Editorial [Hot topic: Infective Endocarditis (Guest Editor: Ioannis Starakis)]

Infective endocarditis (IE) is a microbial infection of the endocardium. In subacute IE, the previously-damaged damaged surface of cardiac valve becomes the starting point for the deposition of platelets and the formation of a platelet-fibrin clot. IE develops after bacteria enter the bloodstream and colonize the clot. Platelets and fibrin mount up over the bacteria, increasing the size of the vegetation. As additional layers of fibrin are added, leukocytes are incapable to break through the vegetation. Treatment with antibiotics can also be problematic because the bacteria within the vegetation often become less metabolically active, and many antibiotics require active bacterial growth to be effective. The overall incidence of infective endocarditis is 1.7 to 4.0 per 100,000 population and in adults older than 50 years, it exceeds 15 per 100,000 population. However, the precise incidence of IE is difficult to determine because case definitions have diverged from decade to decade, among different authors, and among different medical facilities. Moreover, the incidence of predisposing conditions (eg, rheumatic heart disease and injection drug use) has wandered over time and among different areas. Sex and age have an impact on the incidence of IE. Men prevail in most series, with male-to-female ratios ranging from 3:2 to 9:1. Almost 50-60% of cases of acute IE do not necessitate an underlying heart condition to be present. The microorganisms most accountable for the development of acute IE (e.g. S. aureus) are exceedingly virulent and able to colonize normal heart valves. The incidence of acute IE has been progressively rising and now surpasses the number of subacute IE cases. The patients who are more susceptible to IE comprise of those with congenital heart defects, rheumatic heart disease, the elderly, immunocompromised and AIDS patients, intravenous drug abusers (IVDA) and patients with a malignancy. Mitral valve prolapse is the most common (30%) predisposing condition found in young adults, and bicuspid aortic valve is the most common underlying congenital condition (15%). Rheumatic heart disease currently accounts for less than 20% of cases, but 6% of these patients develop IE in their lifetimes. In 75% of cases of IVDA IE, no underlying valvular abnormalities are noted, and 50% of them involve the tricuspid valve. Prosthetic valve endocarditis (PVE) accounts for 10-20% of all cases of IE, and in the long run, 5% of mechanical and bioprosthetic valves become infected. Mechanical valves are more likely to be infected within the first 3 months of implantation, and bioprosthetic valves are more likely to be infected after the first year. The mitral valves are more vulnerable than those in the aortic area. Analogous to PVE are infections of implantable pacemakers (PMs) and cardioverter -defibrillators. Usually, these devices are infected within a few months of implantation. The principle causative agents include Streptococcus viridans (55%), Staphylococcus aureus (30%), Enterococcus (6%) and HACEK bacteria, although on occasions it can also be caused by fungi. Antibiotics are usually administered intravenously for 2-6 weeks and duration usually depends on the pathogen%s virulence. 15-25% of patients with IE are treated surgically. Removal of an infected valve is necessary when antibiotic therapy fails, there are persistent vegetations after systemic embolization or vegetations increase their size after antimicrobial treatment, in valvular dysfunction and in fungal endocarditis.