Valvular and congenital heart disease

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Chapter 21 Valvular and congenital heart disease

VALVULAR HEART DISEASE

Valvular heart disease is still a common cause for symptoms and disability worldwide. In most economically developed countries the main cause is no longer rheumatic heart disease: congenital valve abnormalities such as mitral valve prolapse and bicuspid aortic valves, degenerative valve disease or infective endocarditis are more common causes.1 However, in many parts of the world, rheumatic fever and rheumatic heart disease are still major health problems, especially in the young.2,3 Diseases of heart valves produce stenosis, incompetence or both.

MITRAL STENOSIS

Rheumatic fever is the main cause of mitral stenosis; rarer causes are:

Scarring or fibrosis of the valves, especially at the edges and sometimes involving the subvalvular apparatus, causes narrowing and hence increased left atrial pressure, pulmonary venous hypertension and pulmonary arterial hypertension. Thus the lungs and right ventricle suffer the most burden. Main symptoms are breathlessness on exertion, recurrent bronchitis, fatigue, palpitations due to paroxysmal atrial fibrillation (AF), haemoptysis and stroke. The onset of AF is usually associated with marked symptomatic deterioration and significantly increases the risk for left atrial thrombus formation and embolism.

Classic signs of mitral stenosis are:

The first clue to the diagnosis is often the loud first heart sound, which should prompt a careful search for the diastolic rumble which may be soft, low-pitched and localised to the apex. An opening snap is present if the valve is not calcified and this occurs 0.04–0.10 s after S2.

An electrocardiogram (ECG) shows a broad P-wave in lead 2 due to left atrial hypertrophy. Chest X-ray shows an enlarged left atrium and appendage, prominent upper-lobe pulmonary veins, but heart size is usually within normal limits. The diagnosis can readily be confirmed by echocardiography, which allows assessment of the valve anatomy, and estimation of valve area and gradient. Severe stenosis is considered to be present if the valve area is < 1 cm2 (Figure 21.1).

Treatment is the use of β-blockers to slow the heart rate and increase diastolic filling time diuretics, and digoxin is given if the patient is in AF. Anticoagulation is essential if there is significant mitral stenosis and AF. Mitral balloon valvuloplasty has been shown to be very successful therapy with excellent long-term outcome, and compares well with surgical treatment.5 The main contraindications to balloon valvuloplasty are significant mitral regurgitation and heavy calcification when mutual valve replacement should be done.

MITRAL REGURGITATION

There is a considerable difference between acute and chronic mitral regurgitation (Table 21.1). In chronic mitral regurgitation, there is time for the left ventricle and left atrium to adapt to the increasing regurgitation, leading to their gradual enlargement. In acute mitral regurgitation, the sudden pressure overload of the left atrium and pulmonary veins leads to severe pulmonary oedema. The treatment for acute mitral regurgitation is urgent surgery. The management of chronic mitral regurgitation is more difficult. Initially, medical therapy can be helpful, but the probability of postoperative death or persistent severe heart failure after valve replacement increases abruptly when the left ventricular (LV) end-systolic diameter exceeds 45 mm on echocardiography, or ejection fraction falls below 60%.6 In patients without mitral stenosis, mitral valve repair is preferable to replacement, and evidence suggests that preservation of the chordae improves postoperative LV function.7

Table 21.1 Mitral regurgitation

  Chronic Acute
Causes Mitral valve prolapse Ruptured chordae
Rheumatic heart disease Ruptured papillary muscle
LV dilatation (IHD, cardiomyopathies, etc.) Perforation of leaflet
Prosthetic valves Prosthetic valves
Physiology LV volume overload Sudden pressure overload of LA and pulmonary veins
LV dilatation and hypertrophy  
Increased LA size (mean pressure normal initially because of increased compliance) No change in LV dimension
  LA may be normal size
Symptoms Asymptomatic initially Severe dyspnoea
Fatigue  
Dyspnoea  
Examination Pansystolic apical murmur radiating to axilla/lower sternal edge Harsh pansystolic murmur radiating to axilla and back
Third heart sound Third heart sound
Electrocardiogram LV hypertrophy No change (or acute MI)
LA hypertrophy  
Chest X-ray Increased-size LV Normal LV and LA dimension
Increased-size LA Pulmonary oedema
Echocardiography Diagnostic Diagnostic
Treatment Vasodilators and ACE inhibitors (reduce afterload) Preload and afterload reduction and prepare for urgent surgery
Diuretics and digitalis
Surgery if symptoms and LV size increase (before LV end-systolic diameter > 4.5 cm or LV ejection fraction < 60%)

MI, myocardial infarction; LV, left ventricle/ventricular; IHD, ischaemic heart disease; IE, infective endocarditis; LA, left atrium/atrial; ACE, angiotensin-converting enzyme.

MITRAL VALVE PROLAPSE8

This is a common condition affecting 5% of the adult population – more women than men. It has a number of synonyms, such as Barlow and click–murmur syndrome. It is due to myxomatous degeneration of the valve, with redundancy of the leaflets, which may affect both the anterior and posterior valves. At the end of diastole, the valve closes normally, but as LV pressure rises during systole, a portion of the valve leaflet prolapses in the left atrium, with associated regurgitation. It is usually mild, but can progress and become more severe, and, rarely, the chordae may rupture to produce severe acute regurgitation.

Mitral valve prolapse is usually asymptomatic, but a wide variety of symptoms have been associated, including odd chest pains, palpitations and fatigue. On examination, typical findings are a mid-systolic click and a late systolic murmur, which are separated from the first heart sound, but usually reaching the second heart sound. The murmur may have a crescendo/decrescendo quality. It is usually louder with the Valsalva manoeuvre and on standing. As the prolapse worsens with age the murmur becomes more pansystolic. Echocardiography is diagnostic, and can accurately assess the degree of severity of mitral valve prolapse (Figure 21.2). In most patients, mitral prolapse is a benign condition with a good prognosis. It poses a risk for infective endocarditis, which then leads to a substantial risk of death and need for mitral valve surgery.9 There is a very small increased incidence of embolic neurological ischaemic events.

AORTIC REGURGITATION

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