The innermost layer of the heart, comprised of endothelial cells.
A conical fibro-serous sac surrounding the HEART and the roots of the great vessels (AORTA; VENAE CAVAE; PULMONARY ARTERY). Pericardium consists of two sacs: the outer fibrous pericardium and the inner serous pericardium. The latter consists of an outer parietal layer facing the fibrous pericardium, and an inner visceral layer (epicardium) resting next to the heart, and a pericardial cavity between these two layers.
A fetal heart structure that is the bulging areas in the cardiac septum between the HEART ATRIA and the HEART VENTRICLES. During development, growth and fusion of endocardial cushions at midline forms the two atrioventricular canals, the sites for future TRICUSPID VALVE and BICUSPID VALVE.
The hollow, muscular organ that maintains the circulation of the blood.
Flaps of tissue that prevent regurgitation of BLOOD from the HEART VENTRICLES to the HEART ATRIA or from the PULMONARY ARTERIES or AORTA to the ventricles.
The lower right and left chambers of the heart. The right ventricle pumps venous BLOOD into the LUNGS and the left ventricle pumps oxygenated blood into the systemic arterial circulation.
An impulse-conducting system composed of modified cardiac muscle, having the power of spontaneous rhythmicity and conduction more highly developed than the rest of the heart.
The domestic dog, Canis familiaris, comprising about 400 breeds, of the carnivore family CANIDAE. They are worldwide in distribution and live in association with people. (Walker's Mammals of the World, 5th ed, p1065)
The muscle tissue of the HEART. It is composed of striated, involuntary muscle cells (MYOCYTES, CARDIAC) connected to form the contractile pump to generate blood flow.
A condition characterized by the thickening of ENDOCARDIUM due to proliferation of fibrous and elastic tissue, usually in the left ventricle leading to impaired cardiac function (CARDIOMYOPATHY, RESTRICTIVE). It is most commonly seen in young children and rarely in adults. It is often associated with congenital heart anomalies (HEART DEFECTS CONGENITAL;) INFECTION; or gene mutation. Defects in the tafazzin protein, encoded by TAZ gene, result in a form of autosomal dominant familial endocardial fibroelastosis.
The chambers of the heart, to which the BLOOD returns from the circulation.
The hemodynamic and electrophysiological action of the HEART VENTRICLES.
Recording the locations and measurements of electrical activity in the EPICARDIUM by placing electrodes on the surface of the heart to analyze the patterns of activation and to locate arrhythmogenic sites.
Methods to induce and measure electrical activities at specific sites in the heart to diagnose and treat problems with the heart's electrical system.
Abrupt changes in the membrane potential that sweep along the CELL MEMBRANE of excitable cells in response to excitation stimuli.
Ear-shaped appendage of either atrium of the heart. (Dorland, 28th ed)
A potentially lethal cardiac arrhythmia that is characterized by uncoordinated extremely rapid firing of electrical impulses (400-600/min) in HEART VENTRICLES. Such asynchronous ventricular quivering or fibrillation prevents any effective cardiac output and results in unconsciousness (SYNCOPE). It is one of the major electrocardiographic patterns seen with CARDIAC ARREST.
Recording of the moment-to-moment electromotive forces of the HEART as projected onto various sites on the body's surface, delineated as a scalar function of time. The recording is monitored by a tracing on slow moving chart paper or by observing it on a cardioscope, which is a CATHODE RAY TUBE DISPLAY.
Modified cardiac muscle fibers composing the terminal portion of the heart conduction system.
A spectrum of septal defects involving the ATRIAL SEPTUM; VENTRICULAR SEPTUM; and the atrioventricular valves (TRICUSPID VALVE; BICUSPID VALVE). These defects are due to incomplete growth and fusion of the ENDOCARDIAL CUSHIONS which are important in the formation of two atrioventricular canals, site of future atrioventricular valves.
Regulation of the rate of contraction of the heart muscles by an artificial pacemaker.
An abnormally rapid ventricular rhythm usually in excess of 150 beats per minute. It is generated within the ventricle below the BUNDLE OF HIS, either as autonomic impulse formation or reentrant impulse conduction. Depending on the etiology, onset of ventricular tachycardia can be paroxysmal (sudden) or nonparoxysmal, its wide QRS complexes can be uniform or polymorphic, and the ventricular beating may be independent of the atrial beating (AV dissociation).
Recording of regional electrophysiological information by analysis of surface potentials to give a complete picture of the effects of the currents from the heart on the body surface. It has been applied to the diagnosis of old inferior myocardial infarction, localization of the bypass pathway in Wolff-Parkinson-White syndrome, recognition of ventricular hypertrophy, estimation of the size of a myocardial infarct, and the effects of different interventions designed to reduce infarct size. The limiting factor at present is the complexity of the recording and analysis, which requires 100 or more electrodes, sophisticated instrumentation, and dedicated personnel. (Braunwald, Heart Disease, 4th ed)
Common name for two distinct groups of BIRDS in the order GALLIFORMES: the New World or American quails of the family Odontophoridae and the Old World quails in the genus COTURNIX, family Phasianidae.
This structure includes the thin muscular atrial septum between the two HEART ATRIA, and the thick muscular ventricular septum between the two HEART VENTRICLES.
Theoretical representations that simulate the behavior or activity of the cardiovascular system, processes, or phenomena; includes the use of mathematical equations, computers and other electronic equipment.
The middle germ layer of an embryo derived from three paired mesenchymal aggregates along the neural tube.
The hemodynamic and electrophysiological action of the HEART ATRIA.
Removal of tissue with electrical current delivered via electrodes positioned at the distal end of a catheter. Energy sources are commonly direct current (DC-shock) or alternating current at radiofrequencies (usually 750 kHz). The technique is used most often to ablate the AV junction and/or accessory pathways in order to interrupt AV conduction and produce AV block in the treatment of various tachyarrhythmias.
Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control of gene action during the developmental stages of an organism.
Contractile activity of the MYOCARDIUM.
The development of anatomical structures to create the form of a single- or multi-cell organism. Morphogenesis provides form changes of a part, parts, or the whole organism.
Striated muscle cells found in the heart. They are derived from cardiac myoblasts (MYOBLASTS, CARDIAC).
Conical muscular projections from the walls of the cardiac ventricles, attached to the cusps of the atrioventricular valves by the chordae tendineae.
A potent anti-arrhythmia agent, effective in a wide range of ventricular and atrial ARRHYTHMIAS and TACHYCARDIAS.
The developmental entity of a fertilized chicken egg (ZYGOTE). The developmental process begins about 24 h before the egg is laid at the BLASTODISC, a small whitish spot on the surface of the EGG YOLK. After 21 days of incubation, the embryo is fully developed before hatching.
A condition characterized by the thickening of the ventricular ENDOCARDIUM and subendocardium (MYOCARDIUM), seen mostly in children and young adults in the TROPICAL CLIMATE. The fibrous tissue extends from the apex toward and often involves the HEART VALVES causing restrictive blood flow into the respective ventricles (CARDIOMYOPATHY, RESTRICTIVE).
The study of the generation and behavior of electrical charges in living organisms particularly the nervous system and the effects of electricity on living organisms.
A TIE receptor tyrosine kinase that is found almost exclusively on ENDOTHELIAL CELLS. It is required for both normal embryonic vascular development (NEOVASCULARIZATION, PHYSIOLOGIC) and tumor angiogenesis (NEOVASCULARIZATION, PATHOLOGIC).
An exotic species of the family CYPRINIDAE, originally from Asia, that has been introduced in North America. They are used in embryological studies and to study the effects of certain chemicals on development.
A group of diseases in which the dominant feature is the involvement of the CARDIAC MUSCLE itself. Cardiomyopathies are classified according to their predominant pathophysiological features (DILATED CARDIOMYOPATHY; HYPERTROPHIC CARDIOMYOPATHY; RESTRICTIVE CARDIOMYOPATHY) or their etiological/pathological factors (CARDIOMYOPATHY, ALCOHOLIC; ENDOCARDIAL FIBROELASTOSIS).
One of the POTASSIUM CHANNEL BLOCKERS, with secondary effect on calcium currents, which is used mainly as a research tool and to characterize channel subtypes.
A subclass of LIM domain proteins that include an additional centrally-located homeodomain region that binds AT-rich sites on DNA. Many LIM-homeodomain proteins play a role as transcriptional regulators that direct cell fate.
The heart of the fetus of any viviparous animal. It refers to the heart in the postembryonic period and is differentiated from the embryonic heart (HEART/embryology) only on the basis of time.
The circulation of blood through the CORONARY VESSELS of the HEART.
Any of various animals that constitute the family Suidae and comprise stout-bodied, short-legged omnivorous mammals with thick skin, usually covered with coarse bristles, a rather long mobile snout, and small tail. Included are the genera Babyrousa, Phacochoerus (wart hogs), and Sus, the latter containing the domestic pig (see SUS SCROFA).
The hemodynamic and electrophysiological action of the left HEART VENTRICLE. Its measurement is an important aspect of the clinical evaluation of patients with heart disease to determine the effects of the disease on cardiac performance.
Any disturbances of the normal rhythmic beating of the heart or MYOCARDIAL CONTRACTION. Cardiac arrhythmias can be classified by the abnormalities in HEART RATE, disorders of electrical impulse generation, or impulse conduction.
A disorder of cardiac function caused by insufficient blood flow to the muscle tissue of the heart. The decreased blood flow may be due to narrowing of the coronary arteries (CORONARY ARTERY DISEASE), to obstruction by a thrombus (CORONARY THROMBOSIS), or less commonly, to diffuse narrowing of arterioles and other small vessels within the heart. Severe interruption of the blood supply to the myocardial tissue may result in necrosis of cardiac muscle (MYOCARDIAL INFARCTION).
The fibrous tissue that replaces normal tissue during the process of WOUND HEALING.
Inflammation of the ENDOCARDIUM caused by BACTERIA that entered the bloodstream. The strains of bacteria vary with predisposing factors, such as CONGENITAL HEART DEFECTS; HEART VALVE DISEASES; HEART VALVE PROSTHESIS IMPLANTATION; or intravenous drug use.
Accumulation of purulent material in tissues, organs, or circumscribed spaces, usually associated with signs of infection.
Inflammation of the inner lining of the heart (ENDOCARDIUM), the continuous membrane lining the four chambers and HEART VALVES. It is often caused by microorganisms including bacteria, viruses, fungi, and rickettsiae. Left untreated, endocarditis can damage heart valves and become life-threatening.
Impaired venous blood flow or venous return (venous stasis), usually caused by inadequate venous valves. Venous insufficiency often occurs in the legs, and is associated with EDEMA and sometimes with VENOUS STASIS ULCERS at the ankle.
Pathological conditions involving any of the various HEART VALVES and the associated structures (PAPILLARY MUSCLES and CHORDAE TENDINEAE).

Effect of warfarin on the induction and course of experimental endocarditis. (1/971)

The effect of warfarin treatment on an experimental endocarditis was studied in rabbits. Warfarin had no effect on the induction of a Streptococcus sanguis infection in catheter-induced endocardial vegetations, and the course of this infection was also unaltered. However, warfarin treatment resulted in rapidly progressive bacteremia, probably due to impaired circulation in clearing organs such as the lungs, liver, and spleen. Warfarin also reduced the survival time of the infected rabbits, in which pulmonary edema and extensive lung hemorrhages may have been a contributory factor.  (+info)

Enteroviral RNA replication in the myocardium of patients with left ventricular dysfunction and clinically suspected myocarditis. (2/971)

BACKGROUND: Previous studies dealing with the detection of enteroviral RNA in human endomyocardial biopsies have not differentiated between latent persistence of the enteroviral genome and active viral replication. Enteroviruses that are considered important factors for the development of myocarditis have a single-strand RNA genome of positive polarity that is transcribed by a virus-encoded RNA polymerase into a minus-strand mRNA during active viral replication. The synthesis of multiple copies of minus-strand enteroviral RNA therefore occurs only at sites of active viral replication but not in tissues with mere persistence of the viral genome. METHODS AND RESULTS: We investigated enteroviral RNA replication versus enteroviral RNA persistence in endomyocardial biopsies of 45 patients with left ventricular dysfunction and clinically suspected myocarditis. Using reverse-transcriptase polymerase chain reaction in conjunction with Southern blot hybridization, we established a highly sensitive assay to specifically detect plus-strand versus minus-strand enteroviral RNA in the biopsies. Plus-strand enteroviral RNA was detected in endomyocardial biopsies of 18 (40%) of 45 patients, whereas minus-strand RNA as an indication of active enteroviral RNA replication was detected in only 10 (56%) of these 18 plus-strand-positive patients. Enteroviral RNA was not found in biopsies of the control group (n=26). CONCLUSIONS: These data demonstrate that a significant fraction of patients with left ventricular dysfunction and clinically suspected myocarditis had active enteroviral RNA replication in their myocardium (22%). Differentiation between patients with active viral replication and latent viral persistence should be particularly important in future studies evaluating different therapeutic strategies. In addition, molecular genetic detection of enteroviral genome and differentiation between replicating versus persistent viruses is possible in a single endomyocardial biopsy.  (+info)

Regional electrophysiological effects of hypokalaemia, hypomagnesaemia and hyponatraemia in isolated rabbit hearts in normal and ischaemic conditions. (3/971)

OBJECTIVE: The aims of this study were to establish an isolated working heart model for electrophysiological recordings from the epicardium and endocardium and to examine regional effects of changes in ion concentrations in normal and ischaemic conditions. METHODS: Monophasic action potential duration (MAPD90), effective refractory period (ERP) and conduction delay were measured simultaneously in the epicardium and endocardium of rabbit hearts paced at 3.3 Hz, subjected to 30 min of regional ischaemia and 15 min of reperfusion. The hearts were exposed before and throughout ischaemia and reperfusion to hypokalaemia (K+ = 2 mM), hypomagnesaemia (Mg2+ = 0.5 mM) or hyponatraemia (Na+ = 110 mM). RESULTS: In the control hearts, no regional electrophysiological differences were seen before ischaemia, but ischaemia-induced MAPD90 shortening and postrepolarisation refractoriness were greater in the epicardium than in the endocardium and conduction delay increased only in the epicardium. Hypokalaemia shortened ERP in the epicardium (but not endocardium) and increased conduction delay in all areas before ischaemia, but it had no effects during ischaemia. During reperfusion hypokalaemia increased the incidence of recurrent tachyarrhythmias. Hypomagnesaemia had no effect before ischaemia, increased epicardial (but not endocardial) MAPD90 shortening during ischaemia, although it had no pro-arrhythmic action. Hyponatraemia increased conduction delay in all areas before ischaemia and produced asystole or severe bradycardia in all hearts. During ischaemia, hyponatraemia decreased ERP shortening and inducibility of arrhythmias in the epicardium (but not endocardium). CONCLUSIONS: We conclude that the more pronounced effect of ischaemia upon the epicardium than the endocardium can be explained by the contact of the endocardium with intracavitary perfusate. We also conclude that changes in ion concentrations may have differential regional electrical effects in normal or ischaemic conditions.  (+info)

Requirement of type III TGF-beta receptor for endocardial cell transformation in the heart. (4/971)

Transforming growth factor-beta (TGF-beta) signaling is mediated by a complex of type I (TBRI) and type II (TBRII) receptors. The type III receptor (TBRIII) lacks a recognizable signaling domain and has no clearly defined role in TGF-beta signaling. Cardiac endothelial cells that undergo epithelial-mesenchymal transformation express TBRIII, and here TBRIII-specific antisera were found to inhibit mesenchyme formation and migration in atrioventricular cushion explants. Misexpression of TBRIII in nontransforming ventricular endothelial cells conferred transformation in response to TGF-beta2. These results support a model where TBRIII localizes transformation in the heart and plays an essential, nonredundant role in TGF-beta signaling.  (+info)

Bulbus arteriosus of the antarctic teleosts. I. The white-blooded Chionodraco hamatus. (5/971)

The bulbus arteriosus of teleost fish is a thick-walled chamber that extends between the single ventricle and the ventral aorta. The functional importance of the bulbus resides in the fact that it maintains a steady blood flow into the gill system through heart contraction. Despite of this, a thorough study of the structure of the bulbus in teleost fish is still lacking. We have undertaken a morphologic study of the bulbus arteriosus in the stenothermal teleosts of the Antarctic sea. The structural organization of the bulbus arteriosus of the icefish Chionodraco hamatus has been studied here by conventional light, scanning, and transmission electron microscopy. The inner surface of the bulbus shows a festooned appearance due to the presence of longitudinal, unbranched ridges that extend between the ventricle and the arterial trunk. The wall of the bulbus is divided into endocardial, subendocardial, middle, and external layers. Endocardial cells show a large number of moderately-dense bodies. The endocardium invaginates into the subendocardium forming solid epithelial cords that contain numerous secretory vacuoles. Cells in the subendocardium group into small domains, have some of the morphological characteristics of smooth muscle cells, and appear enmeshed in a three-dimensional network of matrix filaments. Cells in the middle layer are typical smooth muscle cells. They appear arranged into layers and are surrounded by a filamentous meshwork that excludes collagen fibers. Orientation of this meshwork occurs in the vicinity of the smooth muscle cells. Elastin fibers are never observed. The external layer is formed by wavy collagen bundles and fibroblast-like cells. This layer lacks blood vessels and nerve fibers. The endocardium and the endocardium-derived cords are secretory epithelia that may be involved in the formation ofmucins or glycosaminoglycans. These mucins may have a protecting effect on the endocardium. The subendocardium and the middle layer appear to be formed by the same cell type, smooth muscle, with a gradient of differentiation from the secretory (subendocardium) to the contractile (middle layer) phenotype. Despite the absence of elastin fibers, the filamentous matrix could maintain the elastic properties of the bulbus wall. Smooth muscle cells appear to be actively involved in bulbus wall dynamics. The restriction of collagen to the external layer suggests that it may control wall dilatation and bulbus compliance. When comparison was possible, structural differences between C. hamatus and temperate teleosts seemed to be not species-related, but of phenotypic adaptative significance. This is remarkable since Antarctic fishes have lived isolated in freezing waters for the last two million years.  (+info)

Fas expression and apoptosis correlate with cardiac dysfunction in patients with dilated cardiomyopathy. (6/971)

Fas is a transmembranous glycoprotein that mediates apoptosis. To elucidate the roles of Fas and of myocyte apoptosis in patients with dilated cardiomyopathy (DCM), the expression of Fas and the fragmentation of DNA were compared in endomyocardial biopsy specimens obtained from patients with DCM. Endomyocardial biopsy was performed on 19 subjects (16 with DCM and 3 control subjects) who also underwent cardiac catheterization and echocardiography. Fas and bcl-2 expression were assayed immunohistochemically, and in situ TdT staining was performed to estimate the number of apoptotic cells. Samples from the DCM patients stained more intensely with anti-Fas antibody than those from control patients (p<0.05). The percentage of in situ TdT-positive cells was significantly higher in the DCM group than in the control group (p<0.05). A correlation between Fas expression and in situ TdT staining was observed in 67% of myocytes in the DCM group. Moreover, the percentage of in situ TdT staining was significantly higher in subjects with severely impaired left ventricular systolic function than in those whose systolic function was mild to moderately impaired, or who had normal systolic function (p<0.05). The samples showed little expression of bcl-2. These results suggest that Fas expression and apoptosis may be involved in the progression of cardiac dysfunction in DCM.  (+info)

Tracheal aspirate as a substrate for polymerase chain reaction detection of viral genome in childhood pneumonia and myocarditis. (7/971)

BACKGROUND: Infectious respiratory disorders are important causes of childhood morbidity and mortality. Viral causes are common and may lead to rapid deterioration, requiring mechanical ventilation; myocardial dysfunction may accompany respiratory decompensation. The etiologic viral diagnosis may be difficult with classic methods. The purpose of this study was to evaluate polymerase chain reaction (PCR) as a diagnostic method for identification of causative agents. METHODS AND RESULTS: PCR was used to amplify sequences of viruses known to cause childhood viral pneumonia and myocarditis. Oligonucleotide primers were designed to amplify specific sequences of DNA virus (adenovirus, cytomegalovirus, herpes simplex virus, and Epstein-Barr virus) and RNA virus (enterovirus, respiratory syncytial virus, influenza A, and influenza B) genomes. Tracheal aspirate samples were obtained from 32 intubated patients and nucleic acid extracted before PCR. PCR results were compared with results of culture, serology, and antigen detection methods when available. In cases of myocarditis (n=7), endomyocardial biopsy samples were analyzed by PCR and compared with tracheal aspirate studies. PCR amplification of viral genome occurred in 18 of 32 samples (56%), with 3 samples PCR positive for 2 viral genomes. Amplified viral sequences included RSV (n=3), enterovirus (n=5), cytomegalovirus (n=4), adenovirus (n=3), herpes simplex virus (n=2), Epstein-Barr virus (n=1), influenza A (n=2), and influenza B (n=1). All 7 cases of myocarditis amplified the same viral genome from heart as found by tracheal aspirate. CONCLUSIONS: PCR is a rapid and sensitive diagnostic tool in cases of viral pneumonia with or without myocarditis, and tracheal aspirate appears to be excellent for analysis.  (+info)

Oxidized low-density lipoproteins induce apoptosis in aortic and endocardial endothelial cells. (8/971)

AIM: To examine whether oxidized low-density lipoproteins (ox-LDL) might induce apoptosis in bovine aortic and endocardial endothelial cells (BAEC and BEEC). METHODS: Low-density lipoproteins (LDL) were isolated from healthy human plasma by ultracentrifugation and oxidized by CuSO4 10 mumol.L-1. BAEC and BEEC were incubated in a medium containing ox-LDL, LDL, or phosphate-buffer solution (PBS) as control. DNA fragmentation was visualized by agarose gel electrophoresis and determined quantitatively using Hoechst-33258 fluorochrome. RESULTS: Ox-LDL, not LDL, elicited typical apoptotic changes and DNA fragmentation in BAEC and BEEC. In BAEC, dextran sulfate, and cicloheximide (Cic) exhibited no effect on DNA fragmentation induced by ox-LDL. Butylated hydroxytoluene (BHT) 20 mumol.L-1 completely inhibited Cu(2+)-mediated oxidation of LDL as well as the apoptosis-inducing effect of Cu(2+)-exposed LDL. Lysophosphatidylcholine (LPC) did not elicit DNA fragmentation in BAEC and in BEEC. DNA fragmentation induced by ox-LDL in BAEC and in BEEC was blocked by chelating the calcium of the culture medium by egtazic acid. CONCLUSION: Ox-LDL induces apoptosis in BAEC and BEEC without involving the LPC.  (+info)

The exact cause of endocardial fibroelastosis is not known, but it is believed to be due to genetic mutations or environmental factors during fetal development. The condition may be associated with other congenital heart defects, such as ventricular septal defect or atrial septal defect.

Symptoms of endocardial fibroelastosis can vary depending on the severity of the condition, but they may include:

* Difficulty breathing
* Fatigue
* Shortness of breath during exercise
* Swelling in the legs and feet
* Pale or blue-tinged skin
* Poor feeding or growth in infants

If endocardial fibroelastosis is suspected, a doctor may perform various diagnostic tests, such as:

* Echocardiogram (echo): This test uses sound waves to create images of the heart and can help identify thickening or scarring of the endocardium.
* Cardiac catheterization: This test involves inserting a thin tube into the heart through a blood vessel to measure pressure and oxygen levels within the heart.
* Magnetic resonance imaging (MRI): This test uses a strong magnetic field and radio waves to create detailed images of the heart.

Treatment for endocardial fibroelastosis may include:

* Medications: To manage symptoms such as high blood pressure or irregular heart rhythms.
* Catheter ablation: A procedure that uses heat or cold to destroy abnormal electrical pathways in the heart.
* Surgery: To repair or replace damaged heart valves or to correct other congenital heart defects.

The prognosis for endocardial fibroelastosis is generally good if the condition is detected and treated early. However, if left untreated, it can lead to serious complications such as heart failure, stroke, or sepsis. Regular follow-up with a cardiologist is important to monitor the condition and adjust treatment as needed. With appropriate treatment, many people with endocardial fibroelastosis can lead active, fulfilling lives.

In Vfib, the electrical activity of the heart becomes disorganized, leading to a fibrillatory pattern of contraction. This means that the ventricles are contracting in a rapid, unsynchronized manner, rather than the coordinated, synchronized contractions that occur in normal heart function.

Vfib can be caused by a variety of factors, including coronary artery disease, heart attack, cardiomyopathy, and electrolyte imbalances. It can also be triggered by certain medications, such as digoxin, or by electrical shocks to the heart.

Symptoms of Vfib include palpitations, shortness of breath, chest pain, and loss of consciousness. If not treated promptly, Vfib can lead to cardiac arrest and death.

Treatment of Vfib typically involves electrical cardioversion, which involves delivering an electric shock to the heart to restore a normal heart rhythm. In some cases, medications may also be used to help regulate the heart rhythm. In more severe cases, surgery or other interventions may be necessary to address any underlying causes of Vfib.

Overall, ventricular fibrillation is a serious medical condition that requires prompt treatment to prevent complications and ensure effective cardiac function.

Endocardial cushion defects can be classified into several types based on their location and severity. Some common types of endocardial cushion defects include:

1. Atrial septal defect (ASD): A hole in the wall between the two upper chambers of the heart, known as the atria.
2. Ventricular septal defect (VSD): A hole in the wall between the two lower chambers of the heart, known as the ventricles.
3. Endocardial cushion defect (ECD): A defect that affects the endocardial cushions in one or more of the heart's chambers.
4. Double outlet right ventricle (DORV): A condition where two major blood vessels arise from the same ventricle, instead of one.
5. Tetralogy of Fallot: A combination of four heart defects that include a VSD, pulmonary stenosis (narrowing of the pulmonary artery), a thickened muscle wall in the ventricles, and an enlarged aorta.

Endocardial cushion defects can cause a range of symptoms, including shortness of breath, fatigue, and poor growth or development in children. In some cases, these defects may not cause any symptoms at all until later in life.

Diagnosis of endocardial cushion defects typically involves a combination of physical examination, echocardiography (ultrasound imaging of the heart), electrocardiography (ECG or heart rhythm testing), and other tests such as chest X-rays or cardiac catheterization.

Treatment for endocardial cushion defects depends on the severity of the defect and may include medications, surgery, or a combination of both. In some cases, no treatment may be necessary if the defect is mild and not causing any symptoms. Surgical repair of endocardial cushion defects can involve patching or replacing the affected area with healthy tissue, and may also involve other procedures such as balloon dilation or stenting to widen narrowed blood vessels.

In some cases, endocardial cushion defects may be associated with other genetic or chromosomal disorders, such as Down syndrome or Turner syndrome. In these cases, treatment may also involve management of the underlying condition.

Overall, while endocardial cushion defects can be serious and require ongoing medical attention, many people with these conditions can lead active and fulfilling lives with proper treatment and monitoring.

Tachycardia, ventricular can be classified into several types based on its duration and the presence of other symptoms. These include:

1. Paroxysmal ventricular tachycardia (PVT): This is a rapid heart rate that occurs in episodes lasting less than 30 seconds and may be accompanied by palpitations, shortness of breath, or dizziness.
2. Sustained ventricular tachycardia: This is a rapid heart rate that persists for more than 30 seconds and may require medical intervention to return the heart to normal rhythm.
3. Ventricular fibrillation (VF): This is a life-threatening condition in which the ventricles are unable to pump blood effectively due to rapid, disorganized electrical activity.

Symptoms of tachycardia, ventricular may include:

* Palpitations or rapid heartbeat
* Shortness of breath
* Dizziness or lightheadedness
* Chest pain or discomfort
* Fatigue or weakness

Diagnosis of tachycardia, ventricular is typically made based on a physical examination, medical history, and results of diagnostic tests such as electrocardiogram (ECG), echocardiogram, or stress test. Treatment options may include medications to regulate heart rhythm, cardioversion to restore normal heart rhythm, and in some cases, implantation of a cardioverter-defibrillator (ICD) to prevent sudden death.

In summary, tachycardia, ventricular is a rapid heart rate that originates in the ventricles and can be caused by a variety of conditions. It is important to seek medical attention if symptoms persist or worsen over time. With proper diagnosis and treatment, it is possible to manage the condition and improve quality of life.

The exact cause of endomyocardial fibrosis is not known, but it is believed to be related to inflammation and scarring within the heart. The condition is more common in men than women, and typically affects people between the ages of 20 and 50. Symptoms of endomyocardial fibrosis can include shortness of breath, fatigue, swelling in the legs and feet, and chest pain.

There is no cure for endomyocardial fibrosis, but treatment options may include medications to manage symptoms, surgery to repair or replace damaged heart tissue, and lifestyle changes such as a healthy diet and regular exercise. In severe cases, heart transplantation may be necessary. Early diagnosis and treatment can help slow the progression of the condition and improve quality of life for those affected.

There are several types of cardiomyopathies, each with distinct characteristics and symptoms. Some of the most common forms of cardiomyopathy include:

1. Hypertrophic cardiomyopathy (HCM): This is the most common form of cardiomyopathy and is characterized by an abnormal thickening of the heart muscle, particularly in the left ventricle. HCM can lead to obstruction of the left ventricular outflow tract and can increase the risk of sudden death.
2. Dilated cardiomyopathy: This type of cardiomyopathy is characterized by a decrease in the heart's ability to pump blood effectively, leading to enlargement of the heart and potentially life-threatening complications such as congestive heart failure.
3. Restrictive cardiomyopathy: This type of cardiomyopathy is characterized by stiffness of the heart muscle, which makes it difficult for the heart to fill with blood. This can lead to shortness of breath and fatigue.
4. Left ventricular non-compaction (LVNC): This is a rare type of cardiomyopathy that occurs when the left ventricle does not properly compact, leading to reduced cardiac function and potentially life-threatening complications.
5. Cardiac amyloidosis: This is a condition in which abnormal proteins accumulate in the heart tissue, leading to stiffness and impaired cardiac function.
6. Right ventricular cardiomyopathy (RVCM): This type of cardiomyopathy is characterized by impaired function of the right ventricle, which can lead to complications such as pulmonary hypertension and heart failure.
7. Endocardial fibroelastoma: This is a rare type of cardiomyopathy that occurs when abnormal tissue grows on the inner lining of the heart, leading to reduced cardiac function and potentially life-threatening complications.
8. Cardiac sarcoidosis: This is a condition in which inflammatory cells accumulate in the heart, leading to impaired cardiac function and potentially life-threatening complications.
9. Hypertrophic cardiomyopathy (HCM): This is a condition in which the heart muscle thickens, leading to reduced cardiac function and potentially life-threatening complications such as arrhythmias and sudden death.
10. Hypokinetic left ventricular cardiomyopathy: This type of cardiomyopathy is characterized by decreased contraction of the left ventricle, leading to reduced cardiac function and potentially life-threatening complications such as heart failure.

It's important to note that some of these types of cardiomyopathy are more common in certain populations, such as hypertrophic cardiomyopathy being more common in young athletes. Additionally, some types of cardiomyopathy may have overlapping symptoms or co-occurring conditions, so it's important to work with a healthcare provider for an accurate diagnosis and appropriate treatment.

There are many different types of cardiac arrhythmias, including:

1. Tachycardias: These are fast heart rhythms that can be too fast for the body's needs. Examples include atrial fibrillation and ventricular tachycardia.
2. Bradycardias: These are slow heart rhythms that can cause symptoms like fatigue, dizziness, and fainting. Examples include sinus bradycardia and heart block.
3. Premature beats: These are extra beats that occur before the next regular beat should come in. They can be benign but can also indicate an underlying arrhythmia.
4. Supraventricular arrhythmias: These are arrhythmias that originate above the ventricles, such as atrial fibrillation and paroxysmal atrial tachycardia.
5. Ventricular arrhythmias: These are arrhythmias that originate in the ventricles, such as ventricular tachycardia and ventricular fibrillation.

Cardiac arrhythmias can be diagnosed through a variety of tests including electrocardiograms (ECGs), stress tests, and holter monitors. Treatment options for cardiac arrhythmias vary depending on the type and severity of the condition and may include medications, cardioversion, catheter ablation, or implantable devices like pacemakers or defibrillators.

Myocardial ischemia can be caused by a variety of factors, including coronary artery disease, high blood pressure, diabetes, and smoking. It can also be triggered by physical exertion or stress.

There are several types of myocardial ischemia, including:

1. Stable angina: This is the most common type of myocardial ischemia, and it is characterized by a predictable pattern of chest pain that occurs during physical activity or emotional stress.
2. Unstable angina: This is a more severe type of myocardial ischemia that can occur without any identifiable trigger, and can be accompanied by other symptoms such as shortness of breath or vomiting.
3. Acute coronary syndrome (ACS): This is a condition that includes both stable angina and unstable angina, and it is characterized by a sudden reduction in blood flow to the heart muscle.
4. Heart attack (myocardial infarction): This is a type of myocardial ischemia that occurs when the blood flow to the heart muscle is completely blocked, resulting in damage or death of the cardiac tissue.

Myocardial ischemia can be diagnosed through a variety of tests, including electrocardiograms (ECGs), stress tests, and imaging studies such as echocardiography or cardiac magnetic resonance imaging (MRI). Treatment options for myocardial ischemia include medications such as nitrates, beta blockers, and calcium channel blockers, as well as lifestyle changes such as quitting smoking, losing weight, and exercising regularly. In severe cases, surgical procedures such as coronary artery bypass grafting or angioplasty may be necessary.

Cicatrix is a term used to describe the scar tissue that forms after an injury or surgery. It is made up of collagen fibers and other cells, and its formation is a natural part of the healing process. The cicatrix can be either hypertrophic (raised) or atrophic (depressed), depending on the severity of the original wound.

The cicatrix serves several important functions in the healing process, including:

1. Protection: The cicatrix helps to protect the underlying tissue from further injury and provides a barrier against infection.
2. Strength: The collagen fibers in the cicatrix give the scar tissue strength and flexibility, allowing it to withstand stress and strain.
3. Support: The cicatrix provides support to the surrounding tissue, helping to maintain the shape of the affected area.
4. Cosmetic appearance: The appearance of the cicatrix can affect the cosmetic outcome of a wound or surgical incision. Hypertrophic scars are typically red and raised, while atrophic scars are depressed and may be less noticeable.

While the formation of cicatrix is a normal part of the healing process, there are some conditions that can affect its development or appearance. For example, keloid scars are raised, thick scars that can form as a result of an overactive immune response to injury. Acne scars can also be difficult to treat and may leave a lasting impression on the skin.

In conclusion, cicatrix is an important part of the healing process after an injury or surgery. It provides protection, strength, support, and can affect the cosmetic appearance of the affected area. Understanding the formation and functions of cicatrix can help medical professionals to better manage wound healing and improve patient outcomes.

Causes and risk factors:

The most common cause of bacterial endocarditis is a bacterial infection that enters the bloodstream and travels to the heart. This can occur through various means, such as:

* Injecting drugs or engaging in other risky behaviors that allow bacteria to enter the body
* Having a weakened immune system due to illness or medication
* Having a previous history of endocarditis or other heart conditions
* Being over the age of 60, as older adults are at higher risk for developing endocarditis


The symptoms of bacterial endocarditis can vary depending on the severity of the infection and the location of the infected area. Some common symptoms include:

* Fever
* Chills
* Joint pain or swelling
* Fatigue
* Shortness of breath
* Heart murmurs or abnormal heart sounds


Bacterial endocarditis is diagnosed through a combination of physical examination, medical history, and diagnostic tests such as:

* Blood cultures to identify the presence of bacteria in the bloodstream
* Echocardiogram to visualize the heart and detect any abnormalities
* Chest X-ray to look for signs of infection or inflammation in the lungs or heart
* Electrocardiogram (ECG) to measure the electrical activity of the heart


The treatment of bacterial endocarditis typically involves a combination of antibiotics and surgery. Antibiotics are used to kill the bacteria and reduce inflammation, while surgery may be necessary to repair or replace damaged heart tissue. In some cases, the infected heart tissue may need to be removed.


Preventing bacterial endocarditis involves good oral hygiene, regular dental check-ups, and avoiding certain high-risk activities such as unprotected sex or sharing of needles. People with existing heart conditions should also take antibiotics before dental or medical procedures to reduce the risk of infection.


The prognosis for bacterial endocarditis is generally good if treatment is prompt and effective. However, delays in diagnosis and treatment can lead to serious complications such as heart failure, stroke, or death. Patients with pre-existing heart conditions are at higher risk for complications.


Bacterial endocarditis is a relatively rare condition, affecting approximately 2-5 cases per million people per year in the United States. However, people with certain risk factors such as heart conditions or prosthetic heart valves are at higher risk for developing the infection.


Bacterial endocarditis can lead to a number of complications, including:

* Heart failure
* Stroke or brain abscess
* Kidney damage or failure
* Pregnancy complications
* Nerve damage or peripheral neuropathy
* Skin or soft tissue infections
* Bone or joint infections
* Septicemia (blood poisoning)


Preventive measures for bacterial endocarditis include:

* Good oral hygiene and regular dental check-ups to reduce the risk of dental infections
* Avoiding high-risk activities such as unprotected sex or sharing of needles
* Antibiotics before dental or medical procedures for patients with existing heart conditions
* Proper sterilization and disinfection of medical equipment
* Use of antimicrobial prophylaxis (prevention) in high-risk patients.

Emerging Trends:

Newly emerging trends in the management of bacterial endocarditis include:

* The use of novel antibiotics and combination therapy to improve treatment outcomes
* The development of new diagnostic tests to help identify the cause of infection more quickly and accurately
* The increased use of preventive measures such as antibiotic prophylaxis in high-risk patients.

Future Directions:

Future directions for research on bacterial endocarditis may include:

* Investigating the use of novel diagnostic techniques, such as genomics and proteomics, to improve the accuracy of diagnosis
* Developing new antibiotics and combination therapies to improve treatment outcomes
* Exploring alternative preventive measures such as probiotics and immunotherapy.

In conclusion, bacterial endocarditis is a serious infection that can have severe consequences if left untreated. Early diagnosis and appropriate treatment are crucial to improving patient outcomes. Preventive measures such as good oral hygiene and antibiotic prophylaxis can help reduce the risk of developing this condition. Ongoing research is focused on improving diagnostic techniques, developing new treatments, and exploring alternative preventive measures.

There are several types of abscesses, including:

1. Skin abscesses: These occur when a bacterial infection causes pus to accumulate under the skin. They may appear as red, swollen bumps on the surface of the skin.
2. Internal abscesses: These occur when an infection causes pus to accumulate within an internal organ or tissue. Examples include abscesses that form in the liver, lungs, or brain.
3. Perianal abscesses: These occur when an infection causes pus to accumulate near the anus. They may be caused by a variety of factors, including poor hygiene, anal sex, or underlying conditions such as Crohn's disease.
4. Dental abscesses: These occur when an infection causes pus to accumulate within a tooth or the surrounding tissue. They are often caused by poor oral hygiene or dental trauma.

The symptoms of an abscess can vary depending on its location and severity. Common symptoms include:

* Redness, swelling, and warmth around the affected area
* Pain or discomfort in the affected area
* Fever or chills
* Discharge of pus from the affected area
* Bad breath (if the abscess is located in the mouth)

If an abscess is not treated, it can lead to serious complications, including:

* Further spread of the infection to other parts of the body
* Inflammation of surrounding tissues and organs
* Formation of a pocket of pus that can become infected and lead to further complications
* Sepsis, a life-threatening condition caused by the spread of infection through the bloodstream.

Treatment of an abscess usually involves drainage of the pus and antibiotics to clear the infection. In some cases, surgery may be necessary to remove affected tissue or repair damaged structures.

It's important to seek medical attention if you suspect that you have an abscess, as prompt treatment can help prevent serious complications.

Symptoms of endocarditis may include fever, fatigue, joint pain, and swelling in the legs and feet. In some cases, the condition can lead to serious complications, such as heart valve damage, stroke, or death.

Treatment for endocarditis typically involves antibiotics to clear the infection. In severe cases, surgery may be necessary to repair or replace damaged heart tissue. Preventive measures include good dental hygiene, avoiding risky behaviors such as injecting drugs, and keeping wounds clean and covered.

Endocarditis is a serious condition that can have long-term consequences if left untreated. Early diagnosis and treatment are essential to prevent complications and ensure the best possible outcome for patients.

There are several risk factors for developing venous insufficiency, including:

* Age: As we age, our veins become less effective at pumping blood back to the heart, making us more susceptible to venous insufficiency.
* Gender: Women are more likely to develop venous insufficiency than men due to hormonal changes and other factors.
* Family history: If you have a family history of venous insufficiency, you may be more likely to develop the condition.
* Injury or trauma: Injuries or traumas to the veins can damage valves or cause blood clots, leading to venous insufficiency.
* Obesity: Excess weight can put extra pressure on the veins, increasing the risk of venous insufficiency.

Symptoms of venous insufficiency may include:

* Pain, aching, or cramping in the legs
* Swelling, edema, or water retention in the legs
* Skin discoloration or thickening of the skin on the legs
* Itching or burning sensations on the skin
* Ulcers or sores on the skin

If left untreated, venous insufficiency can lead to more serious complications such as:

* Chronic wounds or ulcers
* Blood clots or deep vein thrombosis (DVT)
* Increased risk of infection
* Decreased mobility and quality of life

To diagnose venous insufficiency, a healthcare provider may perform one or more of the following tests:

* Physical examination: A healthcare provider will typically examine the legs and ankles to check for swelling, discoloration, and other symptoms.
* Duplex ultrasound: This non-invasive test uses sound waves to evaluate blood flow in the veins and can detect blockages or other problems.
* Venography: This test involves injecting a dye into the vein to visualize the veins and check for any blockages or abnormalities.
* Imaging tests: Such as MRI, CT scan, or X-rays may be used to rule out other conditions that may cause similar symptoms.

Treatment options for venous insufficiency depend on the underlying cause and severity of the condition, but may include one or more of the following:

* Compression stockings: These specialized stockings provide gentle pressure to the legs and ankles to help improve blood flow and reduce swelling.
* Lifestyle changes: Maintaining a healthy weight, exercising regularly, and avoiding prolonged standing or sitting can help improve symptoms.
* Medications: Such as diuretics, anticoagulants, or pain relievers may be prescribed to manage symptoms and prevent complications.
* Endovenous laser therapy: This minimally invasive procedure uses a laser to heat and seal off the damaged vein, redirecting blood flow to healthier veins.
* Sclerotherapy: This involves injecting a solution into the affected vein to cause it to collapse and be absorbed by the body.
* Vein stripping: In this surgical procedure, the affected vein is removed through small incisions.

It's important to note that these treatments are usually recommended for more severe cases of venous insufficiency, and for those who have not responded well to other forms of treatment. Your healthcare provider will help determine the best course of treatment for your specific case.

There are several types of heart valve diseases, including:

1. Mitral regurgitation: This occurs when the mitral valve does not close properly, allowing blood to flow backward into the left atrium.
2. Aortic stenosis: This occurs when the aortic valve becomes narrowed or blocked, restricting blood flow from the left ventricle into the aorta.
3. Pulmonary stenosis: This occurs when the pulmonary valve becomes narrowed or blocked, restricting blood flow from the right ventricle into the pulmonary artery.
4. Tricuspid regurgitation: This occurs when the tricuspid valve does not close properly, allowing blood to flow backward into the right atrium.
5. Heart valve thickening or calcification: This can occur due to aging, rheumatic fever, or other conditions that cause inflammation in the heart.
6. Endocarditis: This is an infection of the inner lining of the heart, which can damage the heart valves.
7. Rheumatic heart disease: This is a condition caused by rheumatic fever, which can damage the heart valves and cause scarring.
8. Congenital heart defects: These are heart defects that are present at birth, and can affect the heart valves as well as other structures of the heart.

Symptoms of heart valve disease can include shortness of breath, fatigue, swelling in the legs or feet, and chest pain. Treatment options for heart valve disease depend on the specific condition and can range from medication to surgery or other procedures.

The endocardium also provides protection to the valves and heart chambers. The endocardium underlies the much more voluminous ... In infective endocarditis, the endocardium (especially the endocardium lining the heart valves) is affected by bacteria. ... The endocardium is the innermost layer of tissue that lines the chambers of the heart. Its cells are embryologically and ... The endocardium, which is primarily made up of endothelial cells, controls myocardial function. This modulating role is ...
Digitally coloured electron micrograph of mouse ventricular endocardium (burgundy). TC (blue) make an interstitial network in ... Gherghiceanu, Mihaela; Manole, C. G.; Popescu, L. M. (September 2010). "Telocytes in endocardium: electron microscope evidence ...
The endocardium is the last layer to repolarize. The plateau phase of depolarization has been shown to last longer in ...
The heart valves and the chambers are lined with endocardium. Heart valves separate the atria from the ventricles, or the ...
Endocarditis refers to inflammation of the endocardium of the heart. Staphylococcus schleiferi was isolated as the cause of ...
Infective endocarditis: An infection of the endocardium caused by enterococcus; used when the organism is not sensitive to ...
The endocardium, by secreting endothelins, may also play a role in regulating the contraction of the myocardium. The middle ... The innermost layer of the heart is called the endocardium. It is made up of a lining of simple squamous epithelium and covers ... The wall of the heart is made up of three layers: epicardium, myocardium, and endocardium. The heart pumps blood with a rhythm ... In addition to these muscular ridges, a band of cardiac muscle, also covered by endocardium, known as the moderator band ...
The other leaflets are described as being plastered to the endocardium.[citation needed] Tethering the underlying ventricular ...
Damaged valves and endocardium contribute to the development of infective endocarditis. Specifically, the damaged part of a ... Damage to the valves and endocardium can be caused by: Altered, turbulent blood flow. The areas that fibrose, clot, or roughen ...
Cardiac muscle lies between the epicardium and the endocardium in the heart. Cardiac muscle cells generally only contain one ...
... of the interior surfaces of the heart chambers is called endocardium. An impaired function can lead to serious ...
The openings of the smallest cardiac veins are located in the endocardium. Here the smallest cardiac veins return blood into ...
"Pathologische Histologie des Herzens und der Blutgefasse (Myocardium, Endocardium Arterien, Venen und Capillaren)". 1881. [1] ...
... is an inflammation of the inner layer of the heart, the endocardium. It usually involves the heart valves. Other ... not seem to have a preferred location of deposition and may form on the undersurfaces of the valves or even on the endocardium ... structures that may be involved include the interventricular septum, the chordae tendineae, the mural endocardium, or the ...
A small tissue sample of the endocardium and myocardium is taken and investigated. The cause of the myocarditis can be only ...
This notch is far less evident in cells from the endocardium, and the difference between the endocardium and epicardium are ... The differences in electrical properties between the epi- and endocardium are described as a 'transmural dispersion of ... endocardium) and outside (epicardium) of the heart (known as the repolarisation hypothesis). The shape of the action potential ... creating a brief period within each cardiac cycle when current flows from the endocardium to the epicardium creating the ...
"Utica-Reid Line Gets Single Fare: Endocardium Community Association Succeeds After 2-Year Effort". Brooklyn Daily Eagle. June ...
The Purkinje cells are mostly found within both the endocardium and the sub-endocardium. The sinoatrial node shows a small ... It is located in the endocardium of the atrial surface of the right atrioventricular valve. It is not covered by connective ...
Then the heart tube is formed by the endocardium, which is the inner endothelial lining of the heart, and the myocardial muscle ... The inner lining of the heart - the endocardium, lymphatic and blood vessels, develop from endothelium. In the splanchnopleuric ...
Such receptor subtypes have also been discovered in the epicardium, myocardium, and endocardium of the heart. In rats, D1-like ...
While development splanchnopleure undergo EMT and produce endothelial progenitors, these then form the endocardium through MET ...
1997). "Bmx tyrosine kinase is specifically expressed in the endocardium and the endothelium of large arteries". Circulation. ...
In the adult, this valve typically has totally regressed or remains as a small fold of endocardium. Rarely, the inferior vena ...
In the 1980s research staff worked to clarify the differences between epicardium and endocardium, and found that the presence ... They found differences in the response of epicardium and endocardium to a variety of drugs and neurotransmitters. The MMRI ... of an action potential notch in epicardium, but not endocardium, is responsible for inscription of the electrocardiographic J ...
This is done by injecting electric current into the conductive pathways and into the endocardium at various places. Last, the ...
Most commonly, it is a crescentic fold of endocardium arising from the anterior rim of the IVC orifice. The lateral horn of the ...
Pucéat M (Apr 2013). "Embryological origin of the endocardium and derived valve progenitor cells: from developmental biology to ...
The J wave is prominent when there is a larger outward current in the epicardium compared to the endocardium. It has been ... Due to the complexity of the heart, specifically how it contains three layers of cells (endocardium, myocardium and epicardium ...
They are myelinated vagal fibres in the endocardium found at the junction between atria and the vena cava/pulmonary vein. When ...
The second stage is a thrombotic stage wherein the endocardium (i.e. interior wall) of the diseased heart forms blood clots ... In eosinophilic myocarditis, echocardiography typically gives non-specific and only occasional findings of endocardium ... eosinophilic myocarditis may also show enhanced gadolinium uptake in the sub-endocardium. However, the only definitive test for ... eosinophilic myocarditis due to other underlying causes may show little or no eosinophil infiltrations into the endocardium, ...
The endocardium, the endothelial lining of the heart, plays complex and critical roles in heart development, particularly in ... We discuss the lineage relationships between the endocardium and other endothelial populations and between the endocardium and ... Development of the endocardium Ian S Harris et al. Pediatr Cardiol. 2010 Apr. ... Endocardium in Hypoplastic Left Heart Syndrome: Implications from In Vitro Study. Yu Z, Liu Z, Ravichandran V, Lami B, Gu M. Yu ...
... the myocardium and the endocardium. Learn all about them at Kenhub! ... Endocardium. The endocardium is the innermost layer of the heart. It lines the inner surfaces of the heart chambers, including ... Endocardium. Lines inner surface of heart chambers and valves. Comprised of a layer of endothelial cells, and a layer of ... The endocardium has two layers. The inner layer lines the heart chambers and is made of endothelial cells. Superiorly, is the ...
Information about English words derived from Latin and Greek sources and English vocabulary words with etymologies plus explanations. and quizzes
... Written by Bel Marra Health ... Endocarditis, in particular, is a condition of the heart where an infection occurs within the hearts lining, the endocardium. ... Home » Heart Health » Endocarditis, inflammation of endocardium can damage your heart valves ...
... or endocardium. GFP(+) endothelial foci were identified within the endocardium in the infarct zone. These previously ... Arterial endothelial foci within the endocardium reveal extensive endothelial cell plasticity in the infarct zone and identify ... Endothelial plasticity drives arterial remodeling within the endocardium after myocardial infarction.. Miquerol, Lucile; ... to the surrounding endocardium (Cx40(-), VEGFR2(-), and endoglin(+)). Endocardial flowers are contiguous with coronary vessels ...
Electrophysiology of the endocardium. ENDOCARDIUM /*physiol. *ELECTROPHYSIOLOGICAL PHENOMENA /physiopathology Used for function ... Electrophysiologic abnormalities of the endocardium in endocarditis. ENDOCARDIUM /*physiopathol. ENDOCARDITIS /*physiopathol. * ...
Endocardium minimally contributes to coronary endothelium in the embryonic ventricular free walls. Circ. Res. 118, 1880-1893 ( ...
Solving the inverse problem of Electrocardiography on the Endocardium Using a single layer source. ... Home , Publications , Solving the inverse problem of Electrocardiography on the Endocardium Using a single layer source. ...
Endocardium. 1088563. Canada. Quebec. 2008 May. 28. +. +. -. -. +. +. +. +. +. +. +. +. -. -. +. +. Pig. Brain. 1089976. Canada ...
Local changes in topgraphy of the left ventricular endocardium measured by its surface fractal dimension can be used as ... The topography of the endocardium is characterized by its regional values of fractal dimension (FD), computed using a box- ... Regional dynamics of fractal dimension of the left ventricular endocardium from cine computed tomography images. ... to quantify regional left ventricular function using topography variation of the endocardium as a surrogate measure of strain. ...
Homeopathic Digitalis Purpurea - CHEST indications, uses & symptoms by Reversed & reworded Kent repertory
heart; endocardium. pain and great anxiety. rheumatic. heart; pericardium. Movements in and of chest ...
How the Heart Works - Endocardium Pericar .... 02:28 , 7657 views Watch VIDEO. 25928 views ...
... the mural endocardium, or a septal defect. Its intracardiac effects include severe valvular insufficiency, which may lead to ... After 1 week, the connective tissue proliferates, partially embedding the leads in the wall of the vein and endocardium. This ... Nonbacterial thrombotic endocarditis also may form on the endocardium of the right ventricle, opposite the orifice that has ... the mural endocardium, or a septal defect. The history of IE can be divided into several eras. In 1674, Lazaire Riviere first ...
McKenna WJ, Elliott P. Diseases of the myocardium and endocardium. In: Goldman L, Schafer AI, eds. Goldman-Cecil Medicine. 26th ...
The Dental Board Exam Prep, Part I is very important for anyone seeking to obtain licensure in dentistry. Its an exam which has been designed to evaluate q...
Endocardium /. valves. Endocarditis. *infective endocarditis *Subacute bacterial endocarditis. *non-infective endocarditis * ...
Categories: Endocardium Image Types: Photo, Illustrations, Video, Color, Black&White, PublicDomain, CopyrightRestricted 2 ...
... in the OFT endocardium at 51 hpf (N-P), indicating the contribution of cells from external sources to the OFT endocardium ... Cardiac function promotes addition of endothelial cells from the aortic arches to the OFT endocardium. (A-U) Three-dimensional ... D,E,I,J,N,O,S,T,X,Y) Middle cross-sections through the OFTs shown in A′, F′, K′, P′ indicate that the OFT endocardium collapses ... Photoconversion of the OFT endocardium (K-M) at 36 hpf was followed by detection of green cells, which had not been labeled by ...
The Endocardium and Heart Valves. Bailey Dye and Joy Lincoln. MODEL ORGANISMS. Xenopus: Experimental Access to Cardiovascular ...
Development of the endocardium.. Harris IS; Black BL. Pediatr Cardiol; 2010 Apr; 31(3):391-9. PubMed ID: 20135106. [TBL] ... 1. The heart endocardium is derived from vascular endothelial progenitors.. Milgrom-Hoffman M; Harrelson Z; Ferrara N; Zelzer E ... Haemogenic endocardium contributes to transient definitive haematopoiesis.. Nakano H; Liu X; Arshi A; Nakashima Y; van Handel B ... 7. Development of the Heart Endocardium at an Early Stage of Chick Embryos Evaluated at Light- and Electron-Microscopic Levels. ...
Abnormal endocardium morphology Abnormal myocardium morphology Abnormality of femur morphology Achalasia Angina pectoris ...
Endocarditis is inflammation of the endocardium - the inner lining of the heart chambers and valves. Endocarditis is a rare but ... clumps of bacteria or fungi from another part of your body get into your bloodstream and collect on the endocardium. These ...
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The endocardium remained rudimentary in the primitive ventricle, whose lumen failed to close in the atrioventricular area. At ... The E9.0 End+/- embryo shows staining associated with the endocardium in the ventricular compartment (v) and tightly delineated ... Normal End+/- embryos showed signs of a progressively developing endocardium, such as increasing trabeculation and closure of ... Endoglin is present on the endocardium throughout human heart development and is also transiently upregulated on cushion tissue ...
  • Heart inflammation is inflammation in one or more of the layers of tissue in the heart, including the pericardium, myocardium, or endocardium. (
  • As shown in Figure 14.3.2, the wall of the heart is made up of three layers, called the endocardium, myocardium, and pericardium. (
  • A thin layer of connective tissue joins the endocardium to the myocardium. (
  • Poisoning also results in hepatic and renal damage along with congestion of the lungs, petechial hemorrhages of pleura, epicardium, and endocardium. (
  • In addition, indwelling intravascular catheters may directly traumatize the endocardium or valvular endothelium. (
  • 14. Nkx2.5 marks angioblasts that contribute to hemogenic endothelium of the endocardium and dorsal aorta. (
  • Endothelium of the interior surfaces of the heart chambers are called endocardium . (
  • Endocarditis is inflammation of the inside lining of the heart chambers and heart valves (endocardium). (
  • Infective Endocarditis Infective endocarditis is infection of the endocardium, usually with bacteria (commonly, streptococci or staphylococci) or fungi. (
  • Endocardium is the thin inner lining of the heart chambers and also forms the surface of the valves. (
  • Heart development is arrested at day 9.0, and the atrioventricular canal endocardium fails to undergo mesenchymal transformation and cushion-tissue formation. (
  • We are interested in the endocardium, the internal endothelial lining of the heart, as it is a source of instructive signals that regulate patterning, growth and differentiation of adjacent cardiac tissues to give rise to the mature ventricles, valves and coronary vessels. (
  • The endocardium is the inner layer that lines the heart chambers and covers the heart valves. (
  • We study how different pathways regulate the cellular and molecular mechanisms involved in the formation of trabeculae, which are myocardial protrusions covered by endocardium, necessary for embryonic nourishment. (
  • During mouse cardiac development NOTCH activity is restricted to the endocardium (see: Know more). (
  • Although the endocardium is thickened, the ventricular wall (myocardium) thickness is within the reference range. (
  • The underlying pathophysiology of endocardial fibroelastosis (EFE) is believed to be deposition of acellular fibrocartilagenous tissue in the subendothelial layer of the endocardium predominantly involving the inflow tracts, apices of either left or both ventricles. (
  • Dilated endocardial fibroelastosis is characterized by a markedly enlarged globular heart, mainly involving the left ventricle (LV) and left atrium (LA). The LV endocardium is opaque, glistening, milky white, and diffusely thickened to about 1-2 mm. (
  • 17. Malignant solitary fibrous tumors of the left atrial endocardium. (