Heart Conduction System
Electrophysiologic Techniques, Cardiac
Endocardial Cushion Defects
Cardiac Pacing, Artificial
Body Surface Potential Mapping
Gene Expression Regulation, Developmental
Ventricular Function, Left
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
* 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:
* Joint pain or swelling
* 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.
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 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.
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- Heart inflammation is inflammation in one or more of the layers of tissue in the heart, including the pericardium, myocardium, or endocardium. (nih.gov)
- As shown in Figure 14.3.2, the wall of the heart is made up of three layers, called the endocardium, myocardium, and pericardium. (tru.ca)
- A thin layer of connective tissue joins the endocardium to the myocardium. (tru.ca)
- Poisoning also results in hepatic and renal damage along with congestion of the lungs, petechial hemorrhages of pleura, epicardium, and endocardium. (cdc.gov)
- In addition, indwelling intravascular catheters may directly traumatize the endocardium or valvular endothelium. (medscape.com)
- 14. Nkx2.5 marks angioblasts that contribute to hemogenic endothelium of the endocardium and dorsal aorta. (nih.gov)
- Endothelium of the interior surfaces of the heart chambers are called endocardium . (wikidoc.org)
- Endocardium is the thin inner lining of the heart chambers and also forms the surface of the valves. (nih.gov)
- Heart development is arrested at day 9.0, and the atrioventricular canal endocardium fails to undergo mesenchymal transformation and cushion-tissue formation. (jci.org)
- 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. (cnic.es)
- The endocardium is the inner layer that lines the heart chambers and covers the heart valves. (pacificmedicalacls.com)
- 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. (cnic.es)
- During mouse cardiac development NOTCH activity is restricted to the endocardium (see: Know more). (cnic.es)
- Although the endocardium is thickened, the ventricular wall (myocardium) thickness is within the reference range. (medscape.com)
- 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. (medscape.com)
- 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. (medscape.com)
- 17. Malignant solitary fibrous tumors of the left atrial endocardium. (nih.gov)