Overview

The endocardium has three layers. The innermost is a continuous endothelium on a basal lamina. It provides a non-thrombogenic surface in contact with blood. Beneath it is a subendothelial layer of dense connective tissue with elastic fibres and occasional smooth muscle cells. Outermost is a subendocardial layer of loose connective tissue that joins the endocardium to the myocardium. This layer contains small vessels, nerves and, in the ventricles, the branches of the conduction system and the Purkinje fibres.

The valve cusps are folds of endocardium around a dense fibrous core (the lamina fibrosa). The chordae tendineae are also covered by endocardium.

Endocardial endothelial cells also signal to the underlying myocytes, for example through nitric oxide and endothelin, and so help modulate contraction.

Location: Lines all four chambers, the papillary muscles and trabeculae, and covers both surfaces of the valves and the chordae tendineae.

Anatomy

Histology: Simple squamous endothelium on a subendothelial layer of fibroelastic connective tissue. Beneath this is a subendocardial layer of loose connective tissue that, in the ventricles, contains the pale, glycogen-rich Purkinje fibres.
Development: The endocardium forms from the endothelial (endocardial) tube of the primitive heart. In the endocardial cushions, some endocardial cells undergo endothelial-to-mesenchymal transition and build the valves and parts of the septa.

Function

Provides a smooth, antithrombotic lining that reduces turbulence and clotting.
Forms the surface of the valves and chordae.
Houses the subendocardial conduction network (Purkinje fibres).
Modulates myocardial function through paracrine signals such as NO and endothelin-1.

Clinical significance

Infective endocarditis

Infective endocarditis is the growth of microbial vegetations on the endocardium, usually on a valve. Risk factors include damaged or prosthetic valves and intravenous drug use. The mitral and aortic valves are most often affected. In people who inject drugs the tricuspid valve is typical, usually infected by Staphylococcus aureus.

Clinical signs include fever, a new murmur, splinter haemorrhages, Janeway lesions, Osler nodes and Roth spots. The diagnosis rests on blood cultures and echocardiography, combined in the modified Duke criteria.

Mural thrombus

After an anterior myocardial infarction, a dyskinetic apex with damaged endocardium can grow a mural thrombus. Fragments may embolise to the brain or limbs.

Compiled from standard anatomy and physiology references — see the Cardiovascular System sources. For education only; not medical advice.