Materiały źródłowe

• #1 Pathogenesis, Diagnosis, Antimicrobial Therapy, and Management of Infective Endocarditis, and Its Complications

  https://pmc.ncbi.nlm.nih.gov/articles/PMC9572932/

  Infective endocarditis is a potentially deadly disease affecting the host and pathogen changes. The pathophysiology comprises three critical elements: preparation of the cardiac valve for bacterial adherence, adhesion of circulating bacteria to the prepared valvular surface, and survival of the adherent bacteria on the surface with the propagation of the infected vegetation. […] Pathogenic bacteria find ways to enter and exit the bloodstream and the surrounding tissues through the endothelium. It is an interface between circulating blood or lymph in the lumen and the rest of the vessel wall. Platelets, fibrin deposition, and surface disruption may lead to valve trauma and produce endothelial cell alternation. The surface is susceptible to colonization by the circulating bacteria, which render and do not cause any harm. Fibrin platelet matrix is more common than others; some bacterial strains appear to adhere most quickly to the surface lining. The complex, which attaches to the lining, is most commonly polysaccharide (dextran), which affects the virulence factor of the bacteria. The surface vegetation’s complex, and the adherent bacteria survive on the endothelial surface. The clotting cascade is initiated by vegetative propagation. Bacteria and fungi infections usually do not affect the standard endothelial lining of the heart and its valves. Vegetation on the endocardium and a sequence of interrelated consequences occur before microbes are tested. The infecting organism of the vegetative formation depends on pathogenesis.

• #2 Infectious Endocarditis – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK557641/

  Infectious endocarditis refers to the colonization of cardiac valve endocardium by virulent microorganisms. […] Infectious endocarditis is the inflammation of the endocardium, the inner lining of the heart, as well as the valves that separate each of the four chambers within the heart. […] The intact, healthy endocardium is typically resistant to bacterial seeding. Overall, the development of infectious endocarditis requires prodromal endocardial injury followed by a period of bacteremia. The preliminary endocardial disruption may emerge secondary to turbulent flow around diseased valves or from the direct mechanical trauma caused by catheter or electrode insertion. […] As evidenced by the predilection for vegetations to form on the ventricular surface of the aortic valve and the atrial surface of the mitral valve, hemodynamics plays an important role in the pathogenesis.

• #3 Pathogenesis of vegetation formation in infective endocarditis – UpToDate

  https://www.uptodate.com/contents/pathogenesis-of-vegetation-formation-in-infective-endocarditis

  Pathogenesis of vegetation formation in infective endocarditis […] Infective endocarditis (IE) arises when an adherent platelet-fibrin nidus becomes secondarily infected and produces vegetations, which in turn may directly damage the endocardial tissue and/or valves. The pathogenesis of infective endocarditis will be reviewed here. […] Vegetation formation — The endothelial lining of the heart and its valves is normally resistant to infection with bacteria and fungi. Experiments in animal models have demonstrated that a sequence of interrelated events must occur before microbes can establish an infective nidus or vegetation on the endocardium. […] It is likely that the pathogenesis of vegetation formation varies depending on the infecting organism. In most instances, the initial step in the establishment of a vegetation is endocardial injury, followed by focal adherence of platelets and fibrin. The initially sterile platelet-fibrin nidus becomes secondarily infected by microorganisms circulating in the blood, either from a distant infection or as a result of transient bacteremia from a mucosal or skin source. Subsequent microbial growth results in further activation of the coagulation system via the extrinsic clotting pathway, adherent monocytes release a variety of cytokines, and activated endothelial cells continue to lead to further local deposition of fibronectin. These processes culminate in a macroscopic excrescence or vegetation. Bacterial growth occurs within cells and within the matrix of fibronectin inside vegetations, making it difficult for host immune responses to control or eradicate the ongoing infection.

• #4 Pathogenesis of endocarditis

  https://www.periodicos.capes.gov.br/index.php/acervo/buscador.html?task=detalhes&id=W2080057936

  The pathophysiology of infective endocarditis comprises at least three critical elements: preparation of the cardiac valve for bacterial adherence, adhesion of circulating bacteria to the prepared valvular surface, and survival of the adherent bacteria on the surface, with propagation of the infected vegetation. […] Trauma to the valve, however, produces an alteration in the endothelial cells, leading to either disruption of the surface and deposition of platelets and fibrin, or other phenomena that render the surface susceptible to colonization by circulating bacteria. […] Once the surface is prepared, some bacterial strains appear to adhere to the fibrin-platelet matrix more avidly than others. […] The bacterial virulence factors that promote adherence are complex, but at least one, an extracellular polysaccharide (dextran), has been identified.

• #5 Infective endocarditis – Wikipedia

  https://en.wikipedia.org/wiki/Infective_endocarditis

  Damaged valves and endocardium contribute to the development of infective endocarditis. Specifically, the damaged part of a heart valve forms a local blood clot, a condition known as non-bacterial thrombotic endocarditis (NBTE). The platelet and fibrin deposits that form as part of the blood clotting process allow bacteria to take hold and form vegetations. As previously mentioned, the body has no direct methods of combating valvular vegetations because the valves do not have a dedicated blood supply. This combination of damaged valves, bacterial growth, and lack of a strong immune response results in infective endocarditis. […] Damage to the valves and endocardium can be caused by: […] Altered, turbulent blood flow. The areas that fibrose, clot, or roughen as a result of this altered flow are known as jet lesions. Altered blood flow is more likely in high pressure areas, so ventricular septal defects or patent ductus arteriosus can create more susceptibility than atrial septal defects. […] Catheters, electrodes, and other intracardiac prosthetic devices. […] Solid particles from repeated intravenous injections. […] Chronic inflammation. Examples include auto-immune mechanisms and degenerative valvular lesions.

• #6 Pathogenesis, Diagnosis, Antimicrobial Therapy, and Management of Infective Endocarditis, and Its Complications

  https://pmc.ncbi.nlm.nih.gov/articles/PMC9572932/

  Vegetation formation is a multistep process. The first step is endocardial injury. The most common mechanism is injury by turbulent blood movement from congenital intracardiac abnormality. The microorganisms circulate the blood sterile platelet and fibrin formation. The dermal and the mucosal are infections of transient bacteremia. The extrinsic clotting pathway of the coagulation system is activated further, which causes the release of various cytokines from the adherent monocytes. Further deposition of fibronectin continues as the endothelial cells start. Vegetation is the culmination of a microscopic event. The ongoing infection becomes more difficult to eradicate bacteria’s growth inside the fibronectin matrix nectin, making the host’s immune system not respond appropriately. Staphylococcus aureus (S. aureus) is a species with high virulence and can infect the standard cardiac valves of a human being. Subsequent internalization into the endothelial cells and the extracellular matrix binding protein are mechanisms that bind the S. aureus bacterium. They further induce tissue destruction by releasing exoproteins, which endothelial cells activate when the bacteria invade the host’s immune system.

• #7 Infectious Endocarditis – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK557641/

  The damaged endocardium serves as a nidus for platelet aggregation and activation of the coagulation cascade, which fosters the formation of a sterile, non-bacterial thrombotic vegetation. […] Subsequent bacteremia then allows for colonization of the vegetation. […] Even in the setting of endocardial injury and bacteremia, pathogenesis still requires a virulent organism capable of binding to and facilitating platelet-fibrin deposits. […] In theory, expanding the originally sterile platelet-fibrin deposits protects pathogens from the hosts immune response and allows the vegetation to grow.

• #8

  https://journals.lww.com/cardiologyinreview/fulltext/2016/09000/nonbacterial_thrombotic_endocarditis_.6.aspx

  Nonbacterial thrombotic endocarditis (NBTE), formerly known as marantic endocarditis, is a potentially overlooked condition that involves the formation of sterile, fibrin vegetations on heart valve leaflets. […] The pathogenesis is not entirely clear but involves a preexisting hypercoagulable state. […] Therapy for NBTE includes treating the underlying disease, systemic anticoagulation and surgical intervention.

• #9

  https://link.springer.com/article/10.2165/00002512-199404040-00005

  Elderly dental patients are at risk of developing infective endocarditis. Increased longevity is associated with an increased prevalence of cardiac valvular disease and impairment of the immune system. Aortic stenosis commonly occurs in persons between 60 and 75 years of age. Degenerative calcification of the mitral valve ring leading to valve incompetency often develops in those over age 70 years. Men over the age of 60 years with mitral valve prolapse and systolic hypertension are at risk of infective endocarditis because the excessive haemodynamic load placed upon the abnormal valve causes extensive stretching of cusps and loss of valve surface endothelium. […] Dental procedures, that result in mucosal or gingival bleeding (most notably dental extractions, periodontal probing, scaling and surgery, endodontics and restorative procedures which extend below the gingival line), frequently produce a bacteraemia. Anaerobic strains of bacteria are isolated twice as frequently as aerobic strains.

• #10 Infective Endocarditis: Practice Essentials, Background, Pathophysiology

  https://emedicine.medscape.com/article/216650-overview

  The development of subacute IE depends on a bacterial inoculum sufficient to allow invasion of the preexistent thrombus. This critical mass is the result of bacterial clumping produced by agglutinating antibodies. […] In acute IE, the thrombus may be produced by the invading organism (ie, S aureus) or by valvular trauma from intravenous catheters or pacing wires (ie, HCIE). S aureus can invade the endothelial cells (endotheliosis) and increase the expression of adhesion molecules and of procoagulant activity on the cellular surface. […] The microorganisms that most commonly produce endocarditis (ie, S aureus; Streptococcus viridans; groups A, C, and G streptococci; enterococci) resist the bactericidal action of complement and possess fibronectin receptors for the surface of the fibrin-platelet thrombus.

• #11 Pathology of Infectious Endocarditis: Overview, Etiology and Pathophysiology, Affected Sites

  https://emedicine.medscape.com/article/1954887-overview

  Endocarditis begins as endothelial damage and sterile surface microthrombus, which, in the absence of bacteremia, regresses or grows into macrothrombi (noninfectious endocarditis). […] In the presence of bacteremia or fungemia, even transient or those with low microbe counts, microthrombi become infected, by adhesion and colonization of the thrombotic surfaces. Growth of organisms results in an inflammatory response, with neutrophil infiltration, enlargement of the thrombus, recruitment of matrix metalloproteinases (MMPs), and eventual destruction of collagen and cusp perforation. […] The organisms responsible for most cases of infectious endocarditis are gram-positive cocci: streptococci and, increasingly, staphylococci. […] Some cases of culture-negative endocarditis are caused by fastidious gram-negative organisms of the Haemophilus parainfluenzae, Actinobacillus, Actinomycetemcomitans, Cardiobacterium hominis, Eikenella corrodens, Kingella kingae (HACEK) group, which constitutes approximately 1-3% of cases of community-acquired endocarditis on native and prosthetic valves, and may have a relatively good prognosis.

• #12 Infective endocarditis | Nature Reviews Disease Primers

  https://www.nature.com/articles/nrdp201659

  Infective endocarditis (IE) is a rare, life-threatening disease that has long-lasting effects even among patients who survive and are cured. […] In the setting of bacteraemia with a pathogenic organism, an infected vegetation may form as the end result of complex interactions between invading microorganisms and the host immune system. […] Once established, IE can involve almost any organ system in the body. […] This prospective cohort study of 2,781 adults with definite IE demonstrates that IE had shifted from a subacute disease of younger people with rheumatic valvular abnormalities to one in which the presentation is more acute and is characterized by a high rate of S. aureus infection in patients with previous health care exposure. […] This prospective cohort study of 1,779 patients with definite IE demonstrates that S. aureus is the leading cause of IE in many regions of the world.

• #13 Infective endocarditis: diagnosis, treatment and prevention – The Pharmaceutical Journal

  https://pharmaceutical-journal.com/article/ld/infective-endocarditis-diagnosis-treatment-and-prevention

  Infective endocarditis (IE) is defined as an infection of the endocardial surface, the cardiac valves (native or prosthetic) or an indwelling cardiac device. The pathogenesis of IE is through the sequential stages of endothelial damage, adhesion of a bloodstream-borne pathogen and proliferation of the pathogen to cause local infection. Normal endothelial lining of the heart and valves is sterile and naturally resistant to colonisation by microorganisms, but following endothelial damage or injury, platelets and fibrin may form a thrombus with inflammatory cells to which microorganisms can adhere, forming an infected vegetation (irregular growths formed of microorganisms and cells). Opportunistic infection caused by Gram-positive cocci account for up to 90% of IE cases. Oral streptococci found in the mouth and gastrointestinal (GI) tract; Staphylococcus aureus and coagulase-negative staphylococci from the skin; and Enterococci (several species) spp. from the lower GI tract are commonly implicated. Gram-negative bacilli such as the HACEK bacteria (Haemophilus spp., Aggregatibacter actinomycetemcomitans, Cardiobacterium hominis, Eikenella corrodens, Kingella kingae) account for 1–5% of IE cases; other Gram-negative pathogens — which cause a high proportion of all invasive infections — are rarely associated with IE. Fungal endocarditis, caused by yeast (Candida spp.) or by filamentous fungi (Aspergillus spp.), account for about 1% of IE cases, usually in post-surgical or immunocompromised patients in the presence of a prosthetic valve. A small but possibly unrecognised proportion of patients will present with the clinical features of endocarditis with a negative blood culture. This may be a consequence of antimicrobial administration prior to taking blood samples, the presence of fastidious microorganisms undetected by standard culturing techniques or non-infective endocarditis. Non-infective endocarditis aetiology may also be seen as a secondary complication of autoimmune or neoplastic conditions. Here, non-bacterial thrombotic endocarditis may develop, resulting in the formation of sterile vegetations.

• #13 Infective endocarditis: diagnosis, treatment and prevention – The Pharmaceutical Journal

  https://pharmaceutical-journal.com/article/ld/infective-endocarditis-diagnosis-treatment-and-prevention

  The rise in cases of IE is likely to be multifactorial, owing to patient longevity, an increasing number of implantable cardiac devices, prosthetic valves and indwelling catheters, improved diagnostic modalities and more frequent hospital-acquired infections. High-risk activities, such as intravenous drug usage, increase the risk of IE. Non-sterile injection practice can introduce opportunistic bacterial infection and impurities in the drugs can cause endocardial tissue damage.

• #14

  https://link.springer.com/article/10.1007/BF01640778

  Bacterial adherence as a result of specific surface properties may be a contributory factor in the pathogenesis of bacterial endocarditis giving certain types of bacteria a selective advantage to cause this disease. […] Adherence could interact with other pathogenetic mechanisms, and this interaction could promote or hamper the development of endocarditis. […] Dextran production by streptococci, the activation of the clotting system by monocyte tissue thromboplastin, and phagocytic removal of bacteria from the vegetational surface by granulocytes and monocytes are examples of interacting mechanisms that could contribute to the pathogenesis of bacterial endocarditis. […] Die Adhrenz von Bakterien infolge spezifischer Oberflcheneigenschaften ist mglicherweise ein pathogenetischer Faktor in der Entwicklung der bakteriellen Endokarditis.

• #15

  https://www.jci.org/articles/view/109057

  The role of dextran in the pathogenesis of bacterial endocarditis was investigated by studying the adherence of dextran producing oral streptococci to the constituents of nonbacterial thrombotic endocarditis (NBTE) in vitro and in vivo. […] This study demonstrates that dextran production is important in the adherence of oral streptococci to the constituents of NBTE and may play a role in the pathogenesis of bacterial endocarditis by oral streptococci.

• #16 Infective endocarditis | Nature Reviews Cardiology

  https://www.nature.com/articles/nrcardio.2011.43

  Infective endocarditis (IE) is lethal if not aggressively treated with antibiotics alone or in combination with surgery. […] Medical progress has altered the epidemiology of IE. […] Healthcare-associated IE has become a major issue in industrialized countries. […] Successful therapy for IE is being challenged by the development of antibiotic resistance. […] New concepts in the pathophysiology of infective endocarditis. […] Fibrinogen and fibronectin binding cooperate for valve infection and invasion in Staphylococcus aureus experimental endocarditis. […] The fibrinogen- and fibronectin-binding domains of Staphylococcus aureus fibronectin-binding protein A synergistically promote endothelial invasion and experimental endocarditis. […] Contribution of (sub)domains of Staphylococcus aureus fibronectin-binding protein to the proinflammatory and procoagulant response of human vascular endothelial cells.

• #17 Pathogenesis of vegetation formation in infective endocarditis – UpToDate

  https://www.uptodate.com/contents/pathogenesis-of-vegetation-formation-in-infective-endocarditis

  Some organisms with high virulence are capable of infecting normal human heart valves, such as Staphylococcus aureus. One proposed mechanism involves binding of S. aureus bacteria to endothelial cells through extracellular matrix binding proteins and then subsequent internalization into the endothelial cell. Once internalized, S. aureus can evade the host immune response, further activate endothelial cells, and induce tissue destruction by the release of exoproteins.

• #18 Pathogenesis of vegetation formation in infective endocarditis – UpToDate

  https://www.uptodate.com/contents/pathogenesis-of-vegetation-formation-in-infective-endocarditis/print

  Subsequent microbial growth results in further activation of the coagulation system via the extrinsic clotting pathway, adherent monocytes release a variety of cytokines, and activated endothelial cells continue to lead to further local deposition of fibronectin. These processes culminate in a macroscopic excrescence or vegetation. Bacterial growth occurs within cells and within the matrix of fibronectin inside vegetations, making it difficult for host immune responses to control or eradicate the ongoing infection. […] Some organisms with high virulence are capable of infecting normal human heart valves, such as Staphylococcus aureus. One proposed mechanism involves binding of S. aureus bacteria to endothelial cells through extracellular matrix binding proteins and then subsequent internalization into the endothelial cell. Once internalized, S. aureus can evade the host immune response, further activate endothelial cells, and induce tissue destruction by the release of exoproteins.

• #19 Infective Endocarditis: Practice Essentials, Background, Pathophysiology

  https://emedicine.medscape.com/article/216650-overview

  Once microorganisms establish themselves on the surface of the vegetation, the process of platelet aggregation and fibrin deposition accelerates at the site. As the bacteria multiply, they are covered by ever-thickening layers of platelets and thrombin, which protect them from neutrophils and other host defenses. […] The pathogenesis of pacemaker IE is similar. Shortly after implantation, a fibrin-platelet thrombus (similar to the nonbacterial thrombotic endocarditis described above) involves the generator box and conducting leads. After 1 week, the connective tissue proliferates, partially embedding the leads in the wall of the vein and endocardium. This layer may offer partial protection against infection during a bacteremia.

• #20 The Role of Platelets in Infective Endocarditis

  https://www.mdpi.com/1422-0067/24/8/7540

  Some microorganisms, particularly S. aureus, accompany their proliferation with biofilm formation leading to platelet aggregation embedded in a polysaccharide and protein network. Biofilm formation promotes virulence of the bacteria, particularly by protecting them from immune defenses and antimicrobial treatments. […] Platelets play a key role during IE by combining their well-known hemostatic role with their proinflammatory and antibacterial powers. […] It has now been clearly established that platelets are involved from the early stages of endocardial vegetation formation. Platelets possess a panoply of receptors on their surface that can interact with the bacteria involved in IE, with differences between species. […] Platelet aggregation can also be induced by other Gram-positive bacterial species, such as streptococci and enterococci.

• #21

  https://repository.rcsi.com/articles/chapter/Platelet-bacterial_interactions_in_the_pathogenesis_of_infective_endocarditis_Part_I_The_Streptococcus/10783553

  Infective endocarditis (IE) is a life threatening disease caused by a bacterial infection of the endocardial surfaces of the heart. It is typified by the formation of septic thrombi or vegetative growth on the heart valve. Typically, both platelets and fibrin are deposited on exposed extracellular matrix proteins as part of the normal response to damage of the endocardium. However, this sterile platelet-fibrin nidus facilitates colonisation of the endocardium by bacteria in the bloodstream. Following attachment, bacteria can recruit platelets from the circulation inducing platelet activation and platelet aggregation. This results in the development of large macroscopic vegetations which resist infiltration by both immune cells and antibiotics making IE a difficult disease to treat. […] These vegetations commonly occur on the heart valves and can disrupt hemodynamic patterns within the heart. This puts undue force on often already compromised valves, leading to congestive heart failure.

• #22 Clinical Pathology Glossary: Bacterial Endocarditis | ditki medical & biological sciences

  https://ditki.com/course/pathology/glossary/pathophysiologic-disorder/bacterial-endocarditis

  The bacteria Staphylococcus aureus is the leading cause of infective endocarditis; it is associated with a high mortality rate due to its aggressive nature and anti-biotic resistance. The aggressive nature of S. aureus is due to multiple virulence factors that enhance its ability to thrive; in the context of endocarditis, we’ll focus on: Adherence to endothelial cells and extracellular proteins via surface adhesion protein. Invasion of endocardial cells, where it releases toxins and promotes inflammatory processes that are highly destructive to host tissues. Evasion of host defenses via the creation of a protective biofilm and/or phenotype switching to persist as small colony variants. […] S. aureus produces a protective biofilm (sometimes called the slime layer). The biofilm comprises polysaccharides and proteins that inhibit thrombus destruction, thus allowing S. aureus to proliferate and destroy underlying tissues.

• #23 Clinical Pathology Glossary: Bacterial Endocarditis | ditki medical & biological sciences

  https://ditki.com/course/pathology/glossary/pathophysiologic-disorder/bacterial-endocarditis

  S. aureus is particularly virulent and destructive because of its ability to enter host cells. The S. aureus-fibronectin connection enables endocytosis into the endocardial cell. Within the host cells, S. aureus releases toxins and acts as a superantigen to provoke immune responses that ultimately destroy the cells. To protect itself from host defenses and/or antibiotic treatments, S. aureus employs phenotypic switching to become small colony variants; this allows it to lie dormant within the host tissues, evade host defenses, and, when conditions are favorable, reemerge as an infective pathogen.

• #24 Infective Endocarditis: Etiology, Epidemiology and Current Recommendations for the Dental Practitioner | JCDA

  https://jcda.ca/o4

  Acute forms of IE are usually caused by the highly virulent Staphylococcus aureus, with mortality higher than the subacute form and characterized by larger vegetations. The acute form has been found to start more abruptly and progress more rapidly. […] Subacute forms involve the less virulent Streptococcus viridans and are characterized by smaller vegetations on damaged or diseased heart valves. Compared with the acute form, the subacute form starts more subtly, its progression is slower over time and it most commonly affects the mitral and aortic valves.

• #25 Pathogenesis – Primary Care Notebook

  https://primarycarenotebook.com/pages/cardiovascular-medicine/infective-endocarditis/pathogenesis

  The endothelial lining of the chambers of the heart and blood vessels is resistant to bacterial infection. Endothelial damage however, for example from a „jet lesion” caused by mitral regurgitation, may produce a localised, sterile vegetation of platelets and fibrin. This may then allow circulating micro-organisms to adhere to the valve. Once attached, the bacteria may become encased in fibrin and platelets and multiply rapidly. […] In the subacute form of endocarditis, vegetations may have arisen over a number of years following repeated bacteraemia with an organism of low virulence. The clinical course of this condition is therefore more insidious. This should be contrasted with the more dramatic presentation of acute infective endocarditis, where the infecting organism is more virulent, forming larger vegetations which tend to embolise.

• #26 Pathogenesis – Primary Care Notebook

  https://primarycarenotebook.com/pages/cardiovascular-medicine/infective-endocarditis/pathogenesis

  Prosthetic valve endocarditis results from infection of a prosthetic valve. This may occur early, within 60 days of surgery, either during the operation or due to a perioperative bacteraemia e.g. urinary catheterisation. […] Right sided endocarditis accounts for 5% of cases and is most often seen in IV drug abusers or the immunosuppressed; invariably the tricuspid valve is affected and the organism is usually a staphylococcus.

• #27 Tricuspid valve endocarditis – Hussain- Annals of Cardiothoracic Surgery

  https://www.annalscts.com/article/view/14141/15202

  Right-sided infective endocarditis (RSIE) is less common than left-sided infective endocarditis (IE), encompassing only 5-10% of cases of IE. Ninety percent of RSIE involves the tricuspid valve (TV). […] Staphylococcus aureus is the predominant causative organism in TVIE. […] Most patients with TVIE are successfully treated with antibiotics, however, 5-16% of RSIE cases eventually require surgical intervention. […] Earlier surgical intervention may potentially prevent further destruction of leaflet tissue and increase the likelihood of TV repair. […] Patients with concomitant left-sided involvement have worse prognosis than those with RSIE alone, due predominantly to greater likelihood of invasion and abscess formation in left-sided IE. […] S. aureus is the predominant causative microorganism for TVIE, occurring in 60-90% of cases in some studies, irrespective of associated risk factors.

• #28 Pathogenesis, Diagnosis, Antimicrobial Therapy, and Management of Infective Endocarditis, and Its Complications

  https://pmc.ncbi.nlm.nih.gov/articles/PMC9572932/

  The critical damages are possible in infective endocarditis pathogenesis. Including bacteriemia, polycythemia, cyanosis, endothelial damage, and increased blood viscosity are leading to complications. The most noticeable increase is in artificial implants such as prosthetic valves and shunts. It is not astonishing that cyanotic CHD with an unreal shunt or prosthetic valves represents the highest risk for infected endocarditis. Neonatal endocarditis often occurs on the heart’s right side and is associated with disruption of the endocardium or valvular endothelial tissue produced by catheter-induced trauma. The bacteremia combination and the endothelial damage are the critical induction of infective endocarditis.

• #29 Infective Endocarditis

  https://www.utmb.edu/Pedi_Ed/CoreV2/cardiology/Cardiology16.html

  Infective endocarditis (IE) is an inflammation of the endothelial lining of the heart muscle, valves and great vessels. The valves have a particularly high propensity for infection due to the lack of blood supply and limited access to immune cells. […] Bacteremia and the presence of endothelial damage are important factors in the pathogenesis of IE. Cyanosis and polycythemia, if present, increase the viscosity of the blood and further enhance the likelihood of developing IE. Foreign materials such as prosthetic valves or shunts also significantly increase the risk for developing IE. It is not surprising that cyanotic CHD with an artificial shunt or prosthetic valves constitutes the highest risk for IE. […] The combination of endothelial damage and bacteremia is critical for the induction of IE.

• #30 Treatment of Infectious Endocarditis

  https://www.uspharmacist.com/article/treatment-of-infectious-endocarditis

  The pathogenesis of IE involves clot formation, as a result of blood and „subendothelial” particles, on one of the heart valves followed by binding of pathogens from bacteremia to the clot. An immunologic response is then initiated involving cytokines and white blood cells that results in the formation of a vegetation. […] Usually, patients who develop IE have underlying risk factors, such as the presence of a prosthetic heart valve, rheumatic heart disease, mitral valve prolapse, hemodialysis, diabetes, HIV, inadequate dental care, and intravenous drug abuse.

• #31 The role of cytokines in the pathogenesis of infective endocarditis

  https://www.immunologiya-journal.ru/en/jarticles_immunology/93.html?SSr=1101348ad323ffffffff27c__07e6061b170b14-591d

  Infective endocarditis (IE) is a disease of infectious nature with the primary localization of the pathogen on the heart valves and parietal endocardium. […] In this regard, the analyze of current information about the pathogenetic role of cytokines in infective endocarditis is the subject of interest in modern research. […] Do cytokines play a role in predicting some features and outcome in infective endocarditis? […] Cytokine profiles linked to fatal outcome in infective prosthetic valve endocarditis. […] Cytokine signature in infective endocarditis.

• #32 Infective Endocarditis: Inflammatory Response, Genetic Susceptibility, Oxidative Stress, and Multiple Organ Failure | IntechOpen

  https://www.intechopen.com/chapters/66253

  Infective endocarditis is defined by a focus of infection within the heart. The challenges in this clinical entity have several aspects such as the diversity of germs that cause endocarditis, and the most important epidemiologically has generated resistance to antimicrobial treatment along with the possibility of apoptosis in their host-germ interaction. Inflammation, local and systemic, is complex, with the genesis of reactive oxygen species, which are harmful when the antioxidant defenses are exceeded, causing the break in the mitochondrial electron transport chain with the fall in energy genesis, multiple organ failure, and death. […] The pathogenesis and the prognosis of IE can be simply described in a general way as the interaction between the host and the germ; however, these factors are not independent and are very importantly linked both in the susceptibility characteristics of the host (advanced age, higher prevalence of comorbid conditions, and exposure to health care) to survive or not to an infectious state, as of the characteristics of the germ involved.

• #33 Infective Endocarditis: Inflammatory Response, Genetic Susceptibility, Oxidative Stress, and Multiple Organ Failure | IntechOpen

  https://www.intechopen.com/chapters/66253

  The interaction of S. aureus-host allows us to develop in a substantive way, on one hand, the importance of the virulence of the germ and, on the other, the defense mechanisms of the host, showing how the inflammation is generated and amplified to offer a step to oxidative stress. […] One of the clinical disorders that selectively damage the endocardium and subendocardial interstitial tissue is endocarditis. This entity causes activation of the vascular and endocardial endothelial system, as well as poor adaptation or failure characterized by hemodynamic abnormalities, neurohormonal imbalance, cytokine expression, and endothelial dysfunction. […] The sequence of events that begin with an infectious state, such as IE, alerts and promotes inflammation through the immune system, both cellular and humoral to eliminate the infectious agent; however, this has the ability to evade the immune system. […] The activity of antioxidant enzymes is exceeded, so that ROS cannot be eliminated, generating a state of oxidative stress, with a profound effect on the mitochondrial level by breaking the chain of electron transport, and, consequently, the genesis of the energy is compromised.

• #34 Pulsenotes | Infective endocarditis notes

  https://app.pulsenotes.com/medicine/cardiology/notes/infective-endocarditis

  As well as local cardiac damage, embolic events can occur due to vegetations breaking off and being deposited in other organ systems. The embolisation of fragments of vegetations can lead to the formation of abscesses (e.g. cerebral abscess in left sided endocarditis or pulmonary abscesses in right-sided endocarditis). Alternatively, activation of the immune system and clustering of immune complexes within vegetations can lead to immune-mediated vasculitis within distant vessels following embolisation (e.g. glomerulonephritis).

• #35 Infective endocarditis – etiopathogenesis, morphology and complications – Histopathology.guru

  https://www.histopathology.guru/infective-endocarditis-etiopathogenesis-and-morphology/

  Bacteria from blood stream in any of the above mentioned routes are implanted on the cardiac valves or mural endocardium as they have surface adhesion molecules which mediate their adherence to endocardium. […] These conditions causes damage to endothelium on valves, favoring the formation of platelet-fibrin thrombi which get infected from circulating bacteria where they proliferate and form vegetations. […] Vegetations can embolize and as their embolic fragments contain virulent organisms, abscesses develop where they lodge, leading to sequelae such as septic infarcts or mycotic aneurysms. […] Vegetations of subacute endocarditis are associated with less valvular destruction than acute endocarditis.

• #36 Stroke Specialists and Infective Endocarditis: Why They’re Critical to the Care Team

  https://consultqd.clevelandclinic.org/stroke-specialists-and-infective-endocarditis-why-theyre-critical-to-the-care-team

  A major complication of infective endocarditis (IE) is embolic stroke caused by bits of infective material that break off from a heart valve vegetation and travel to the brain. […] Cardiac surgery can be a definitive treatment for IE, remove the source of potential embolism and reduce the risk of subsequent stroke. […] To mitigate the risk of a cerebrovascular accident resulting from IE repair, Cleveland Clinic takes care to routinely image the brain and include a stroke specialist in the preoperative evaluation of IE patients. […] If the patient has had an embolic stroke and has large vegetations on a heart valve, the question may not be whether to operate, but when. […] When a patient with IE has suffered a brain hemorrhage, heart surgery ideally should be postponed for four weeks or at least two weeks if they’ve had a large stroke to minimize the risk of further bleeding or hemorrhagic transformation. […] Mycotic aneurysms may be coiled before the cardiac IE surgery is performed. We have seen a decrease in the incidence of stroke with this approach over the last several years, says Dr. Unai. It’s rare to have a large or significantly debilitating stroke after IE surgery.

• #37 Unusual mechanism of myocardial infarction in prosthetic valve endocar | IMCRJ

  https://www.dovepress.com/unusual-mechanism-of-myocardial-infarction-in-prosthetic-valve-endocar-peer-reviewed-fulltext-article-IMCRJ

  A 46-year-old man with bicuspid aortic valve and severe calcific aortic stenosis was submitted to aortic valve replacement with a stented bioprosthesis. He developed Staphylococcus epidermidis prosthetic valve endocarditis a month later, presenting in the emergency room with acute myocardial infarction. The mechanism of myocardial ischemia was a large aortic root abscess causing left main extrinsic compression. […] Acute coronary syndromes are uncommon in prosthetic valve endocarditis, with a prevalence of between 1% and 3%. The most likely mechanisms responsible for myocardial ischemia are the presence of preexisting coronary artery disease and coronary emboli from aortic vegetations. Other less frequent mechanisms have been described, such as obstruction of the coronary ostium due to large vegetation and severe aortic insufficiency. External coronary artery compression due to infective endocarditis is also a described mechanism, but is a rare occurrence with only few cases reported in medical literature.

• #38 Unusual mechanism of myocardial infarction in prosthetic valve endocar | IMCRJ

  https://www.dovepress.com/unusual-mechanism-of-myocardial-infarction-in-prosthetic-valve-endocar-peer-reviewed-fulltext-article-IMCRJ

  The present case describes a rare complication of prosthetic valve endocarditis, an aortic root abscess causing external coronary artery compression and acute myocardial infarction. This mechanism of myocardial infarction has already been described. The most likely mechanisms responsible for myocardial infarction during infective endocarditis are preexisting coronary artery disease and coronary artery emboli from vegetations. […] Although uncommon, external compression of coronary artery should be considered in the differential diagnosis of these patients, and adequate diagnostic work-up and treatment should be indicated. Treatment with anti-platelet agents increased the risk of cerebral bleeding and certainly complicated the operative treatment in this patient. […] Operative findings confirmed the severity of infection. The root abscess perforated the membranous septum, causing aortic to right atrium fistula, and there was a huge invasion of the left coronary cuspid around the left main coronary artery, which caused its extrinsic compression and myocardial ischemia.

• #39 Infective endocarditis – Knowledge @ AMBOSS

  https://www.amboss.com/us/knowledge/infective-endocarditis/

  Pathogenesis [3] Damaged valvular endothelium exposure of the subendothelial layer adherence of platelets and fibrin sterile vegetation (microthrombus) […] Localized infection or contamination bacteremia bacterial colonization of vegetation formation of fibrin clots encasing the vegetation valve destruction with loss of function (valve regurgitation) [13]

• #40 Infective endocarditis | Calgary Guide

  https://calgaryguide.ucalgary.ca/infective-endocarditis/infective-endocarditis-2024/

  Infective Endocarditis: Pathogenesis, complications, and clinical findings […] A sterile thrombus forms […] Thrombus forms on the surface of a cardiac valve […] Bacteria adhere to thrombi on the cardiac valve endothelium […] Infection of the thrombus typically produces a vegetation on the flow surface of a valve […] Immune complexes (complexes of antibody bound to antigen) form secondary to infection […] Parts of vegetation embolize systemically, obstructing arteries […] Infection destroys infected valve […] Vegetation seen on ultrasound/echocardiogram […] Regurgitation (blood leaks back through the insufficient valve despite it being closed) […] Valve unable to fulfill normal functions (valve insufficiency)

• #41 Infective endocarditis and oral health—a Narrative Review – Bumm – Cardiovascular Diagnosis and Therapy

  https://cdt.amegroups.org/article/view/63403/html

  As the described odontogenic infections are associated with pathogenic microorganisms, gingival or mucosal trauma or the manipulation of the periapical region of the tooth may cause a transient bacteremia of these microorganisms that, in a patient at risk, can cause infective endocarditis. […] Since, it is commonly accepted that the presence and the magnitude of bacteremia caused by odontogenic infections are directly proportional to the severity of oral inflammation, good oral and dental health has to be highlighted as a major factor regarding prevention of infective endocarditis. […] Eventually, it has to be emphasized that besides antibiotic prophylaxis prior to certain dental procedures the maintenance of good oral health in patients at risk seems to play an even more important role in preventing IE, since persisting odontogenic infections may remain undetected causing bacteremia with high frequency and intensity during every-day activities.

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