Editing Endocardium (section)

==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>