Disease relevance of Endocardium

• The depletion of left ventricular endocardium ATP during normothermic ischemia was significantly delayed after direct mechanical ventricular actuation compared with cardiopulmonary bypass.(ABSTRACT TRUNCATED AT 250 WORDS)[1]
• Patients with congestive noncoronary cardiomyopathy, regardless of the type of their arrhythmia, have a relatively normal endocardium [2].
• Because electrical depression attending myocardial ischemia is more accentuated in ventricular epicardium than in endocardium, we endeavored to contrast the effects of pinacidil-induced IK-ATP activation on the electrophysiology of canine ventricular epicardium and endocardium [3].
• Thus ablation of the superficial ventricular endocardium with Lugol's solution results in a profound increase in the ventricular fibrillation threshold with only minimal tissue destruction [4].
• MAPs were obtained from the right and left ventricular endocardium in six patients with congenital long QT syndrome (LQT group, 18 recording sites) and in eight control patients (control group, 19 recording sites) [5].

High impact information on Endocardium

• Thus, NFAT signaling functions sequentially from myocardium to endocardium within a valvular morphogenetic field to initiate and perpetuate embryonic valve formation [6].
• Within the endocardium, specific inductive events appear to activate NF-ATc: it is localized to the nucleus only in endocardial cells that are adjacent to the interface with the cardiac jelly and myocardium, which are thought to give the inductive stimulus to the valve primordia [7].
• METHODS AND RESULTS: MAPs were recorded simultaneously from two or three sites on the right ventricular and left ventricular endocardium in 6 patients with a congenital form of LQT1 syndrome with KvLQT1 defect (17 sites) and 8 control patients (24 sites) [8].
• Effects of quinidine on repolarization in canine epicardium, midmyocardium, and endocardium: II. In vivo study [9].
• Terminals arising from nerve fibers (diameter, 6 to 10 microns) immunoreactive for myelin basic protein were identified in the atrial endocardium, epicardium, and coronary sinus, and four types were distinguished by differences in immunostained nerve area (range, 358 to 797 microns 2) and dispersion (range, 620 to 4684 microns 2) [10].

Chemical compound and disease context of Endocardium

• METHODS: Monophasic action potentials were recorded from right and left ventricular endocardium during atrial pacing at heart rates from 70 to 140 beats/min at baseline and from 100 to 140 beats/min during epinephrine infusion (0.1 microgram/kg body weight per min) in 11 patients with congenital LQTS and 10 control patients [11].
• Results showed that ischemia-induced conduction delay was significantly less in verapamil treated dogs throughout period of ischemia and reperfusion, both in epicardium and endocardium [12].
• These findings suggested that the effect of ischemia is marked in the endocardium and, also, that the protective effect of diltiazem is seen only during a decrease in endocardial flow following short-term and reversible ischemia [13].
• INTRODUCTION: Substrate-based catheter ablation of postmyocardial infarction (post-MI) ventricular tachycardia necessitates electroanatomic definition of the scarred endocardium [14].
• Coronary collateral flow in the endocardium was similar for all of the experimental groups; however, hearts subjected to ischemia with low-flow perfusion of Ringer's lactate demonstrated significantly higher epicardial coronary collateral flow levels compared with controls.(ABSTRACT TRUNCATED AT 250 WORDS)[15]

Biological context of Endocardium

• Delayed afterdepolarizations and triggered activity were evoked in focal areas of myocardium in vivo by local exposure of endocardium to ouabain by means of a catheter electrode system capable of recording monophasic action potentials (MAPs) and delivering ouabain to the recording site [16].
• Transgenic mice generated with a homologous regulatory region of the mouse DSCR1 gene linked to lacZ (DSCR1(e4)/lacZ) show gene activation in the endocardium of the developing valves and aorticopulmonary septum of the heart, recapitulating a specific subdomain of endogenous DSCR1 cardiac expression [17].
• Increased endothelin-1 gene expression in the endothelium of coronary arteries and endocardium in the DOCA-salt hypertensive rat [18].
• These results show that the dextro-isomer of sotalol possesses similar class III action to the parent compound and that this action is homogeneous with respect to left ventricular endocardium and epicardium at heart rates of 100 beats/min and 150 beats/min over a wide dose range. d-Sotalol may be a useful anti-arrhythmic agent in man [19].
• In contrast to the marked occurrence of natriuretic peptide receptor binding sites seen in the ventricular endocardium of control rats, the sympathectomized rats exhibited a decreased number of binding sites for natriuretic peptides in the endocardium of both the right and left chambers [20].

Anatomical context of Endocardium

• Under sodium pentobarbital, the CP/ATP ratio ranged from 1.92 +/- 0.06 to 2.51 +/- 0.08 from endocardium to epicardium, resulting in a transmural slope in the CP/ATP ratio of 0.149 +/- 0.047 (n = 22) [21].
• Addition of eosinophils from hypereosinophilic patients to muscles with selectively damaged endocardium (by previous transient [1-second] exposure to 1% Triton X-100) produced no further change in contractile performance [22].
• These results suggest that intact endocardium may enhance performance of the heart by increasing the myofilament Ca2+ responsiveness through endothelium-derived compounds such as endothelin [23].
• ET converting enzyme-1 (ECE-1), however, is expressed preferentially in endothelial cells of the endocardium and coronary arteries where Purkinje fiber recruitment takes place [24].
• Histologically, TNF-alpha-induced fractalkine expression was observed markedly in arterial and capillary endothelial cells, endocardium, and endothelium of intestinal villi, and slightly in venous endothelial cells, but not at all in lymphatic endothelial cells of intestine [25].

Associations of Endocardium with chemical compounds

• The role of the endocardium was investigated by selectively damaging it by very brief (1 second) exposure to 1% Triton X-100 in some muscle preparations before experiments [26].
• Hydroxyproline in the stunned endocardium was not different from control [27].
• Flecainide (10-20 microM) produced either prolongation or marked abbreviation of APD in epicardium but only minor changes in the APD of endocardium [28].
• Lugol's solution was applied through small ventriculotomies to the left and right ventricular endocardium of 10 dogs on cardiopulmonary bypass [4].
• When LV wall stresses during adenosine were reduced in a subgroup of 5 dogs with LVH, the endocardium/epicardium ratio during adenosine infusion was no longer different from that in control dogs (0.63 +/- 0.11), nor was the level of subendocardial blood flow different (3.42 +/- 0.60 mL.min-1.g-1) [29].

Gene context of Endocardium

• Consistent with roles in cardiac development, Tll1 expression was specific to precardiac tissue and endocardium in 7.5 and 8.5 days p.c. embryos, respectively [30].
• In the mouse, Tbx20 is expressed in the cardiac crescent, then in the endocardium and myocardium of the linear and looped heart tube before it is restricted to the atrioventricular canal and outflow tract in the multi-chambered heart [31].
• Deletion of the Bmp type 1A receptor, Bmpr1a, in endocardium also resulted in failed cushion formation, indicating that Bmp2 signals directly to cushion-forming endocardium to induce EMT [32].
• There is an increased expression of Pal-E, ICAM-1, VCAM-1, and DR antigen on endocardium from rejecting heart biopsies [33].
• Popdc2 expression was absent from the endocardium and propepicardial organ [34].

Analytical, diagnostic and therapeutic context of Endocardium

• After 90 min of reperfusion the sum of ATP, adenosine diphosphate, adenosine monophosphate, inosine, and hypoxanthine levels was decreased in the endocardium by 10.2 nmol X mg protein-1 in the untreated group, but no change was observed in verapamil-treated animals [35].
• Using microelectrode techniques we compared the effects of tetrodotoxin (TTX, 2-3 microM), DL-propranolol (1-3 micrograms/ml), and flecainide acetate (10-15 microM) on isolated canine ventricular epicardial (epicardium) and endocardial (endocardium) tissues [36].
• Expression of endothelial nitric oxide synthase (eNOS) protein in the ischemic endocardium of left anterior descending coronary artery area (as determined by Western blotting) significantly decreased (79 +/- 4%) compared with the nonischemic endocardium of LCX area (100 +/- 7%), which was improved by hydroxyfasudil (105 +/- 6%, p < 0.01) [37].
• In situ hybridization of embryonic and new born mouse tissues revealed expression of laminin alpha 4 mRNA in a subset of endothelium, in particular aortic endothelium, endocardium and endothelium of blood vessels in the skin and in the brain [38].
• Immunohistochemistry demonstrated that IL-1beta and IL-6 immunoreactive cells were widely distributed in the myocardium in the earlier time intervals, and mainly localized in the regions close to the endocardium in the later time intervals [39].

References