**1. Introduction**

Infective endocarditis (IE) is characterised by a microbial infection that involves the endocardial surface of the heart; it most often denotes infection of the heart valves or an intracardiac device [1]. Less commonly it involves septal defects, mural endocardium and the subvalvular apparatus [2]. The classic lesion is a vegetation, which is composed of platelets, fibrin enmeshed with microorganisms and inflammatory cells [3]. Infective endocarditis is caused by many different species of bacteria such as staphylococci, streptococci, enterococci and slow-growing Gramnegative coccobacilli.

In the 1950s IE secondary to intravenous drug use was first described [4]. Rightsided infective endocarditis (RSIE) secondary to intravenous drug use is a distinct entity and will be reviewed in this chapter.

### **2. Epidemiology**

Intravenous drug abuse (IVDA) is a recognised risk factor for IE. Intravenous drug users are at a seven times higher risk for infective endocarditis compared to patients with rheumatic heart disease or prosthetic valves [3].

#### *Infective Endocarditis*

 Over the last decade there has been a steady increase in number of cases related to IE due to intravenous drug use. Between 2000 and 2008 the rate of IE due to IVDA has increased from 6 to 8% hospitalisation to 12% in the year 2013. During this period there has been an increase in IVDA related IE cases amongst younger white population. A similar distribution was noted between males and females [5].

In United States, North Carolina, a study reported a 12-fold increase in hospitalisations for intravenous drug use related IE over the last decade [6].

In the past IE related to IVDA was predominantly disease of men. A recent study has shown that there is a general increase in the rate of IVDA associated IE in the United States, with a relatively higher proportion of women compared to previous studies [5, 6]. In a recent South African Study, Meel et al. reported an increase in the incidence of IE related to IVDA amongst Africans. These were predominantly male and majority were HIV infected [7].

Infective endocarditis involving the right side accounts for 5–10% of cases of IE [8, 9].

RSIE may occur in patients with intracardiac devices but in intravenous drug users it is usually associated with HIV infection [9].

 HIV infection in intravenous drug users is associated with a higher rate of IE compared to HIV uninfected users [10, 11]. Further, immunosuppression with lower CD4 count is associated with a higher predisposition to IE [9].

Intravenous drug use related IE involves the tricuspid valve in 46–78% of the cases, mitral valve in 24–32% of cases and the aortic valve in 8–19%. About 16% of the patients have multiple valve involvement. In the majority the infection occurs on the native valves. Intravenous drug use is characterised by recurrent infective endocarditis of the native valves [3].

### **3. Etiopathogenesis**

The most common organism isolated in IVDA related IE is *Staphylococcus aureus*. It accounts for greater than 50% of the organisms cultured [3]. It tends to commonly infect the native tricuspid valve. In contrast streptococci and enterococci infect damaged valves, mostly aortic and the mitral valve. Other organisms include fungi, *Pseudomonas aeruginosa* and Gram-negative bacilli. Injection of contaminated material predisposes drug addicts to less commonly encountered organisms such as *Corynebacterium* species, *Lactobacillus*, *Neisseria* species and *Bacillus cereus*. In 3–5% of cases Polymicrobial infection is present [3].

 The tricuspid valve is the most commonly involved valve in RSIE due to IVDA. Injection of recreational drugs results in entry of particulate matter such as talc into the circulatory system resulting in structural damage to the endothelium of the valve [12, 13]. Similarly, the left-sided valves get damaged by particulate matter that is less than 10 mm in size and is able to cross the pulmonary circulation [14]. The use of cocaine is associated with greater frequency of IE in IVDA. The possible mechanisms postulated include the ability of cocaine to cause vasospasm and tissue damage to the myocardium. It is also procoagulant and thus can cause thrombus formation and thus producing a nidus for bacterial seeding the damaged valve tissue [8]. Further, it has been postulated that intravenous drugs can result in pulmonary hypertension leading to increased turbulent blood flow across the valve resulting in endothelial damage to the right-sided heart valves.

The pathogenesis of formation of vegetation is complex. It involves interaction between the host, the organism, the endothelium, hemostatic pathways, the ability of the hosts immune system to eliminate the organism and the virulence of the specific microorganism [3].

*Right-Sided Infective Endocarditis Secondary to Intravenous Drug Abuse DOI: http://dx.doi.org/10.5772/intechopen.84319* 

The microorganism once in the blood stream tend to attach themselves to the valve surface and proliferate at sites of endothelial damage resulting in further damage to the valve tissue. The microorganisms initially attach to the plateletfibrin nidus and then proliferate [15]. Microbial growth results in activation of the extrinsic coagulation pathway, monocytes release a myriad of pro-inflammatory cytokines and there is increased expression of fibronectin on the surface of the endothelial cells with resultant formation of a vegetation.

The vegetation grows further, with subsequent embolization and continued bacteraemia, if the host is unable to contain the infection [16].
