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PubMed1987

Mesenchymal tissue of the interventricular septum. Structural and ultrastructural study.

Light and electron microscopic studies of frontal and sagittal sections of embryonic chick hearts (Stages 25, 28-29), reveal mesenchymal tissue in the cephalic portion of the interventricular septum. The endocardium of this cephalic portion contains reoriented and invaginated cells with pseudopodia; in addition there are cells immediately subjacent to the endocardium. Similar cellular events take place during the formation of mesenchymal tissue in the atrioventricular and conotruncal regions. In these regions the mesenchymal tissue originates by means of an endocardial activation process. The structural characteristics of the formation of the cephalic portion of the interventricular septum suggest that local mesenchymal tissue is contributed by the endocardium. However, based upon the close anatomic relationship observed by us between the mesenchymal tissues of the atrioventricular canal, conotruncal region and the cephalic portion of the interventricular septum; we do not discard a contribution by migration of cells from atrioventricular and conotruncal regions to the interventricular septum.

Animals↗
PubMed1989

Changes in endocardial cell morphology during development of the endocardial cushions.

This paper presents a scanning electron microscope study of the morphologic changes undergone by the endocardium during development of the atrioventricular (A-V) endocardial cushions. Prior to cell seeding into the cushions, endocardial cells show a regular, uniform morphology, many of them appearing to be oriented in the direction of the blood flow. Concomitant with the appearance of cells in the A-V cushions, endocardial cells lose their elongated appearance, become more flattened and adopt a variable morphology. Endocardial cells at this stage develop filopodia and lamellipodia, overlap each other and show a variable number of microvilli and different degrees of flattening. After completion of endocardial migration, the endocardial cells that remain in the plane of the endocardium become extremely flattened, the degree of overlapping decreases and the cells adopt a polygonal morphology. These changes in endocardial cell morphology appear to be related to endocardial cell activity. It is suggested that the whole endocardial cushion, not just the cells that migrate into the cushions, is involved in cushion development. The activity of the endocardial cells may be related to the maintenance of the integrity of the endocardium.

Animals↗
PubMed1993

Diagnosis of cardiac thrombosis in patients with atrial fibrillation in the absence of macroscopically visible thrombi.

Cardiac thrombosis due to atrial fibrillation (AF) has been recognized as the most common cause of cerebral embolism. However, sometimes no macroscopic thrombus is found at autopsy in the heart of a victim of this type of cerebral embolism. We investigated morphological changes in the left atrial endocardium of 31 patients (including 21 cases with AF) who had died of cerebral embolism. "Rough endocardium" (RE) seen macroscopically provided evidence for the existence of atrial thrombosis. The RE that appeared in AF cases was due to a granular and wrinkled appearance of the endocardium associated with oedematous and fibrous thickening. Fibrin-thread deposits were also always distinguishable. Mural thrombi and oedema with neutrophil infiltration in the subendocardium could be seen under the microscope. Small areas of endothelial denudation and thrombotic aggregations were commonly observed by scanning electron microscopy (SEM). These SEM lesions were significantly more frequent in cases with AF than in controls (P < 0.001). The diagnostic success rate for atrial thrombosis among cases with AF increased from 33.3% to 81% when thrombi proven by histological investigation of the areas with RE were added. Left atrial RE may be an anatomically relevant finding for the existence of atrial thrombosis with AF, when the thrombosis cannot be detected upon gross observation at autopsy.

Adult↗
PubMed1994

Relation between impedance and endocardial contact during radiofrequency catheter ablation.

Lesion size during radiofrequency catheter ablation in patients with paroxysmal supraventricular tachycardia (PSVT) is thought to be related to multiple factors, including contact pressure at the catheter-endocardial interface. Therefore a predictor of contact pressure at a potential target site for ablation might be useful. In this study 25 patients underwent duplicate 2 W applications of radiofrequency energy with the catheter in poor and firm contact with the right ventricular endocardium after successful ablation treatment for PSVT. The mean age of the patients was 44 +/- 15 years. Fifteen patients underwent slow pathway ablation for atrioventricular nodal reentrant tachycardia, and 10 patients underwent ablation for an accessory pathway. The mean impedance for low-energy applications in firm contact (139 +/- 24 ohms) was 22% +/- 13% greater (p 0.0001) than in poor contact with the right ventricle (113 +/- 16 ohms). The maximum impedance was 27% greater when the catheter was in firm (147 +/- 28 ohms) rather than poor contact (116 +/- 16 ohms), with the endocardium (p 0.0001). These results suggest that higher impedance measurements may be obtained with low-energy applications of 2 W when the ablation catheter is in firm contact with the endocardium.

Adult↗
PubMed1981

Relation of the endocardial and epicardial ventricular fibrillation thresholds of the right and left ventricle.

Ventricular fibrillation thresholds were measured on the endocardium and epicardium of the right or left ventricle, or both, in 13 dogs. The electrodes, introduced through a right or left atriotomy to avoid injury to the ventricles, were aligned opposite and parallel to each other on the endocardium and epicardium. The ventricular fibrillation threshold was measured during atrial pacing by delivering a train of impulses to the ventricle during the vulnerable period after every 12th paced complex in 1 milliampere (mA) increments of current until fibrillation ensued. The mean (+/- standard deviation) right ventricular epicardial and endocardial fibrillation thresholds were 18.3 +/- 5.3 and 17.6 +/- 5.3 mA, respectively, (values not significantly different). However, the fibrillation threshold of 36.1 +/- 9.5 mA in the left ventricular epicardium was significantly higher than the value of 20.7 +/- 9.4 mA on the left ventricular endocardium. These data suggest that the proximity of the fibrillating electrodes and Purkinje network may be a factor in the measurement of ventricular vulnerability.

Animals↗
PubMed2006

I(Kr) contributes to the altered ventricular repolarization that determines long-term cardiac memory.

OBJECTIVE: Cardiac memory (CM) is characterized by an altered T-wave morphology, which reflects altered repolarization gradients. We hypothesized that the delayed rectifier currents, I(Kr) and I(Ks), might contribute to these repolarization changes. METHODS: We studied conscious, chronically instrumented dogs paced from the postero-lateral left ventricular (LV) wall at rates 5-10% faster than sinus rate for 3 weeks. ECGs during sinus rhythm were recorded on days 0, 7, 14 and 21 of pacing. Within 3 weeks, CM achieved steady state, hearts were excised, and epicardial and endocardial tissues and myocytes were studied. RESULTS: In unpaced controls, action potential duration to 50% and 90% repolarization (APD) in epicardium was shorter than in endocardium (P < 0.05); in CM epicardial APD increased at CL > or = 500 ms, while endocardial APD was either unchanged or decreased such that the transmural gradient seen in controls diminished (P < 0.05). A transmural I(Kr) gradient occurred in controls (epicardium>endocardium, P < 0.05) and was reversed in CM. No I(Ks) transmural gradient was found in controls, while in CM endocardial I(Ks) was greater than epicardial at greater than +50 mV. Canine ERG (cERG) mRNA and protein in epicardium > endocardium in controls (P < 0.05), and this difference was lost in CM. Expression levels of KCNQ1 and KCNE1 protein were similar in all groups. CONCLUSIONS: A transcriptionally induced change in epicardial I(Kr) contributes to the altered ventricular repolarization that characterizes CM.

Action Potentials↗
PubMed2003

Tissue factor expression in atrial endothelia associated with nonvalvular atrial fibrillation: possible involvement in intracardiac thrombogenesis.

INTRODUCTION: Tissue factor plays a key role in the extrinsic coagulation pathway and is induced by inflammatory cytokines. Atrial myocarditis has been detected recently in some patients with lone atrial fibrillation. Virchow's triad of low blood flow, hypercoagulability, and endothelial dysfunction, enhances thrombus formation. The present study was designed to elucidate the role of endothelial dysfunction in thrombogenesis associated with nonvalvular atrial fibrillation. MATERIAL AND METHODS: We investigated tissue factor expression in the endothelia of left atrial appendages obtained from seven patients with nonvalvular atrial fibrillation and cardiogenic thromboembolism. Tissues were divided into 7-13 sections and compared with control specimens from four patients who died of noncardiac events. Expression of tissue factor, von Willebrand factor and tissue factor pathway inhibitor was evaluated by immunohistochemistry. RESULTS: Histopathologically, inflammatory cells infiltrated the endocardium and all seven patients showed features of persistent myocarditis. Activated T cells [15.3+/-9.4 cells/high power field (HPF, mean+/-S.D.) vs. control 2.2+/-4.4/HPF (P=0.0294)] and a few macrophages [5.1+/-8.4 cells/HPF vs. control 2.4+/-3.5 cells/HPF (P=NS)] infiltrated the endocardium. Tissue factor was overexpressed in the endothelia particularly in tissues containing inflammatory cells and denuded matrix of the endocardium, compared with the control group. Von Willebrand factor, but not tissue factor pathway inhibitor, was also overexpressed in these tissues. CONCLUSION: Tissue factor expression induced by local inflammation is involved in the pathogenesis of thrombosis in patients with nonvalvular atrial fibrillation.

Aged↗
PubMed1986

Endocardial photoablation by excimer laser.

A xenon-chlorine excimer laser was used to irradiate normal endocardium of fresh sheep and pig hearts as well as unfixed human endocardial scar. Forty pulses of 370 J and 35 ns each resulted in penetration of up to 12 mm in normal tissue and only 3.5 mm in scarred endocardium. Dosimetry indicated that the volume of vaporized scarred tissue was 1/10th that of normal endocardium (0.19 to 0.40 versus 1.35 to 3.22 mm3/J). Ultrastructurally, there was a sharp demarcation of only 10 mu between the region of injury and normal myocardium, with little evidence of heat injury. The high power and short duration of these lasers coupled with the lack of a boundary zone of injury suggest that excimers may be an ideal tool for arrhythmia ablation.

Animals↗
PubMed2002

Effects of procainamide on transmural ventricular repolarisation.

To investigate the pharmacological effect of procainamide on transmural ventricular repolarisation in normal heart, the transmural activation-recovery intervals (ARI) and their responses to procainamide (20 mg/min i.v. for 20 min) were studied in 6 open-chest, pentobarbitone-anaesthetised sheep. ARI was measured from the unipolar ECGs acquired with 4 plunge needles inserted into the basal and apical parts of the left ventricular wall. During sinus rhythm (cycle length 500-700 ms), there was no significant difference in the pooled ARI between the epicardium (266.0 +/- 30.5 ms), midmyocardium (265.0 +/- 28.9 ms) and endocardium (265.7 +/- 28.1 ms) (p > 0.05). Procainamide prolonged ARI in all myocardial layers. The pooled ARI prolongation from the epicardium, midmyocardium and endocardium of the 6 animals was 66.8 +/- 18.3, 70.3 +/- 14.7 and 65.3 +/- 15.7 ms (p > 0.05), respectively. In conclusion, sodium channel blocker procainamide results in a similar repolarisation prolongation in the left ventricular epicardium, midmyocardium and endocardium of a healthy heart.

Animals↗
PubMed2005

Epicardial and endocardial dispersion of ventricular repolarization. A study of monophasic action potential mapping in healthy pigs.

OBJECTIVES: To investigate the total dispersion of ventricular repolarization of the epi- and endocardium. DESIGN: Monophasic action potentials (MAP) were recorded from 211+/-54 (151-353) left and right ventricular epi- and endocardial sites during atrial pacing in 10 pigs using the CARTO system. The activation time (AT), MAP duration (MAPd) and end of repolarization time (EOR) were measured. RESULTS: The total dispersion of AT, EOR and MAPd, defined as the maximal differences of these parameters over both the epi- and endocardium, were 57+/-10, 84+/-20, and 75+/-21 ms respectively and were significantly larger than the respective epi- and endocardial dispersions (p<0.05). The epicardial dispersion of AT, EOR and MAPd of both the right and left ventricles were significantly larger than that of each ventricle alone (p<0.02). Sternotomy did not affect these dispersion parameters. CONCLUSION: Detailed mapping of epicardial repolarization in vivo using the MAP mapping technique is feasible. Both the epi- and endocardium of the two ventricles contribute significantly to the total dispersion of repolarization.

Action Potentials↗
PubMed1994

Modulation of myocardial relaxation by basal release of endothelin from endocardial endothelium.

OBJECTIVE: The aim was to study the potential role of basal endothelin-1 release from endocardial endothelium in isolated ferret papillary muscle preparations. METHODS: The following interventions were studied: (1) no treatment (time control); (2) endothelin-1 (5 nM); (3) endothelin-1 (5 nM) in the presence of the specific ETA receptor antagonist, BQ123 (10 microM); (4) BQ123 (10 microM) in endocardium-intact muscles; and (5) BQ123 (10 microM) in endocardium-denuded muscles (n = 6 in each group). RESULTS: Untreated muscles remained stable throughout the experiment. BQ123 fully inhibited the positive inotropic effect of exogenous endothelin-1. In endocardium-intact preparations (n = 6), exposure to BQ123 induced a progressively earlier onset and time course of isometric twitch relaxation [time to peak tension -12.3(SEM 1.8)%, relaxation half time -13.3(1.1)%; both p < 0.01], but had no effect on peak tension or on rate of tension development. Selective denudation of endocardial endothelium induced similar relaxant effects, but also significantly reduced peak tension. In endocardial endothelium-denuded preparations (n = 6), addition of BQ123 did not result in further contractile changes. CONCLUSIONS: Endocardial endothelium in situ on papillary muscle preparations tonically releases endothelin, resulting in a significantly delayed onset of isometric twitch relaxation. There is no evidence for basal endothelin-1 release from microvascular endothelial cells in this superfused preparation. A similar release of endothelin-1 from endocardial endothelium in the intact heart could influence myocardial contractile behaviour independently of changes in coronary perfusion. Endothelin-1 may have a physiological role in modulating myocardial relaxation.

Animals↗
PubMed1997

Endomyocardial fibrosis in Behçet's disease.

OBJECTIVE: To report on four patients with Behçet's disease associated with endomyocardial fibrosis involving the right or the left ventricle. METHODS: Charts of more than 350 patients with Behçet's disease were reviewed. Endomyocardial fibrosis was confirmed because of cardiac failure in three patients and incidentally discovered by histological examination of an operative specimen in one patient. Echocardiography displayed bright echogen endocardium. Angiocardiography showed a reduced ventricular size. Electron beam computed tomography demonstrated a lowdense area involving the endocardium. Magnetic resonance imaging showed a mass of intermediate intensity on T1 weighted images. Diagnosis of endomyocardial fibrosis was based on histological study of a biopsy specimen in one patient and of an operative specimen in three. RESULTS: Six other similar cases of endomyocardial fibrosis complicating Behçet's disease were previously reported in the medical literature. Endomyocardial fibrosis predominantly involved the right ventricle. It can be considered a feature of Behçet's disease because: (a) no other cause was discovered; (b) arteritis, valvulopathy, and intraventricular thrombus were closely linked, and (c) all patients with endomyocardial fibrosis had vasculo-Behçet pattern. CONCLUSION: Endomyocardial fibrosis may be the sequelae of vasculitis involving endocardium or myocardium, or both and complicated with intraventricular thrombosis. Behçet's disease should be added to the list of causes of endomyocardial fibrosis.

Adult↗
PubMed1971

Endocardial fibroelastosis in children with special reference to the lesions of cardiac ganglia.

In all cases of primary endocardial fibroelastosis investigated diffuse degenerative changes in the ganglion cells were detected. Thickened endocardium was formed by the proliferation of mesenchymal cells located under the endothelial endocardium and of the mesenchyme surrounding the necrobiotic muscle cells. In some cases ;axial' vacuolar degeneration, necrobiosis, and necrosis of muscle cells, interstitial oedema, and dilatation of capillaries and lymphatic spaces were found in the whole myocardium. In all cases these changes were in the subendocardial layer.In the cases discussed morphological changes in the endocardium were seen to be secondary to lesions in myocardial and possibly in neural structures.

Child, Preschool↗
PubMed2004

Triggered activity due to delayed afterdepolarizations in sites of focal origin of ischemic ventricular tachycardia.

This study for the first time systematically evaluated the site of origin of focal ventricular tachycardia (VT) induced 1-3 h after acute coronary artery ligation in dogs. We determined whether delayed afterdepolarizations (DADs) and triggered activity (TA) are more often recorded from ischemic endocardium excised from focal sites of VT origin. A total of 145 alpha-chloralose-anesthetized dogs were studied: in 54 dogs without inducible VT, normal or ischemic endocardium was investigated in vitro; in 91 dogs, inducible VT was studied by three-dimensional activation mapping, with in vitro study of 51 endocardial foci compared with 40 endocardial ischemic sites not of VT origin. Incidence of DADs (71% vs. 33%, P <0.05) and TA (32% vs. 11%, P <0.05) was greater in ischemic than in normal Purkinje tissues. Purkinje sites of origin of focal VT demonstrated the greatest frequency of DADs (92%, P <0.05) and TA (75%, P <0.05), with repetitive TA predominating. Similar results were obtained in endocardial sites of origin. Action potentials were mildly depolarized and prolonged in the focal sites of origin. These abnormalities were stable up to 2.5 h of recording. This study demonstrated that DADs and TA may underlie a majority of focal VTs in ischemic endocardium and Purkinje tissue.

Action Potentials↗
PubMed2004

Direct measurement of transmural laminar architecture in the anterolateral wall of the ovine left ventricle: new implications for wall thickening mechanics.

Laminar, or sheet, architecture of the left ventricle (LV) is a structural basis for normal systolic and diastolic LV dynamics, but transmural sheet orientations remain incompletely characterized. We directly measured the transmural distribution of sheet angles in the ovine anterolateral LV wall. Ten Dorsett-hybrid sheep hearts were perfusion fixed in situ with 5% buffered glutaraldehyde at end diastole and stored in 10% formalin. Transmural blocks of myocardial tissue were excised, with the edges cut parallel to local circumferential, longitudinal, and radial axes, and sliced into 1-mm-thick sections parallel to the epicardial tangent plane from epicardium to endocardium. Mean fiber directions were determined in each section from five measurements of fiber angles. Each section was then cut transverse to the fiber direction, and five sheet angles (beta) were measured and averaged. Mean fiber angles progressed nearly linearly from -41 degrees (SD 11) at the epicardium to +42 degrees (SD 16) at the endocardium. Two families of sheets were identified at approximately +45 degrees (beta(+)) and -45 degrees (beta(-)). In the lateral region (n = 5), near the epicardium, sheets belonged to the beta(+) family; in the midwall, to the beta(-) family; and near the endocardium, to the beta(+) family. This pattern was reversed in the basal anterior region (n = 4). Sheets were uniformly beta(-) over the anterior papillary muscle (n = 2). These direct measurements of sheet angles reveal, for the first time, alternating transmural families of predominant sheet angles. This may have important implications in understanding wall mechanics in the normal and the failing heart.

Animals↗
PubMed1994

Positive inotropic effect of Streptococcus faecalis in isolated cardiac muscle.

Infective endocarditis is caused by bacterial colonization of the endocardium. Because endocardium modulates mechanical performance of subjacent myocardium, we studied acute effects of bacteria on isolated cardiac muscle and on the functional role of the endocardium. Bacteria, grown in broth at 37 degrees C, were added at increasing concentrations (10(2) to 10(6) bacteria/ml) to cat papillary muscles in Krebs-Ringer solution (1.25 mM Ca2+, 35 degrees C). The endocardial surface was damaged by exposing muscles to a stream of dry air for 30 s. Streptococcus (Enterococcus) faecalis induced significant increases in total peak isometric twitch tension (TT) and maximal velocity of unloaded shortening (Vmax) and significant decreases in time to TT (TtTT) and time to half isometric twitch tension decline (RT 1/2), both before and after removal of endocardial endothelium. This response could also be elicited with bacterial filtrate, after boiling the filtrate or after extracting the polysaccharides from it with KIO4. Increasing Ca2+ concentrations progressively reduced the response to the filtrate. Propranolol slightly, although not significantly, diminished the effects on TT and Vmax while abolishing the effects on TtTT and on RT 1/2. By contrast, Streptococcus bovis and Staphylococcus aureus did not affect TT or Vmax but induced a slight but significant decrease in TtTT at the highest concentration of bacteria. Accordingly, the filtrate of Strep. faecalis induces a positive inotropic effect. The active component is neither a protein nor a polysaccharide, and its effect may be partly beta-adrenoceptor mediated. Strep. bovis and Staph. aureus have negligible acute effects on contractility.

Adrenergic beta-Antagonists↗
PubMed2001

Ventricular hypertrophy amplifies transmural repolarization dispersion and induces early afterdepolarization.

The effects of left ventricular hypertrophy (LVH) on the generation of phase 2 early afterdepolarization (EAD) and transmural dispersion of repolarization (TDR) were assessed using arterially perfused rabbit ventricular wedge preparations. Transmembrane action potentials from epicardium, subendocardium, and endocardium were simultaneously recorded together with a transmural ECG. Transmural action potential duration (APD) was also mapped. LVH (renovascular hypertension model) produced significant prolongation in ventricular APD and QT interval. Preferential APD prolongation in subendocardium and endocardium was associated with a marked increase in TDR. Phase 2 EADs were generated from subendocardium or endocardium in all LVH rabbits (15 of 15) in the absence of APD prolonging agents at basic cycle lengths of 2,000-4,000 ms. Phase 2 EAD could produce "R on T" extrasystoles, initiating polymorphic ventricular tachycardia (VT). This study provides the first direct evidence from intracellular recordings that phase 2 EAD could be generated from rabbit intact hypertrophied LV wall in the absence of APD prolonging agents, resulting in R on T extrasystoles capable of initiating polymorphic VT under enhanced TDR.

Action Potentials↗
PubMed1987

Morphologic study of ventricular trabeculation in the embryonic chick heart.

This paper presents a morphologic study of ventricular trabeculation in chick embryo hearts between days 2 and 5 of incubation. Trabeculation appears to be the expression of three closely interrelated events: the formation of endocardial outgrowths that eventually invade the myocardium; the development of large intercellular spaces between the myocytes, and the decrease in thickness of the cardiac jelly. Endocardial cells present morphologic differences between trabeculated and nontrabeculated areas of the ventricular region. The elongation of the endocardial cells in the endocardial outgrowths and the presence of mitoses suggest that the endocardium grows out by means of an increase in cell number and by redistribution and elongation of the preexisting endocardial cells. The intercellular spaces of the myocardium appear filled with abundant extracellular material. It is suggested that the continuous synthesis of extracellular material by the myocytes may increase the hydrostatic pressure within the myocardium, inducing the formation and the enlargement of these intercellular spaces. The development and later rupture of endocardium-covered cords is described here. These cords are made up of a core of cardiac jelly material revested by endocardium. The cords may be engaged in the removal of substantial amounts of cardiac jelly during the formation of the trabeculae.

Animals↗