Heart inflammation

Infektive endocarditis
Infective endocarditis (IE) is a disease caused by an infectious agent that affects the endocardium, heart valves and related structures. Inflammation can be caused by bacteria, fungi, chlamydia, rickettsiae or viruses.

Risk factors
Risk factors - children:


 * congenital heart defects;
 * rheumatic heart defects (rare);
 * iatrogenic - long-established central venous catheters;
 * intravenous drug use;
 * bicuspid aortic valve;
 * mitral valve prolapse with regurgitation;
 * stp. cardiac surgery using conduits and vascular prostheses, with artificial valves[1].

In congenital heart disease, IE occurs most commonly in:


 * Tetralogy of Fallot,
 * ventricular septal defect,
 * aortic stenosis, and
 * patent ductus arteriosus

The risk is significantly lower in pulmonic stenosis and IE is virtually absent in atrial septal defect.


 * The bicuspid aortic valve is a frequent site of IE, regardless of whether it causes stenosis or regurgitation.
 * In mitral valve prolapse, patients are at risk of IE if the valve regurgitates.

IE is rare in neonates, infants, and young toddlers except for iatrogenic IE in critically ill children with catheter infection. The risk of IE increases with increasing age in individuals with heart disease.

Etiology
In children,  the most common cause of IE are:


 * Streptococcus viridans,
 * staphylococci,
 * more rarely enterococci.
 * Coagulase-negative staphylococci (Staphylococcus epidermidis) are typical triggers of IE after cardiac surgery.


 * Gram-negative microorganisms and fungi rarely cause IE. They usually affect immunosuppressed individuals, patients with artificial valves and drug addicts. Mycotic IE is also a serious complication of long-term central venous catheters usually after repeated administration of broad-spectrum antibiotics

Pathogenesis
An important factor in the development of IE is the presence of turbulent blood flow that disrupts the endothelium. However, vegetations can also form as a result of the Venturi effect at the site of slow blood flow. A cluster of platelets and fibrin forms in the damaged endothelium, which is subsequently colonized by infectious agents. Bacteremia occurs in association with various diagnostic or therapeutic procedures. Transient bacteraemia may also occur during tooth brushing or biting of solid food. This mechanism explains the occurrence of IE in patients where a clear causative bacteraemia cannot be identified.

The main macroscopic findings are vegetations on the endocardium. They contain microbes and are covered by a layer composed of fibrin and leukocytes. Less virulent bacteria nestle in the thrombi, where fibrin protects them from phagocytosis and antibiotics.

The adjacent affected tissue is edematous, with cellular infiltration and poorly vascularized, which impairs antibiotic penetration. Fragility of vegetations causes recurrent bacteremia and embolization to the lungs or systemic circulation, depending on the site of cardiac involvement and the presence of intracardiac shunts. Embolization into the lung mimics pneumonia; an unrecognized lung abscess may perforate into the vascular system with subsequent fatal hemorrhage. In embolization into the systemic circulation, the skin, kidneys, spleen and brain are most commonly affected. In prolonged disease, the heart valves are destroyed. Virulent bacteria (Staphylococcus aureus) cause rapid destruction of the valve or invasion of the myocardium leading to abscess formation. Septic embolization into the coronary arteries is also a frequent finding. IE significantly activates the humoral and cellular immune system. For example, circulating immune complexes are responsible for the development of glomerulonephritis[1].

Classification

 * IE native valves,
 * IE of toxics (predisposes to tricuspid valve involvement with risk of pulmonary embolisation),
 * IE of valve prostheses (early/late onset - threshold 2 months after surgery).

The division of IE into acute and subacute forms is obsolete and not used anymore. The division according to the causing agent is recommended. Microorganisms with low virulence (e.g. α-haemolytic streptococcus) usually induce the "subacute" form, whereas Staphylococcus aureus and other pyogenic bacteria induce the "acute" form.

Risks of infective endocarditis
High risk;


 * Valve prostheses (lifelong),
 * stp. cardiac surgery (up to 6 months after surgery),
 * aortic defects,
 * tetralogy of Fallot,
 * mitral insufficiency,
 * PDA,
 * VSD,
 * CoA,
 * Marfan syndrome,
 * history of IE.

Intermediate risk;


 * Mitral stenosis,
 * tricuspid defects,
 * mitral prolapse,
 * hypertrophic cardiomyopathy.

Zdroj

 * HAVRÁNEK, Jiří: Srdeční záněty. (upraveno)

Související články

 * Infekční endokarditida
 * Myokarditida
 * Perikarditida