| Endocardium | |
|---|---|
 Interior of right side of heart | |
| Details | |
| Identifiers | |
| Latin | endocardium |
| MeSH | D004699 |
| TA98 | A12.1.05.001 |
| TA2 | 3962 |
| FMA | 7280 |
| Anatomical terminology | |
Theendocardium (pl.:endocardia) is the innermost layer oftissue that lines the chambers of theheart. Itscells areembryologically and biologically similar to theendothelial cells that lineblood vessels. The endocardium also provides protection to the valves and heart chambers.[1]
The endocardium underlies the much more voluminousmyocardium, the muscular tissue responsible for the contraction of the heart. The outer layer of the heart is termedepicardium and the heart is surrounded by a small amount of fluid enclosed by a fibrous sac called thepericardium.[2]
The endocardium, which is primarily made up of endothelial cells, controls myocardial function. This modulating role is separate from thehomeometric and heterometric regulatory mechanisms that controlmyocardial contractility.[3] Moreover, the endothelium of the myocardial (heart muscle) capillaries, which is also closely appositioned to the cardiomyocytes (heart muscle cells), is involved in this modulatory role.[4] Thus, the cardiac endothelium (both the endocardial endothelium and the endothelium of the myocardial capillaries) controls the development of the heart in the embryo as well as in the adult, for example during hypertrophy. Additionally, the contractility and electrophysiological environment of the cardiomyocyte are regulated by the cardiac endothelium.[5]
The endocardial endothelium may also act as a kind of blood–heart barrier (analogous to theblood–brain barrier), thus controlling the ionic composition of the extracellular fluid in which thecardiomyocytes bathe.[6]
Inmyocardial infarction,ischemia of themyocardium starts at the endocardium and might extend up to the epicardium, disrupting the entire heart wall ("transmural"infarction).[7] Less extensive infarctions are often "subendocardial" and do not affect the epicardium. In the acute setting, subendocardial infarctions are more dangerous than transmural infarctions because they create an area of dead tissue surrounded by a boundary region of damagedmyocytes. This damaged region will conduct impulses more slowly, resulting in irregular rhythms.[8] The damaged region may enlarge or extend and become more life-threatening.[9] In the chronic setting, transmural infarctions are more dangerous due to the greater amount of muscular damage and the development of scar tissue leading to impaired systolic contractility, impaired diastolic relaxation, and increased risk for rupture and thrombus formation.[10]
During depolarization the impulse is carried from endocardium to epicardium, and during repolarization the impulse moves from epicardium to endocardium.Ininfective endocarditis, theendocardium (especially the endocardium lining theheart valves) is affected bybacteria.[11]
