersed scant elastic fibers [Figure 3]. The fibrous tissue bundles subjacent to the mesothelium tend to have a cephalocaudal orientation; whereas the more external bundles have a more weaved organization which allows for some distensibility of the pericardial fibrosa.
The fibrosa contains scant connective tissue cells and small vessels. The outer pericardial layer shows somewhat more abundant elastic fibers, adipose tissue, neural elements, and blood vessels. Rare mast cells and mononuclear cells have been described in this layer. The visceral pericardium [Figure 3] is formed by a thin layer of fibrous tissue overlying the myocardium invested by mesothelial cells the serosal component of the visceral pericardium over the entire surface of the heart.
While the fibrous tissue bundles in the inner fibrosa with its cephalocaudal orientation do not distend very much; in comparison, the weaved organization of the fibrous tissue bundles of the external fibrosa allows for some distention of the pericardial sac before physiologic constriction is clinically evident. The specialized nature of the mesothelial cells with abundant microvilli and the fluid transport systems through these cells allow for high transport capacity through the serosal pericardium.
The highly vascularized epicardium can provide large transfer of fluid to the mesothelial cells for these to produce transudates and exudates. The pericardium parietal and visceral has a limited response to injury, which is initially manifested as increased production of pericardial fluid.
The fibrinous exudate forms adhesions and strands between the parietal and visceral pericardium. These fibrinous adhesions are the basis of the friction rub detected on physical examination [Figure 7]. With fibrinolysis, the fibrin deposits usually organize or heal into loose fibrous strands rather than dense fibrous tissue [Figure 8]. This type of repair does not result in constriction, since pockets lined with normal mesothelial cells are formed, which lubricate the remaining pericardial space.
On the other hand, repeated bouts of fibrinous depositions or a more severe inflammatory injury can elicit a fibrogenic repair process. The healing process may show several alternative predominant patterns as shown in Figure 9. These responses can be of a single type or combined processes [Figure 10]. In some patients, the inflammatory infiltrates involve both the serosa of the pericardium and the serosa of the pleura [Figure 10]. If no further injurious stimuli are present, the inflammatory cells within the fibrinous exudate promote neovascularization and fibroblast proliferation.
Extracellular matrix is laid down and as it matures, the loose granulation tissue becomes organized with more mature fibrous tissue while the neovascularization and chronic inflammation become less conspicuous [Figure 11]. If the injurious stimulus that originated the effusion does not relapse, the healing process eventually leads to the maturation of the granulation tissue into a dense fibrous scar.
The fibrous proliferation of the pericardium may predominantly involve only one of the serosal components or may involve both the parietal and visceral pericardium. Thus, chronic effusions may be associated with pericardial thickening. The neovascularization present in different stages of the organization of the pericardial effusion is the anatomic substrate of the late gadolinium enhancement on CMR imaging studies of pericarditis.
Calcific deposition may be focal or extensive and likely represents an end-stage reaction to injury [Figure 14]. The fiber bundles such as atrioventricular bundle and Purkinje fibers conduct the impulses from the center of the heart to the ventricles, triggering the contraction of the ventricles. Pericardium is the fibrous encase that covers the heart.
It consists of two layers of connective tissue. Serous pericardium, pericardial cavity, and fibrous pericardium are the three layers of the pericardium. The main function of the pericardium is to provide protection against infections while lubricating the heart. Also, it fixes the heart to the mediastinum. Myocardium refers to the muscular tissue of the heart, which is made up of heart muscles while pericardium refers to the membrane enclosing the heart, consisting of an outer fibrous layer and an inner double layer of serous membrane.
Further, the myocardium is the middle layer of the heart wall while the pericardium is the outermost layer of the heart. Also, myocardium is made up of heart muscles while pericardium is made up of connective tissue. Moreover, myocardium makes up a single layer while pericardium makes up two layers.
Regarding the function, the myocardium is responsible for heart contractions while the pericardium is responsible for the protection of the heart while preventing overfilling. Myocardium is the middle, muscular layer of the heart made up of heart muscles.
On the other hand, pericardium is the outermost, membranous structure of the heart, which protects the heart and prevent the overfilling.
The main difference between myocardium and pericardium is their structure and function. Bailey, Regina. WikiJournal of Medicine 1 2. ISSN
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