The normal gross and microscopic structure of the human pericardium is reviewed in information. Based on the structural components of the pericardium, the pathologic responses commonly checked out in clinical specimens are presented. This offers a corfamily member explanation to clinical evolution and also diagnostic imaging findings such as delayed improvement in the workup of pericardial condition.

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We existing the gross and microscopic structure of the pericardium as a framework of recommendation that have the right to be associated through present cardiac imaging methods and also interventions. The limited collection of responses of the pericardium to varied pathologic stimuli is depicted in the context of its normal framework.

A. Gross Structure of the Parietal and Visceral Pericardium

The pericardium is a roughly flask-shaped sac that consists of the heart and proximal parts of the great vessels

. The lateral surdeals with of the pericardium are invested by the mediastinal component of the parietal pleura other than in those areas wright here ligaments anchor the pericardium to the sternum, the diaphragm, and the vertebral column. The phrenic nerves and also pericardiophrenic vessels are included in two bundles flanking the lateral contours of the heart
.

The pericardium is conventionally separated right into parietal and also visceral pericardium . The parietal pericardium is composed of an outer fibrous connective tproblem sac lined by serosa. The serosal component is composed of a solitary continuous layer of mesothelium that invests the fibrosa layer of the pericardium and extends over the root of the good arteries to completely cover the outside surface of the heart. The layer of mesothelium investing the external surconfront of the heart is referred to as the visceral pericardium or epicardium. The fibrosa layer of the parietal pericardium is in between 0.8 and also 1 mm thick however may show up slightly thicker on imaging.1 The pericardial sac is covered by variable quantities of adipose tconcern in its mediastinal surconfront, especially in the cardiophrenic angles

.

Figure 1A


*

Anterior view of the undamaged pericardial sac. An undamaged pericardium attached to the diaphragm is presented via the mediastinal pleura extending the lateral surdeals with of the pericardial sac. Note the numerous epipericardial adipose tconcern in the anterior mediastinum and also anterior cardiophrenic angles. The arrowheads flank the borders of the sternopericardial ligament. LCC = left common carotid artery. SVC = superior vena cava.

Figure 1B


*

Right lateral watch of the heart and also pericardium. The ideal phrenic nerve and also pericardiophrenic vessels lie in between the parietal pericardium and also mediastinal pleura anterior to the pulmonary hilum. The arrowheads highlight these structures. Note the numerous adipose tproblem spanning the mediastinal surchallenge of the pericardium in the anterior and also lateral surfaces. RIPV = appropriate inferior pulmonary vein. RPA = best pulmonary artery. RSPV = appropriate superior pulmonary vein. SVC = Superior vena cava.

Figure 1C


*

Left lateral watch of the heart and pericardium. The course of the left phrenic nerve and also steustatiushistory.orgompanying vessels are highlighted by the arrowheads. Ao = aorta. LIPV = left inferior pulmonary vein. LPA = left pulmonary artery. LSPV = left remarkable pulmonary vein.

Figure 2


*

Parietal vs. visceral pericardium. The pericardium has, as many various other serosal surfaces, a parietal and also a visceral component. The parietal pericardium is created of two layers: a serosal lining (thin red line) and a fibrous sac (thicker yellow line). The visceral pericardium or epicardium is composed of a single layer of serosal investment extending the entire heart (thin red line overlying the myocardium in blue). Note that the serosal lining of the parietal and also visceral pericardium is a continuous layer of mesothelial cells. The serosal layer of the parietal and visceral pericardium challenge each other. The potential area lined by the serosal layers is the pericardial cavity.

Figure 3


*

Parietal and also visceral pericardium. A: Coronal section of the heart reflects the ventricles, ascfinishing aorta (Ao), and partial views of the ideal and also left atrial appendages, the premium vena cava (SVC), the aortic valve, and also the pulmonary artery trunk (PA). B: The incollection of the left lateral ventricular wall is enhanced. The visceral and parietal pericardium are in close apposition and also the area between these 2 layers is virtual. The arrowheads present a space of folding of the parietal pericardium wbelow it separates from the visceral pericardium. Keep in mind the lack of subepicardial fat in the lateral left ventricle. C: Light microscopic exam mirrors a thin layer of fibrous tworry (yellow) overlying the cardiac muscle (red). The "hobnail" cells lying over the thin fibrous sheet are the mesothelial cells which create the visceral pericardium. Note the close proximity of the myocardial capillaries to the mesothelium of the visceral layer. This rich network of vessels have the right to administer quick deliver of liquid material in and also out of the pericardial area. D: A cshed up of the incollection on the ideal ventricle in 3A is presented. Tbelow is a distinctive space in between the parietal pericardium (arrowheads) and the epicardium extending the adipose tproblem that overlies the best ventricular myocardium (RV). E: Light microscopy of the mesothelial lining over the adipose tworry of the best ventricle (visceral pericardium). Short elastic fibers (black) are existing in the subepicardium. F: This micrograph of full thickness pericardial sac shows the fibrosa layer of the parietal pericardium. Note the sporadic vascularization of the fibrosa. The mesothelial cells of the parietal pericardium are directly attached to the fibrosa in the top component of the photo. The mediastinal aspect (lower part) of the pericardium shows adipose tconcern which, in turn, is likewise spanned by mesothelial cells forming the serosa of the mediastinal pleura. Ao = aorta. LV = left ventricle. PA = pulmonary artery. RV = best ventricle. SVC = exceptional vena cava. * = inferior aortic recess. ** = left pulmonic recess.

B. Pericardial Sinoffers and also Recesses

The reflections of the serosa about the good vessels entering and leaving the heart form the pericardial sinprovides and also recesses.2 The ascfinishing aorta and major pulmonary artery together are completely ensheathed by an investment of the visceral pericardium. This investment creates a potential room, the transverse sinus, which sepaprices the anteriorly located good arteries from the veins posteriorly

. The floor of the transverse sinus is developed by the roof of the left atrium. The transverse sinus is continuous via the remarkable aortic recess between the aorta and also the exceptional vena cava and the inferior aortic recess in between the aorta and also the right atrium
. The lateral extensions of the transverse sinus are dubbed the best and also left pulmonic recesses.

A second investment of visceral pericardium separately covers the venae cavae and pulmonary veins. The postcaval recess lies behind the premium vena cava and is bounded by the best pulmonary artery superiorly and ideal remarkable pulmonary vein inferiorly. The ideal and left pulmonary venous recesses are created by the pericardial reflection in between the particular superior and also inferior pulmonary veins. The cul-de-sac located behind the posterior wall of the left atrium is the oblique sinus

. It is bounded by the pericardial reflection alengthy inferior pulmonary veins and the inferior vena cava. It straight abuts the carina and also the esophagus posteriorly.

Figure 4


Sinsupplies and recesses of the pericardium. In this picture the anterior (ventral) percent of the pericardium and also the heart have actually been rerelocated to display the good vessels at the base of the heart. The aorta and pulmonary artery has actually been transected to display the course of the transverse sinus (dotted line) that sepaprices the arteries from the venae cavae and also pulmonary veins. The pericardial reflection exhas a tendency to the proximal aortic arch and also the recess between the aorta and also the premium vena cava is called the remarkable aortic recess (dotted line). The left lateral expansion of the transverse sinus is the left pulmonic recess bordered by the left pulmonary artery and left premium pulmonary vein. The oblique sinus is the cul-de-sac behind the left atrium and also bound by the pericardial reflection over the inferior pulmonary veins and also the inferior vena cava. IVC = inferior vena cava. LPA = left pulmonary artery. LPV = left pulmonary veins. RPA = ideal pulmonary artery. RPV = best pulmonary veins. SVC = premium vena cava.

C. Microscopic Organization of the Pericardium

Three unique layers can be characterized in the parietal pericardium by microscopic exam: the serosa, the fibrosa, and also an outer layer of epipericardial connective tconcern. The serosa is the innermany surface of the pericardial sac and also is formed by mesothelial cells

. The mesothelial cells are level to cuboidal epithelial cells well-off in microvilli which are important for the formation and reabsorption of pericardial fluid
. The fibrosa is created of dense collagen bundles through interspersed scant elastic fibers
. The fibrous tproblem bundles subjacent to the mesothelium tend to have a cephalocaudal orientation; whereas the more external bundles have actually a more weaved company which enables for some distensibility of the pericardial fibrosa. The fibrosa includes scant connective tproblem cells and small vessels. The outer pericardial layer mirrors rather more abundant elastic fibers, adipose tworry, neural elements, and also blood vessels. Rare mast cells and also mononuclear cells have been defined in this layer.3

The visceral pericardium

is developed by a thin layer of fibrous tworry overlying the myocardium invested by mesothelial cells (the serosal component of the visceral pericardium) over the whole surface of the heart.

Figure 5


A sheet of mesothelial cells is presented at high magnification. These cells deserve to differ from level to cuboidal in shape. Microvilli (arrowheads) are present on the surface dealing with the pericardial cavity to rise the surconfront area of these cells. The microvilli impart a "fuzzy" look to the luminal border of the mesothelial cells.

D. Pericardial Responses to Injury

1. Distensibility

While the fibrous tproblem bundles in the inner fibrosa via its cephalocaudal orientation perform not distend incredibly much; in comparison, the weaved company of the fibrous tworry bundles of the outside fibrosa enables for some distention of the pericardial sac prior to physiologic constriction is clinically noticeable. The specialized nature of the mesothelial cells through plentiful microvilli and also the liquid deliver devices through these cells allow for high transfer capacity via the serosal pericardium. The extremely vascularized epicardium can provide huge move of liquid to the mesothelial cells for these to produce transudays and also exudates. This defines how basic transudays and/or extremely fibrinous exudates have the right to easily form in the pericardial cavity when tright here is injury.

2. Exudative and also inflammatory response

The pericardium (parietal and visceral) has actually a restricted response to injury, which is initially materialized as increased production of pericardial liquid.4 The effusion could be a transuday which is composed largely of thin liquid or an exuday which has huge quantities of fibrin and, as a role of severity, variable numbers and also types of inflammatory cells

. The fibrinous exuday creates adhesions and strands in between the parietal and visceral pericardium. These fibrinous adhesions are the basis of the friction rub detected on physical examination
. With fibrinolysis, the fibrin deposits normally organize or heal into loose fibrous strands quite than dense fibrous tproblem
. This kind of repair does not cause constriction, because pockets lined through normal mesothelial cells are created, which lubricate the remaining pericardial room. On the other hand, repeated bouts of fibrinous depositions or an extra serious inflammatory injury have the right to elicit a fibrogenic repair procedure.

Figure 6


Fibrinous exuday. Light micrograph of the epicardial surface of the myocardium reflecting mild inflammatory infiltprice in the myocardium and also an exuberant eosinophilic fibrinous exudate on the surconfront of the visceral pericardium. The gross pathology of this fibrinous exuday is illustrated in Figure 7.

Figure 7


Gross specimen of a heart of a patient through uremic pericarditis completely spanned through fibrinous strands which in enhancement present yellow/green discoloration as the patient had jaundice. Keep in mind that the fibrin strands surround the root of the good vessels as these segments are intrapericardial. Ao = aortic valve and aortic root. LV = left ventricle. PA = pulmonary artery and valve. RV = ideal ventricle. RVOT = right ventricular outcirculation tract. SVC = premium vena cava.

Figure 8


Coronal area of the heart mirroring organized fibrous (not fibrinous) strands (asterisk) formed in between the visceral pericardium and the parietal pericardium. Keep in mind that the parietal pericardium is slightly thicker than the normal examples in Figure 3. LA = left atrium. LAA = left atrial appendage. LLL = left lower lobe of the lung. PA = pulmonary artery at bifurcation.

3. Reabsorption, company and repair of the exudative inflammatory response

The healing process may show a number of alternate preleading fads as displayed in Figure 9. These responses have the right to be of a single form or merged processes

. In some patients, the inflammatory infiltprices involve both the serosa of the pericardium and also the serosa of the pleura
.

Figure 9


Usual responses of the pericardium to noxious stimuli cause varied non-exclusive kinds of effusions. A serous effusion may take place and be reabsorbed entirely without leaving any kind of histologic modification. On the various other hand also, exudative effusions always leave a trace of the pericardial response to the injury. The exuday of fibrin is the a lot of common finding regardmuch less of the resource of injury: chemical (uremic, pharmaceuticals), physical (open heart surgery, therapeutic ablation, radiation), or contagious (viral, bacterial, fungal, parasitic). Once the fibrinous or fibrino-hemorrhagic exudate occurs, there is usually an inflammatory response elicited that will certainly "clean" the fibrinous debris. During this phase, the inflammatory cells promote the development of neovascularization and also early on extracellular matrix deplace (granulation tissue). If the noxious stimulus ends, the result is commonly mild fibrosis. If the noxious stimulus persists, the response of the pericardium is extended in regards to the process of exudation, inflammation, and also repair. In recurrent pericarditis, the inflammatory response may wax and also wane. The red arrows illustrate points where a reexisting insult deserve to happen aacquire, hence editing and also lengthening the healing process. The repetitive injury-repair cycles lead to thickening of the parietal pericardium and also adhesion to the visceral pericardium through obliteration of the pericardial cavity. While generally checked out, calcification is not always a feature present during the healing of the pericardium.

Figure 10


Acute fibrinous pericarditis. A and also B: Fibrinous exudates via abundant inflammatory cells are presented. The fibrosa layer mirrors dilated vessels. The incollection mirrors a cshed up of the inflammatory infiltprices intermingled via the fibrinous strands and also reenergetic mesothelial cells in the serosa layer of the parietal pericardium. C and also D: Parietal pericardium through abundant inflammatory infiltrates and also beforehand deplace of extracellular matrix (yellow green color in D on optimal and listed below the fibrosa). This is a very early phase of organization of the exudate. The newly created connective tissue eventually is got into by capillaries that form extensive vascular network-related. The fibrosa layer of the parietal pericardium is delineated by the dotted lines. Note that in this example the inflammatory procedure is including both the pericardial serosa (mesothelial) layer and also the mediastinal pleural serosa layer. If a pericardiectomy is perdeveloped, the inflammation existing in the mediastinal pleura might still current clinically as residual "pericardial" referred pain. (A and C: H&E stain. B and D: Movat pentachrome stain).

If no further injurious stimuli are present, the inflammatory cells within the fibrinous exudate promote neovascularization and also fibroblast proliferation. Extracellular matrix is laid dvery own and as it matures, the loose granulation tworry becomes organized via even more mature fibrous tproblem while the neovascularization and also chronic inflammation end up being less conspicuous

. If the injurious stimulus that originated the effusion does not relapse, the healing process ultimately leads to the maturation of the granulation tproblem into a dense fibrous scar.

Figure 11


Organizing pericarditis via conspicuous neovascularization. Note that the fibrosa layer does not have actually extremely conspicuous vessels compared to the area of arranging fibrosis. (H&E stain and also Movat pentachrome stain).

The fibrous proliferation of the pericardium might mostly involve only among the serosal components or might involve both the parietal and also visceral pericardium. If repeated episodes of pericarditis happen (regardmuch less of the etiology), the response of the pericardium is comparable in developing new acute fibrinous and/or fibrino-hemorrhagic exudays which cause new granulation tproblem and even more neovascularization . Therefore, chronic effusions might be connected through pericardial thickening. The neovascularization current in various stages of the organization of the pericardial effusion is the anatomic substrate of the late gadolinium improvement on CMR imaging researches of pericarditis. Calcific deplace may be focal or substantial and also likely represents an end-stage reactivity to injury

. Since of the limited collection of tproblem response of the pericardium to noxious stimuli, the histologic features of excised pericardium for constrictive pericarditis are primarily noncertain in regards to etiologic diagnosis and also most often reflect a spectrum from arranging fibrinous pericarditis to arranged fibrocalcific pericarditis.

Figure 12


Maturing arranging pericarditis. Loose edematous granulation tworry becomes arranged right into denser, thicker fibrous tconcern as the amount of extracellular matrix and inflammation diminishes. Relative abundance of fibroblasts (fibroplasia) and also newly-formed blood vessels are indications of the task of the process. Compare to Figure 13. (H&E stain and also Movat pentachrome stain).

Figure 13


Organized pericarditis through represent insult. These micrographs display dense, mature bundles of fibrous tconcern overlying the fibrosa layer of the pericardium. The neovascularization is much less conspicuous than in the earlier stages of organization (Figures 11 and also 12). In this instance, tbelow is boosted cellularity in the top strata of the pericardium in the direction of the pericardial cavity. This innermost area in the direction of the pericardial cavity shows plentiful fibroblast proliferation or fibroplasia, displayed as dark blue infiltrates in upper left area of the imperiods. In enhancement, tbelow is also fibrin and hemorrhage. This is a typical example of a represent process. (H&E stain and also Movat pentachrome stain).

Figure 14


Dense fibrous pericarditis without calcification. The parietal pericardium is thickened as a result of the additional dense (yellow) fibrous tproblem that mirrors no fibroblasts, inflammatory infiltprices or neovascularization. This represents a quiescent phase however may currently be linked via pericardial constriction. (H&E stain and Movat pentachrome stain).

If the cause of the pericardial effusion is main or metastatic malignant neoplasm, the malignant cells have the right to be readily watched in the time of microscopic examination

.

Figure 15


Metastatic lung adenocarcinoma. An organizing fibrinous exuday containing metastatic tumor cells is present. Mild inflammatory infiltrate is detailed in the fibrosa layer of the parietal pericardium. The inset shows a cluster of metastatic tumor cells with large pleomorphic nuclei in a channel lined by level endothelial cells. (H&E stain and Movat pentachrome stain).

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References

Ferrans VJ IT, Roberts WC. Anatomy of the pericardium. In: Reddy PS LD, Shaver JA, eds. Pericardial Disease. New York: Raven Press; 1982:15-29.Levy-Ravetch M, Auh YH, Rubenstein WA, Whalen JP, Kazam E. CT of the pericardial recesses. AJR Am J Roentgenol 1985;144:707-14.Ishihara T, Ferrans VJ, Jones M, Boyce SW, Kawanami O, Roberts WC. Histologic and ultrastructural functions of normal human parietal pericardium. Am J Cardiol 1980;46:744-53.Klein AL, Abbara S, Agler DA, et al. Amerihave the right to Society of Echocardiography clinical references for multimodality cardiovascular imaging of patients via pericardial disease: endorsed by the Society for Cardiovascular Magnetic Resonance and also Society of Cardiovascular Computed Tomography. J Am Soc Echocardiogr 2013;26:965-1012.

Clinical Topics: Cardiac Surgery, Invasive Cardiovascular Angiography and Intervention, Noninvasive Imaging, Pericardial Disease, Vascular Medicine, Aortic Surgery, Interventions and Imaging, Interventions and Vascular Medicine

Keywords: Pericardium, Adenocarcinoma, Adipose Tissue, Aorta, Thoracic, Aortic Valve, Cardiac Imaging Techniques, Carotid Artery Thrombosis, Cicatrix, Coloring Agents, Constriction, Endothelial Cells, Epithelial Cells, Extracellular Matrix, Fibrinolysis, Heart Ventricles, Inflammation, Mast Cells, Microvilli, Myocardium, Pericardial Effusion, Pericardiectomy, Pericarditis, Constrictive, Phrenic Nerve, Pulmonary Artery, Pulmonary Veins, Sagittaria, Vena Cava, Inferior, Vena Cava, Superior


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