Two main mechanisms may contribute to the occurrence of infection.

• mechanical damage to connective tissue in the presence of electrodes and catheters in the heart; entry into the body of highly virulent strains that have strong adhesive properties.
• Diffuse connective tissue diseases.
• Connective tissue diseases are accompanied by an inflammatory process and the response of the body's immune system.
• As a result, immune complexes enter the endocardium and the typical stages of fighting inflammation develop - the production of tissue factor, the deposition of fibrin and platelets.

Changes in the structure of the endocardium and the appearance of tissue heterogeneity facilitate the adhesion of bacterial pathogens when they enter the systemic circulation by any means. Mechanical damage to cardiac tissue leads to a corresponding reaction of the immune system and transport of extracellular matrix proteins to the area of damage. Tissue healing is accompanied by heterogeneity of connective tissue and an increased likelihood of infection.

The presence of a strong allergic reaction contributes to the release of tetracycline of biologically active substances into the systemic bloodstream. Inflammatory mediators damage the vascular endothelium, as well as heart tissue. Over time, a hemodynamic disorder occurs and an inflammatory process develops on the endocardium. Non-infectious endocarditis reduces the protective properties of the inner layer of the heart and creates favorable conditions for bacterial colonization. The body's response to inflammation results in the formation of fibrin-platelet patches, which are more susceptible to pathogens than the original endocardial tissue. Eosinophilic endocarditis is often isolated as a separate form of the disease, but it has not yet been fully studied.

Intoxication endocarditis develops as a secondary non-infectious lesion. In the absence of proper treatment, it leads to changes in the structure of the endocardium and the susceptibility of tissues to the adhesion of pathogens. Intoxication endocarditis is not an independent disease, but is a consequence of other pathologies.

Infection entering the endocardial cavity contributes to the appearance of primary infective endocarditis. In this case, as a rule, a person has provoking factors that increase the ability of pathogens to attach to connective tissue. In the clinical picture, typical symptoms of sepsis are observed, leukocytosis occurs in the blood and ESR increases. The causative agents of infective endocarditis are exogenous bacteria and toxins that have entered the systemic circulation and reached the main organ.

Violation of the structure of the heart leads to disruption of tetracycline online, and the development of pathogenic microflora contributes to the spread of bacteria through the bloodstream throughout the body. Due to this, complications of infective endocarditis can manifest themselves in almost all organ systems. Main complications of the disease.

Heart failure. It occurs due to the destruction of the heart valves, which leads to their inability to function properly. The inflammatory-infectious process eventually spreads to deeper layers of tissue (myocardium), and also causes destruction of the aortic valve cusp. Neurological complications. The cause is embolism of cerebral vessels, which leads to disruption of tissue trophism and insufficient oxygen supply to them. In the future, patients may experience ischemic or hemorrhagic stroke, meningitis, and toxic damage to the meninges.