Editing Endocardium

{{short description|Innermost layer of tissue lining the chambers of the heart}}
{{Infobox anatomy
| Name        = Endocardium
| Latin       = endocardium
| Image       = Gray493.png
| Caption     = Interior of right side of heart
| Image2      =
| Caption2    =
| Precursor   =
| System      =
| Artery      =
| Vein        =
| Nerve       =
| Lymph       =
}}
[[File:Blausen 0470 HeartWall.png|thumb|Illustration depicting the layers of the heart wall including the innermost endocardium]]

The '''endocardium''' ({{plural form}}: '''endocardia''') is the innermost layer of [[Tissue (biology)|tissue]] that lines the chambers of the [[heart]]. Its [[Cell (biology)|cells]] are [[embryology|embryologically]] and biologically similar to the [[endothelium|endothelial]] cells that line [[blood vessel]]s. The endocardium also provides protection to the valves and heart chambers.<ref>{{cite journal |last1=Brutsaert |first1=D. L. |last2=Andries |first2=L. J. |title=The endocardial endothelium |journal=American Journal of Physiology-Heart and Circulatory Physiology |date=October 1992 |volume=263 |issue=4 |pages=H985–H1002 |doi=10.1152/ajpheart.1992.263.4.H985 |pmid=1415782 }}</ref>

The endocardium underlies the much more voluminous [[myocardium]], the muscular tissue responsible for the contraction of the heart. The outer layer of the heart is termed [[epicardium]] and the heart is surrounded by a small amount of fluid enclosed by a fibrous sac called the [[pericardium]].<ref>{{cite book |last1=Tran |first1=Dan B. |last2=Weber |first2=Carly |last3=Lopez |first3=Richard A. |title=StatPearls |date=2025 |publisher=StatPearls Publishing |chapter-url=http://www.ncbi.nlm.nih.gov/books/NBK545195/ |chapter=Anatomy, Thorax, Heart Muscles |pmid=31424779 }}</ref>

==Function== 
[[File:Endocardium and subendocardium histology.png|thumb|Histology of the endocardium and subendocardium.]]The endocardium, which is primarily made up of endothelial cells, controls myocardial function. This modulating role is separate from the [[Autoregulation|homeometric and heterometric regulatory mechanisms]] that control [[myocardial contractility]].<ref>{{cite journal |last1=Milgrom-Hoffman |first1=Michal |last2=Harrelson |first2=Zachary |last3=Ferrara |first3=Napoleone |last4=Zelzer |first4=Elazar |last5=Evans |first5=Sylvia M. |last6=Tzahor |first6=Eldad |title=The heart endocardium is derived from vascular endothelial progenitors |journal=Development |date=November 2011 |volume=138 |issue=21 |pages=4777–4787 |doi=10.1242/dev.061192 |pmid=21989917 |pmc=3190386 }}</ref> 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.<ref>{{Cite web |title=Endothelial Dysfunction |url=https://stanfordhealthcare.org/medical-conditions/blood-heart-circulation/endothelial-dysfunction.html |access-date=2023-02-23 |website=[[Stanford University|stanfordhealthcare.org]]}}</ref> 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.<ref>{{cite journal |last1=Brutsaert |first1=Dirk L. |last2=De Keulenaer |first2=Gilles W. |last3=Fransen |first3=Paul |last4=Mohan |first4=Puneet |last5=Kaluza |first5=Grzegorz L. |last6=Andries |first6=Luc J. |last7=Rouleau |first7=Jean-Lucien |last8=Sys |first8=Stanislas U. |title=The cardiac endothelium: Functional morphology, development, and physiology |journal=Progress in Cardiovascular Diseases |date=November 1996 |volume=39 |issue=3 |pages=239–262 |doi=10.1016/s0033-0620(96)80004-1 |pmid=8970576 }}</ref>

The endocardial endothelium may also act as a kind of blood–heart barrier (analogous to the [[blood–brain barrier]]), thus controlling the ionic composition of the extracellular fluid in which the [[cardiomyocytes]] bathe.<ref>{{cite book |last1=Dotiwala |first1=Ary K. |last2=McCausland |first2=Cassidy |last3=Samra |first3=Navdeep S. |title=StatPearls |date=2025 |publisher=StatPearls Publishing |chapter-url=http://www.ncbi.nlm.nih.gov/books/NBK519556/ |chapter=Anatomy, Head and Neck: Blood Brain Barrier |pmid=30137840 }}</ref>

==Clinical significance==
In [[myocardial infarction]], [[ischemia]] of the [[myocardium]] starts at the endocardium and might extend up to the epicardium, disrupting the entire heart wall ("transmural" [[infarction]]).<ref>{{cite journal |last1=Algranati |first1=Dotan |last2=Kassab |first2=Ghassan|last3=Lanir |first3=Yoram |title=Why is the subendocardium more vulnerable to ischemia? A new paradigm |journal=American Journal of Physiology. Heart and Circulatory Physiology |year=2010 |volume=300 |issue=3 |pages=H1090–H1100 |doi=10.1152/ajpheart.00473.2010 |pmid=21169398 |pmc=3064294 }}</ref> 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 damaged [[myocyte]]s. This damaged region will conduct impulses more slowly, resulting in irregular rhythms.<ref>{{cite journal |last1=Moir |first1=Thomas W. |title=Subendocardial Distribution of Coronary Blood Flow and the Effect of Antianginal Drugs |journal=Circulation Research |date=June 1972 |volume=30 |issue=6 |pages=621–627 |doi=10.1161/01.res.30.6.621 |doi-access=free |pmid=4623628 }}</ref> The damaged region may enlarge or extend and become more life-threatening.<ref>{{cite book |doi=10.1016/B978-0-12-803997-7.00014-4 |chapter=Cardiac Involvement in Systemic Vasculitis |title=The Heart in Systemic Autoimmune Diseases |series=Handbook of Systemic Autoimmune Diseases |date=2017 |last1=Sebastiani |first1=M. |last2=Manfredi |first2=A. |last3=Ferri |first3=C. |volume=14 |pages=335–382 |hdl=11380/1141341 |isbn=978-0-12-803997-7 }}</ref> 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.<ref>{{cite book |last1=Warner |first1=Matthew J. |last2=Tivakaran |first2=Vijai S. |title=StatPearls |date=2025 |publisher=StatPearls Publishing |chapter-url=http://www.ncbi.nlm.nih.gov/books/NBK470572/ |chapter=Inferior Myocardial Infarction |pmid=29262146 }}</ref>
 
During depolarization the impulse is carried from endocardium to epicardium, and during repolarization the impulse moves from epicardium to endocardium.
In [[endocarditis|infective endocarditis]], the ''endocardium'' (especially the endocardium lining the [[heart valve]]s) is affected by [[bacterium|bacteria]].<ref>{{cite book |last1=Wei |first1=Xingyu |last2=Yohannan |first2=Sandesh |last3=Richards |first3=John R. |title=StatPearls |date=2025 |publisher=StatPearls Publishing |chapter-url=http://www.ncbi.nlm.nih.gov/books/NBK537194/ |chapter=Physiology, Cardiac Repolarization Dispersion and Reserve |pmid=30725879 }}</ref>

==References==
{{Reflist}}

==External links==
* {{OklahomaHistology|64_06}} - "Heart and AV valve" (atrial endocardium)
* {{OklahomaHistology|64_07}} - "Heart and AV valve" (ventricular endocardium)

{{Heart anatomy}}
{{Authority control}}

[[Category:Cardiac anatomy]]