Valve Disorders/Diseases

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Valve Disorders/Diseases

Heart valves can become narrowed or fail to close properly

Chronic rheumatic heart disease:
• >50% of those affected with rheumatic fever with carditis  chronic valvular heart disease due to progressive fibrosis
• most commonly mitral valve

Mitral stenosis:
mostly rheumatic in origin; can be calcified in elderly
results in dyspnoea on exertion, palpitations, fatigue, nocturnal dyspnoea, right heart failure ( ankle oedema), pulmonary oedema, increased risk for emboli  eg stroke, fatigue (from diminished cardiac output, loud first heart sound, mid-diastolic murmur
management – anticoagulants (decrease risk of embolism), digoxin (control of atrial fibrillation), antibiotics (prophylaxis of infective endocarditis), mitral balloon valvuloplasty, mitral valve replacement

Mitral regurgitation:
due to prolapse of mitral valve (‘floppy mitral valve’), dilation of mitral valve ring (eg coronary artery disease, rheumatic fever), damage to valve cusps (eg rheumatic fever), myocardial infarction
clinically – exertional and nocturnal dyspnoea, pulmonary oedema, reduced cardiac output (eg fatigue), right side heart failure ( ankle oedema); atrial fibrillation, cardiomeagaly
management – diuretics, vasodilators, digoxin, anticoagulants, antibiotic prophylaxis

Aortic stenosis:
characterised by narrowing of the aortic valve opening
can be congenital (aortic bicuspid valve) or acquired (calcification/fibrosis, rheumatic disease, atherosclerosis)
if acquired, cardiac output is initially maintained by left ventricular hypertrophy and remains asymptomatic if mild  eventually develop dyspnoea on exertion, angina, pulmonary oedema and syncope on exertion. Sudden death can occur
diagnostic tests – cardiac catheterisation, chest x-rays, echocardiography, ECG
management – early valve replacement if indication

Aortic regurgitation/insufficiency:
• characterised by back flow of blood into left ventricle during diastole; ventricle is overloaded and dilated  hypertrophies; eventually affects left atrium and pulmonary system
• causes - congenital (eg bicuspid valves) or acquired (eg rheumatic disease, hypertension, infective endocarditis, dilation – from, eg , Marfan’s syndrome)
• if mild  asymptomatic, may be aware of ‘palpitations’
• if severe  angina, heart failure
• diagnostic tests – cardiac catheterisation, chest x-rays, echocardiography, ECG
• management – valve replacement if symptomatic, before significant ventricular function occurs (not always possible as symptoms mild); management of left sided heart failure (eg cardiac glycosides, low sodium diet, diuretics, vasodilators, ACE inhibitors)

Tricuspid stenosis:
• uncommon - usually due to rheumatic disease – almost always the mitral and aortic valves are also affected
• obstructs blood flow from the right atrium to right ventricle  right atrium dilates and hypertrophies
• clinically – have features of mitral and/or aortic valve disease, as well as features of right heart failure
• management – balloon valvuloplasty if isolated (rare) or surgical replacement

Tricuspid regurgitation/insufficiency:
Common. Incompetent tricuspid valve  back flow into right atrium during systole  decreased blood flow to lungs and left side of heart
Most are functional as valve is not structurally damages – valve usually ‘stretched’ from right ventricular dilation (eg cor pulmonale). Also can be due to rheumatic heart disease, endocarditis (especially in IV drug users), pulmonary hypertension, right ventricular infarction
clinically signs are non-specific – tiredness, oedema. hepatic enlargement, large systolic wave in the jugular venous pulse

Pulmonary stenosis:
• usually always congenital or associated with other cardiac abnormalities (eg Fallot’s tetralogy)
• clinically – right heart failure, systolic murmur
• if severe  balloon valvuloplasty

Infective Endocarditis (IE):
• infection of valve – mostly Strep. viridans or Staph. aureus
• more likely to occur at sites where endothelium is damaged by high pressure jet of blood or on damaged valves – can be further damaged by bacterial lytic enzymes; high risk in those with prosthetic heart valves and IV drug users
• Septic emboli from infected valvular ‘vegetation’ can break off  brain, kidney’s, fingers, toes
• clinical features – classical features (FAME) – fever, anaemia, heart murmur and emboli phenomena.
• 30% develop arthralgias, arthritis and myalgias – usually large proximal joints (may be confused with rheumatoid arthritis as RF factor often high in IE)
• in foot – loss of pulses; splinter haemorrhages in nails; digital clubbing if long standing; nontender haemorrhagic macules on soles (also on hands – Janeway’s lesions; cutaneous vascular embolic symptom of IE); painful nodules on toe pads (also in finger pads – Osler’s nodes; last from a few hours to days; uncommon; immunological process)
• management – antibiotics; surgical correction of valve defect
• prevention – antibiotic prophylaxis in those with heart disease.

Podiatric implications:
• haemodynamic abnormalities  thrombus/embolism
• prophylactic antibiotic if undergoing any minor surgical procedure
• often on anticoagulants  wound healing problems
• bacteraemia risk
• symptoms in foot

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