The Innermost Lining of the Heart Wall Continuous With the Lining of the Blood Vessels

Cardiac Embryology

Richard J. Martin MBBS, FRACP , in Fanaroff and Martin's Neonatal-Perinatal Medicine , 2020

Endocardial Development: Formation of Cushion Tissue

Septation of the heart begins with the swelling of the extracellular matrix between the endocardium and the myocardium at specific regions of the heart tube. These regions include the AV junction, the outflow tract, the leading edge of the primary atrial septum, and the ridge of the interventricular septum. A complex set of inductive events has been elucidated by studying cushion formation of the AV junction and the outflow tract. ⁵⁴ These events include signaling between the specialized myocardium and a subset of competent endocardial cells through growth factors (e.g., transforming growth factor-βs [TGFβs], vascular endothelial growth factor [VEGFs], bone morphogenetic proteins [BMPs]) and extracellular matrix molecules. Various proteases and homeobox genes are also involved.

The subsequent cascade of events includes release and migration of cells from the endocardial epithelium (termedendothelial-mesenchymal transition, EMT) into the previously acellular cardiac jelly and proliferation, death, and differentiation of these endocardial mesenchyme cells within a complex matrix. In the outflow tract, the cushions are also populated by cardiac neural crest cells. The endocardial cushions of the AV junction are also invaded by cells originating from the embryonic epicardium. The cushions eventually give rise to, or at least greatly influence, the subsequent development of septa and valves of the heart. Because a number of factors, cell types, and tissues are involved in this process at multiple levels and at different stages, there are many sites where mistakes can occur. It is, therefore, not surprising that septation defects are so common. The differentiation of resilient valves requires remodeling of the extracellular matrix, an aspect that is poorly understood. However, it has been revealed that steps in cardiac valve differentiation and maturation share mechanisms with those of cartilage, tendon, and bone development. ⁴²

In the primitive atrium, a ring of tissue, the septum primum, grows toward the endocardial cushions near the AV junction (Fig. 71.8). Through apoptosis, fenestrations form in this tissue, creating the osteum secundum. The osteum primum, between the tip of this outgrowth of the septum primum and the endocardial cushion, closes as the tissue advances. The atrial roof folds inward, and the septum secundum begins to grow down on the right of the septum primum and continues in a crescent shape to form to the right of the base of the septum primum. This makes the septum primum a flap over the foramen ovale, allowing only right-to-left flow across the atria.

Ventricular and outflow tract septation occur in tandem, and aberrations in one may have structural consequences for the other. The myocardium from the outer curvature of the ventricle invaginates, growing cranially. AV canal endocardial cushions grow toward the myocardium, completing the ventricular septum. Outflow tract endocardial cushions form ridges that spiral along the conotruncus (Fig. 71.9). These ridges grow together to divide the conotruncus into the trunks of the aorta and pulmonary arteries. The AV canal and outflow tract endocardial cushions join, completing ventricular septation.

Systems Toxicologic Pathology

Brian R. Berridge , ... Eugene Herman , in Haschek and Rousseaux's Handbook of Toxicologic Pathology (Third Edition), 2013

Endocardium

The endocardium is a delicate layer that invests the entire inner surface of the heart. Its structure and thickness are very variable from one chamber to another, and even within different regions of a given chamber. The endocardial connective tissue is continuous with that in the myocardial interstitium and valvular leaflets. Endocardium is thicker in the atria than in the ventricles, in the left- than in the corresponding right-sided chambers, and in the outflow tracts than in the inflow tracts of the ventricles. The ventricular endocardium is composed of five distinct layers: the endothelial layer, the inner connective tissue layer, the elastic tissue layer, the smooth muscle cell layer, and the outer connective tissue layer or subendocardial layer.

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Diseases of the Myocardium and Endocardium

Lee Goldman MD , in Goldman-Cecil Medicine , 2020

Cardiovascular System and Lymphatic Vessels1

Lisa M. Miller , Arnon Gal , in Pathologic Basis of Veterinary Disease (Sixth Edition), 2017

Endocardium and Heart Valves

The endocardium lines the myocardium and contains Purkinje nerve fibers, which transmit a rhythmic action potential throughout the myocardium leading to contraction. The endocardium is lined by endothelial cells, which modulate many aspects of normal hemostasis. In normal states, the endothelial cells are antithrombotic, preventing circulating cells from attaching and thus allowing normal flow of blood through the heart and blood vessels. The endocardium is continuous with the endothelium of blood and lymphatic vessels. Normal flow of blood through the heart depends on functional valves (see Chapter 2). Properly functioning valves serve as one-way valves, allowing blood either to flow from one chamber to another (through AVVs) or to exit from the heart and enter either the pulmonary circulation (pulmonic valve) or the systemic circulation (aortic valve).

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Left and Right Ventricular Systolic Function

Catherine M. Otto MD , in Textbook of Clinical Echocardiography , 2018

Endocardial Definition

Accurate identification of the ventricular endocardium is key in the echocardiographic evaluation of LV systolic function regardless of whether M-mode, 2D, or 3D approaches are used. Speckle tracking stain also is most accurate with high-quality images of the myocardium. Endocardial definition is affected by the physics of ultrasound instrumentation, by anatomic factors, and by technical factors, including the skill of the sonographer. The endocardial-ventricular cavity interface is curved from any imaging window, so the endocardium appears as a thin, bright line where it is perpendicular to the ultrasound beam (axial resolution), but as a broad, "blurred" line where the beam is parallel to the endocardial-ventricular cavity interface (lateral resolution). As for other ultrasound targets, lateral resolution is depth dependent. In addition, "dropout" of signals may result from attenuation, a parallel intercept angle, acoustic shadowing, or reverberations.

Anatomically, the endocardium is not a smooth surface but has numerous trabeculations that are most prominent at the LV apex. The ultrasound beam is reflected from the inner edge of these trabeculations, so that the "endocardium" identified by echocardiography differs from the "endocardium" identified by contrast ventriculography or cardiac magnetic resonance imaging, in which contrast fills these trabeculations and outlines their outer edges.

Several technical factors affect endocardial definition during image acquisition, and meticulous examination technique is needed for optimal image quality. First, acoustic access can be optimizing by:

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Patient positioning

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Use of an echo-stretcher with an apical cutout

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Having the patient suspend respiration

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Careful adjustment of transducer position

Instrument settings can dramatically affect image quality, including:

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Transducer frequency

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Gain

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Gray-scale settings

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Focal depth

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Tissue harmonic imaging

2D endocardial borders are traced from digitally acquired images using the real-time motion of the images to aid in identification of the endocardial border during the tracing process. End-diastolic and end-systolic images are traced on the same cardiac cycle, with end-diastole defined as onset of the QRS complex and end-systole defined as minimal ventricular volume. The trained human observer remains the most accurate means for endocardial border tracing, thus limiting the wide application of quantitative methods because manual tracing of endocardial borders at end-diastole and end-systole in at least two views remains a tedious and time-consuming task. 3D imaging uses semiautomated border detection but continues to rely on manual identification of key anatomic landmarks and usually requires adjustment of the automated borders for accurate volumes measurements. Similarly, the speckle tracking strain images are visually inspected and adjusted to ensure that the myocardium is tracked correctly.

The Heart in Systemic Autoimmune Diseases

M. Sebastiani , ... C. Ferri , in Handbook of Systemic Autoimmune Diseases, 2017

3.1.4 Endocarditis and Valvular Disease

Endocardium involvement is thought to be rare in vasculitides. Functional inorganic murmurs or valvular pathologies that are not related to vasculitis comprise most of the reported cases. However, especially in EGPA, myocardial vasculitis, in addition to predisposing to arterial thromboembolus, endocardial thickening, and thrombus may extend down the myocardial surface to engulf the valvular apparatus or leaflets, classically affecting the atrioventricular valves, leading to significant valve dysfunction ( Ramakrishna et al., 2000). Also in GPA, significant valvular stenosis or regurgitation is frequently detected by echocardiography (about 15% of patients), with the mitral and tricuspid valves most commonly affected (Oliveira et al., 2005).

Moreover, specific valve damage may sometimes occur during the acute phase of the vasculitis and progress to valve distortion during lesion repair and cicatrization (Davenport et al., 1994).

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Anatomic Considerations and Examination of Cardiovascular Specimens (Excluding Devices)

J.J. Maleszewski , ... J.P. Veinot , in Cardiovascular Pathology (Fourth Edition), 2016

Endocardium

The endocardium lines the entire inner surface of all the heart chambers and is continuous with the inner layer of the blood vessels. For the most part, its structure is similar throughout the heart; however, the endocardial layer tends to be thicker in the left-sided chambers than the right-sided ones, in the atria than the ventricles, and in the outflow tracts than the inflow tracts. There are three recognized layers in the endocardium, which includes the endothelium with its basal lamina, the subendothelial layer, and the elastic layer ( Figure 1.29a and b). At times, these layers are ill-defined and they may exhibit some variation even within the same chamber.

Figure 1.29. Endocardium. (a) Three layers can be recognized in the endocardium: the endothelium with its basal lamina (arrowheads); a subendothelial layer (short arrows) comprising delicate, loosely dispersed, and multidirectional collagen fibrils; and the elastic layer (HPS stain; 200   ×). (b) The latter (arrows) is best appreciated with an elastic stain (Movat stain; 200   ×). (c) The subendothelial layer (asterisks) is more prominent in the atrial endocardium, particularly the left atrium (HPS stain; 40   ×). (d) The smooth muscle component (asterisks) in the elastic layer is especially prominent in the left atrium as well as the left ventricular septal region (not shown). Note the epicardial serosal lining (arrowheads) (Movat stain; 40   ×).

The endothelium consists of a single layer of flat, polygonal endothelial cells with rounded or oval nuclei. Similar to endothelial cells that line blood and lymphatic vessels, they possess an irregular cell membrane, Weibel-Palade bodies, and micropinocytotic vesicles. Complex lateral interdigitations are common in this site [139]. Occasionally, the cytoplasm of atrial endothelial cells contains microtubules and microfilaments, which are structures not typically found in ventricular endothelial cells. Micropinocytotic vesicles suggest that these cells may be active in the transport of materials. The subendothelial layer contains delicate, loosely dispersed, and multidirectional collagen fibrils, which are often associated with fibroblasts. This layer, in particular, is more prominent in the atrial endocardium (Figure 1.29c and d). The thick elastic layer constitutes the bulk of the endocardium. In addition to collagen fibers and some smooth muscle cells, this layer contains prominent elastic fibers that progressively increase in size from the endothelium to the area adjacent to the myocardium. The smooth muscle component may be especially prominent, particularly in the left atrium and the left ventricular septal region.

The subendocardium lies deep to the endocardium and binds the latter to the myocardium. This layer contains thick elastic and collagen fibers and a prominent number of blood vessels, mostly continuous capillaries and some arterioles. In the right atrium and right ventricle, small arteries may superficially protrude from the endocardial surfaces into the cardiac chambers [140]. Nerve fibers and branches of Purkinje cells are seen. This layer may also contain undifferentiated mesenchymal cells, fibroblasts, and macrophages. Adipose tissue may be noted in this layer, especially in the right ventricle, and should not be over interpreted on endomyocardial biopsy. The subendocardium is continuous with the extracellular matrix that surrounds the myofibers in the myocardium [141].

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AUTOIMMUNITY AND THE MUSCULOSKELETAL SYSTEM

Nicholas Manolios , in The Musculoskeletal System (Second Edition), 2010

Cardiac involvement

The endocardium, myocardium and pericardium can be involved. Clinical features include a murmur, tachycardia, arrhythmia and heart failure. Cardiovascular and coronary artery disease has been reported to be a major cause of premature morbidity and mortality in lupus. The pathogenesis is multifactorial, with contributions from vascular wall inflammation, corticosteroid effects on the lipid profile, renal disease, hypertension and thrombosis in the setting of anti-phospholipid antibodies. With the exception of anti-phospholipid antibody-induced thromboses, the other factors tend to impact after 10–20 years of lupus activity.

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Giant Cell Arteritis

M.J. Koster , ... K.J. Warrington , in The Heart in Rheumatic, Autoimmune and Inflammatory Diseases, 2017

3.4.3 Endocardium

Involvement of the endocardium in the context of GCA has not been reported clinically or in autopsy studies. Dilation of the ascending aorta and aortic annulus (annuloaortic ectasia) can occur in the context of proximal aortitis, resulting in aortic valve insufficiency [160,161]. Significant regurgitation through the aortic valve is secondary to the dilated aortic root and not due to inflammatory destruction of the valve leaflets. Aortic valve insufficiency in isolation of annuloaortic ectasia has not been described. Similarly, mitral, tricuspid, and pulmonary valve insufficiency do not occur unless in conjunction with advanced heart failure from severe aortic insufficiency [162].

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Prophylaxis of Infective Endocarditis

David T. Durack , in Mandell, Douglas, and Bennett's Principles and Practice of Infectious Diseases (Eighth Edition), 2015

Inhibition of Bacterial Adherence to Endocardium

Adherence of bacteria to the endocardium or to localized deposits of platelets and fibrin on the endocardium are essential early events in the development of IE (see Chapter 82). Bacterial infection established on the surface of a prosthetic valve or other implanted prosthetic material has many of the characteristics of a biofilm. Inhibitors of adherence or of biofilm formation theoretically might prevent endocarditis. In earlier experiments, anticoagulants and antiplatelet agents did not reliably prevent IE in animals, ⁷⁹ but as knowledge of the determinants of bacterial adherence progresses, newer agents to prevent bacterial adherence may be developed. For example, an anticoagulant (dabigatran) and a monoclonal antibody to platelet fibrinogen receptor (abciximab) have been recently shown to prevent experimental staphylococcal IE in rats. ⁸⁰ A drug, an antibody, or a vaccine that prevented adherence of circulating bacteria to the endocardium or formation of a biofilm could have major advantages in the prevention of IE because, unlike antibiotics, its effect would not be limited by antibiotic resistance, nor would it promote antibiotic resistance in the microbiome. However, no such drug, antibody, or vaccine for prevention of IE is currently available for human use.

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