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CHAPTER
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A A A A Acquired Valvular Heart Disease
Denise Ledoux
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de devellopedd countries in whichh soocioeconomic conditions ennable the
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DEFINITION, CLASSIFICATION, sp spread off streptococcal bacteria and limit acceess to adequate he l hth
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AND EPIDEMIOLOGY ca care. Acutee rheumatic fever involves diffuse exudative and prolifer-
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ative inflammatory reactions in the heart, joints,, andd skin.
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Valv lular heart diisease continues to bbe a common source off ca diac J Jones criiteria, based on expert opinion rather than clinical
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dysfunction and mortality. Competent cardiac valves maintain a trials, were introduced in 1944 for the diagnosis of rheumatic
unidirectional flow of blood through the heart as well as to the fever. Major diagnostic criteria include carditis, polyarthritis,
pulmonary and systemic circulations. Diseased cardiac valves that chorea, erythema marginatum (pink skin rash), and subcutaneous
restrict the forward flow of blood because they are unable to open nodules. Minor criteria include arthralgia, fever, and elevated
fully are referred to as stenotic. Stenotic valves elevate afterload and C-reactive protein. 1
cause hypertrophy of the atria or ventricles pumping against the Carditis is the most important clinical manifestation of acute
increased pressure. Cardiac valves that close incompetently and rheumatic fever, causing inflammation of the endocardium, my-
permit the backward flow of blood are referred to as regurgitant, ocardium, and pericardium. Myocarditis is characterized by in-
incompetent, or insufficient. Regurgitant valves cause an elevated terstitial inflammation that may affect cardiac conduction. En-
volume load and dilation of the cardiac chambers receiving the docarditis causes extensive inflammatory changes, resulting in
blood reflux. Valvular dysfunction may be primarily stenotic or re- scarring of the heart valves and acute heart failure. Warty lesions
gurgitant, or may be “mixed,” which refers to a valve that neither of eosinophilic material build-up at the bases and edges of the
opens nor closes adequately. Valvular heart disease is usually de- valves. As the lesions progress, granulation tissue and subsequent
scribed by the duration of the dysfunction (acute vs. chronic), the vascularization develop, and fibrosis occurs. The annulus, cusps,
valves involved, and the nature of the valvular dysfunction (steno- and chordae tendineae are scarred and, as a result, they thicken
sis, insufficiency, or a combination of stenosis and insufficiency). and shorten. Acute heart failure develops because of interstitial
The degree of cardiac dysfunction is defined by the New York myocarditis. Fibrinoid degeneration develops, followed by the
Heart Association’s (NYHA) Functional and Therapeutic Classifi- appearance of Aschoff nodules, the characteristic pathologic le-
cation. Acquired valvular heart disease most commonly affects, sion of acute rheumatic fever. As Aschoff nodules heal, fibrous
and is most symptomatic with, the aortic and mitral valves. This scars remain. In severe cases, death from acute heart failure may
chapter focuses on the mitral and aortic valves, with a brief dis- result. Carditis frequently does not cause any symptoms and is
cussion of tricuspid valve disease. Because the cause of pulmonic detected only when the patient seeks help because of arthritis or
disease is primarily congenital, it is described in Chapter 31. chorea.
Auscultatory signs of aortic and mitral insufficiency are fre-
quently apparent. In more than 90% of patients with carditis, the
mitral valve is affected. When the mitral valve is affected, there
CAUSES OF ACQUIRED may be a high-pitched, blowing, pansystolic murmur. A Carey
VALVULAR HEART DISEASE Coombs murmur, a low-pitched, mid-diastolic murmur of short
duration, may be noted at the apex. The Carey Coombs murmur
Rheumatic Heart Disease may be attributed to swelling and stiffening of mitral valve
leaflets, increased flow across the valve, and alteration in left ven-
Rheumatic fever is an acute autoimmune disorder that results as a tricular compliance.
complication of streptococcal upper respiratory tract infections. Rheumatic fever can be prevented by aggressive treatment of
Tissues involved in rheumatic fever include the lining and valves the initial episode of streptococcal pharyngitis: penicillin G, 500
of the heart, skin, and connective tissue (Fig. 29-1). The group A mg as the first dose and then 250 mg four times daily for a dura-
-hemolytic streptococcal organism is responsible for initial and tion of 10 days. If the patient is allergic to penicillin, erythromy-
recurrent attacks of rheumatic fever. Lymphatic channels from the cin or cephalosporins may be used. Effective antibiotic treatment
tonsils are thought to transmit group A streptococci to the heart. started less than 10 days after the onset of infection almost com-
The incidence of rheumatic fever has declined to less than pletely eliminates the risk of rheumatic fever. 1
1/100,000 in industrialized nations but remains higher than
1
100/100,000 in endemic, less developed countries. Reasons for Infective Endocarditis
the decline in rheumatic fever include the use of antibiotics to treat
and prevent streptococcal infections, as well as improved social Infective endocarditis is an endovascular infection that supports con-
conditions such as decreased crowding, better housing and sanita- tinuous bacteremia from the source of the infection, usually a vege-
2
tion, and access to health care. Rheumatic fever persists in under- tation on a heart valve. While endocarditis is uncommon, affecting
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