**9.1. Background and pathologic changes**

The most common type of postinflammatory valve disease occurs as a sequela of rheumatic fever, leading to RHD. As discussed earlier in this chapter, the incidence has dramatically reduced in high-income countries, except in certain indigenous populations and remains a major global health burden across middle and low-income countries. In Australia, the estimated rate of ARF in young indigenous Australians aged 5–14 years is 150–380 per 100,000 person-years [68].

Rheumatic AV changes include thickening of the cusps, extending to the free margins and associated with commissural fusion. Calcification may eventually develop and occurs predominantly at the commissures and cusp margins. Concomitant changes at the MV are usual and involve thickening and retraction of the leaflets and chords along with commissural fusion. With 'pure' aortic regurgitation, there is cusp fibrosis with leaflet retraction. Fusion of the cusps may mimic a congenital BAV and a 'fish mouth' appearance of the MV on echo. Systemic lupus erythematosus and other inflammatory and autoimmune conditions can mimic rheumatic changes [16]. Rheumatic heart disease may involve all cardiac valves, but the mitral is most commonly affected. Stenosis is more commonly present at the mitral valve and regurgitation involving the aortic [49].

with human immunodeficiency virus (HIV). The majority of cases (right-sided > left-sided) are thought to involve structurally normal cardiac valves [8, 72]. Staphylococcus is the usual microorganism however infections are not infrequently polymicrobial [57]. Various fungi and pseudomonas are noteworthy for severe cases of IVDU-associated IE [8]. Interestingly, streptococci and enterococci more commonly affect left-sided valves, often with underlying struc-

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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According to Mathew et al. [75], the overall incidence of left-sided cardiac involvement was similar to right-sided IE, with a minority involving both right and left-sided valves [75]. Others have reported a predominance of right-sided lesions in patients with IVDU [72, 76]. The overall

The increased risk of IVDU patients acquiring IE is likely attributable to a multitude of factors. Proposed explanations include: (i) particulate matter injury to endothelium from substance injection, (ii) drug-induced thrombus formation and vasospasm, (iii) immune complex deposition on valves, (iv) altered host immune function, (v) frequent exposure to high volume bacterial inoculation, (v) increased prevalence of staphylococcal skin carriage, and (vi) sympathomimetic -induced PHTN resulting in an increase in valvular regurgitation velocity and endothelial trauma. A preference for right-sided involvement of structurally normal valves may also be related to altered host and microorganism factors [71, 74, 78]. It is theorised particulate matter up to 8–10 μm in size can transit across the normal pulmonary vasculature and potentially traumatise left-sided valvular endothelium [75]. However, the relatively high prevalence of left-sided valve involvement in the IVDU cohort without apparent underlying valve disease, may not be completely explained by the above theories and warrants further research. Transthoracic echocardiography is often very useful in IVDU patients for excluding predisposing underlying structural heart disease and providing confirmation of IE, especially for TV endocarditis. Patients with IVDU are often younger and with satisfactory acoustic windows. In addition, the TV is located anteriorly within chest, being in close proximity to the imaging transducer. The use of TOE is preferred for complicated cases of right and left-sided IE, such as periannular extension, prosthetic valves, nondiagnostic TTE, CHD and for excluding infection at other sites within the right heart, such as the Eustachian valve, atrial wall or vena cavae.

incidence of IE in IVDU is estimated at 0.7–20 cases per 1000 patient-years [74, 77].

**11. Prosthetic cardiac valves, devices and risk of endocarditis**

The estimated risk of prosthetic valve endocarditis (PVE) overall is 0.3–1.2% per patient year (3–12 per 1000 patient-years) [57]. Recent study data from the National Health Service in England [70] reported an incidence of 4.64 cases per 1000 patient-years. In a landmark early study from the 1980s, the risk for mechanical valve IE was shown to be higher in first 3 months post-surgery, whilst for porcine valves, the IE risk was higher >12 months. The cumulative risk by 5 years was not significantly different between mechanical and

tural abnormalities [73, 74].

**11.1. Surgical valves**

porcine [79].

#### **9.2. Echocardiographic diagnosis of rheumatic heart disease**

The revised Jones Criteria [69] for diagnosis of ARF, importantly has now incorporated Doppler echo for both acute and chronic valvulitis. In the previous guideline (1992), cardiac involvement was based on clinical auscultation. Modern-era echo has been validated for diagnosis of subclinical carditis. Echo may either help confirm or exclude carditis when a murmur is present, or it may detect subclinical carditis. The most common cardiac changes are cardiac valve involvement (valvulitis) and may be accompanied by a pancarditis with or without a myopericarditis [69].

#### *9.2.1. Echocardiographic diagnosis: Doppler haemodynamics and 2D features*

With acute rheumatic mitral and aortic valvulopathy, functional and haemodynamic changes are readily diagnosed by Doppler echocardiography. The regurgitation must be demonstrated in at least 2 views with a peak jet velocity of >3 m/s, a pan systolic or diastolic jet respectively and a jet length of ≥2 cm for MR and ≥1 cm for AR. Morphological changes may or may not be present early during infection [69]. The morphological change(s) seen at the MV during acute valvulitis/carditis include: (i) annular dilatation, (ii) chordal elongation/rupture, (iii) leaflet prolapse and/or (iv) beading/nodular thickening of the leaflet tips. Chronic changes of the mitral valve apparatus include: (i) thickening of the leaflets/chords, (ii) chordal fusion, (iii) restriction of leaflet motion and/or (iv) calcification [69]. Acute and chronic aortic valve changes of rheumatic valvulitis/carditis demonstrated with 2-D echo include: (i) irregular and/or focal thickening of the leaflets, (ii) leaflet retraction/restriction with or without coaptation defects and/or (iii) leaflet prolapse [69].

#### *9.2.2. Risk of endocarditis*

Incidence of IE in persons with RHD is 3.8–440 per 1000 patient-years [61]. Data published from the National Health Service in England [70], revealed a marginally lower incidence of 3.05 cases per 1000 patient-years, compared with nonrheumatic valve disease at 2.73 per 1000 patient-years in the same study. The incidence of IE in rheumatic mitral stenosis is estimated at 0.17 per 1000 patient-years. Severity of valvular haemodynamics in RHD and risk of IE is not well described.
