**Peter Magnusson (editor) and Robin Razmi (co-editor) Peter Magnusson, MD**

Centre for Research and Development, Uppsala University, Sweden, Cardiology Research Unit, Department of Medicine, Karolinska Institutet, Stockholm, Sweden

### **Robin Razmi**

**C**entre for Research and Development, Uppsala University, Sweden

**1**

**Chapter 1**

**1. Introduction**

Introductory Chapter: Infective

Endocarditis - An Introduction

Infective endocarditis (IE) is a rare but potentially fatal condition. Almost always it is caused by bacteria, even though fungal endocarditis may occur. The infectious agent enters the bloodstream where it may adhere to the endocardium and predominantly the cardiac valves. While infective endocarditis (IE) may occur in any person, some risk factors are well known. Among these, the most significant are patients with valvular anomalies, prosthetic valves, cardiac implantable electric devices (CIEDs), and intravenous drug users. The clinical presentation may vary greatly depending on factors pertaining to the host as well as the causative microbe. Initial symptoms may be low-grade and unspecific but occasionally fulminant and severe. The diagnosis is often challenging and based on a combination of several clinical, microbiological, and radiological findings. The cornerstone of treatment is high-dose antibiotics, which are generally administered intravenously. However, pharmaceutical treatment alone is sometimes insufficient, and surgical intervention is required. This is particularly true in complicated cases, as well as in prosthetic valve endocarditis and CIED infection.

Bacteremia is a prerequisite for the development of infective endocarditis [1], and it is a more common phenomenon than might be assumed. In fact, transient bacteremia often occurs in various dental and surgical procedures, as well as in toothbrushing, flossing, and even chewing [2]. Despite the ubiquity of transient bacteremia, infective endocarditis is a rare condition with annual incidence in the USA varying between 11 and 15 cases per 100,000 population in the first 12 years of the new millennium [3]. It can thus be surmised that bacteremia alone is insufficient to cause the condition. Data from animal models suggest that the development of IE is dependent on the existence of a valvular lesion, which may be symptomatic, previously unknown or even microscopic, and clinically insignificant. The lesion in turn allows bacteria to adhere to the endocardial surface, promoting the establish-

ment of the principal lesion in infective endocarditis: the vegetation [4].

The degree of valvular damage that is sufficient to cause disease varies greatly depending on the causative agent. *Staphylococcus aureus* has an exceptional status in this regard, owing to its recognized tendency to cause IE in patients without a preexisting valvular condition. Infectious material in the bloodstream causes an upregulation of the body's inflammatory response. Fractions of the vegetation may come loose and cause embolization of other organs. Additionally, the presence of a vegetation on the endocardial surface may contribute irreversible structural damage [3]. The topic of antibiotic prophylaxis to prevent IE is a subject of controversy. As described above, transient bacteremia is very common in the general population,

*Robin Razmi and Peter Magnusson*

**2. Epidemiology, pathophysiology, and prophylaxis**
