**2. Predisposing cardiac disease: a changing epidemiology**

Since mid-last century, the epidemiology of IE has continued to change across high-income countries (HIC), from predominantly young patients with rheumatic heart disease (RHD) to the current era of an ageing population with IE, infrequent RHD and prevalent degenerative valve disease (DVD). A history of acute rheumatic fever (ARF) in patients with IE had declined from ~38 to 22.5% in the 30 years up to 1967 [1]. By the 1980s, this had reduced to 6% [2]. According to data from the International Collaboration on Endocarditis—Prospective Cohort Study (ICE-PICS), DVD is the most common underlying pathology in IE, with significant mitral regurgitation (MR) and aortic regurgitation (AR) accounting for 43.3 and 26.3% of cases, respectively, compared with rheumatic mitral valve, present in only 3.3% cases. Prosthetic valve endocarditis (PVE) accounts for up to 22.2% of cases [3], whilst the prevalence of cardiac device-related infective endocarditis (CDRIE) has increased along with health-care associated IE (HCAIE) [4]. Endocarditis patterns in congenital heart disease (CHD) have changed due to patients surviving into adulthood with more complex disease, the availability of improved surgical techniques and implantation of prosthetic material [5, 6].

Regurgitant valves are at higher risk of IE than stenotic valves [9]. In a large clinical-pathological study on native valve endocarditis (NVIE), 84% of valves were regurgitant [10]. Another found the majority of cases of IE presenting to surgery were for regurgitant valves compared to a control-group of non-IE cases undergoing surgery (9% of regurgitant bicuspid aortic valves (BAV), 1.2% of calcified BAVs, 1.6% of calcified trileaflet aortic valves (AV) and 7% of mitral valve prolapse (MVP)) [11]. Aortic regurgitation (AR) is a predisposing lesion in

The Role of Modern-Era Echocardiography in Identification of Cardiac Risk Factors for Infective…

http://dx.doi.org/10.5772/intechopen.75760

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The pathogenesis of IE in structural cardiac abnormalities is characterised by the hydrodynamic theory [13]. A high velocity turbulent jet exerts a shearing effect on endothelium, at the site of a restrictive orifice (e.g. ventricular septal defect (VSD) or MR jet) and/or a distal point of contact (jet lesion). The narrowest diameter of flow is the vena contracta (VC), just distal to the restricted anatomical orifice. This is where the pressure is minimal and retrograde flow may occur, permitting platelets and bacteria to deposit [13]. The typical location of vegetation is on the upstream side of the valve, that is, the atrial aspect of the MV, tricuspid valve (TV)

Structurally normal native right-sided valves in the absence of significant pulmonary hypertension, are exposed to lower pressure flows and are far less commonly involved with IE.In children, without CHD, native right-sided IE involving normal valves is rare but may occur in association with trauma to the valve from central lines or catheters [14, 15]. Other factors are important in risk of acquiring IE and include an interplay between microorganism virulence, altered host defence

Infective endocarditis does occur in some patients without pre-existing known structural abnormalities. Whether the valves were completely normal is uncertain. Early degenerative changes can be present without clinical detection [17]. Modern-era echo with high image resolution and careful scrutiny of valve morphology and function, has the potential to shed more

There is an increasing prevalence of IE involving structurally normal cardiac valves, accounting for 26–43% of native left-sided IE cases [2, 18, 19]. Sun et al. [18] reported the commonest underlying cardiac predisposition was mitral valve prolapse (MVP) followed by normal valves (26%). Olmas et al. [20] found in an IE cohort, normal left-sided native valves in 39.8% of patients aged >65 years and in 53.8% of those aged ≤65 years, whilst DVD comprised 23.4% of the cohort. However, details regarding Doppler valve function were not available. This is important, for even normal valves may be regurgitant, exposing endothelium to shearing forces. Limitations include assessing valves for pre-existing pathology when already involved by infection and absence of pathological correlation to exclude subtle underlying pathology. In vitro studies have demonstrated certain microorganisms can attach to and/or be internalised by healthy valve endothelium, however in vivo, animal studies have required trauma to the endothelium to initiate IE following an inoculum of bacteria [9]. This raises the

mechanisms, predisposing systemic illness, and environmental and social factors [16].

17–36% of cases of IE, whilst mitral regurgitation (MR) accounts for 10–18% [12].

and ventricular aspect AV, pulmonary valve (PV) [9].

**5. Structurally normal native cardiac valves**

light on this research question.

The 2015 European Society of Cardiology IE management guidelines now consider the following cardiac conditions to pose the highest risk of IE: (i) prosthetic cardiac valves and/or repairs with prosthetic material, (ii) previous IE, (iii) cyanotic CHD, and (iv) any CHD that has been repaired for up to 6 months post procedure or indefinitely if a residual defect or valve incompetence persists. Repair or intervention includes both surgical and transcatheter procedures. Antibiotic prophylaxis is recommended for these patients when exposed to procedures considered high-risk [7].
