Rachel Matthews, MSc, RGN.
Lead Patient Care Adviser for Extending Choice in Heart Surgery, Cardiac and Renal Services, Barts and the London NHS Trust
Coronary heart disease (CHD) has enjoyed a high profile in recent years due to the introduction of the National Service Framework for CHD (Department of Health, 2000). Cardiac valve disease is less common, but causes disability and death. As advances are made in the research and treatment of aortic and mitral valve disease, it is timely for cardiac nurses to revisit the management of these patients.
Anatomy and physiology
The valves of the heart ensure that blood flows in one direction. Both the aortic and mitral valve are located on the left side of the heart and are covered in squamous epithelium, which forms the endocardium.
The aortic valve is a semilunar valve. It has three cusps, and its structure is strong to compensate for the high pressure of blood leaving the left ventricle. The aortic valve sits between the outflow tract of the left ventricle and the aorta. The coronary arteries open near the upper part of the aortic sinuses of the valsalva.
The aortic valve opens when the pressure in the left ventricle during systole increases and is higher than pressure in the aorta. As the pressure in the aorta becomes higher than that in the left ventricle, blood begins to flow backwards, causing the valve to close (Novak et al, 2002).
The mitral valve is an atrioventricular valve. It sits between the left atrium and the left ventricle. It is bicuspid, indicating it has two leaflets - an anterior leaflet that moves more freely and a posterior leaflet that is less mobile (Margereson and Riley, 2003). Like the aortic valve, it is attached to an annulus or ring of fibrocollagenous tissue. This is particularly important, as it gives flexibility to the annulus and valve during the cardiac cycle (Novak et al, 2002).
The mitral valve differs from the aortic valve by the presence of chordae tendinae and papillary muscles. These structures prevent the mitral valve being forced back into the left atrium as pressure rises in the left ventricle. The mitral valve is larger than the aortic valve and has an opening of 2-4cm2.
The opening and closing of the heart valves is linked with the cardiac cycle, which synchronises electrical activity with systole and diastole, and pressure changes in the heart chambers (Herbert and Alison, 1996).
Both valves are key components of cardiac activity, and if their function is disrupted it can have serious and catastrophic consequences for the patient.
Aortic valve disease
Aortic stenosis is obstruction to the flow of blood leaving the left ventricle. The obstruction can be:
- At the level of the valve (valvular)
- Above the valve (supravalvular)
- Below the valve (subvalvular) (Keon and Masters, 2000).
Valvular stenosis is the most common, but supravalvular and subvalvular stenosis may be seen in younger patients, who may also have additional cardiac abnormalities (Swanton, 2003).
Aortic valve stenosis may be congenital or acquired. The most common causes of acquired stenosis are rheumatic and calcific (Keon and Masters, 2000). However, as the incidence of rheumatic fever decreases in the developed world, more attention has been focused on the pathophysiology of calcific aortic stenosis.
Evidence is emerging that calcific degeneration of the aortic valve may be the result of an active process that is similar to atherosclerosis and is not simply due to ageing or ‘wear and tear’ (Wallby et al 2002; Otto, 2002; Boon and Bloomfield, 2002; Rajamannan et al, 2003). This has implications for primary and secondary prevention of heart disease and should prompt health-care professionals to reconsider their approach to patients with valve disease. Clinical risk factors for aortic valve disease calcification include age, being male, diabetes, hypertension and renal failure. Biochemical risk factors include hyperlipidaemia, hypercalcaemia and increased serum creatinine (Boon and Bloomfield, 2002).
Patients with a congenital abnormality of the aortic valve may have a unicuspid or bicuspid valve. They may present at an early age or, more commonly with a bicuspid valve, in the fourth and fifth decades (Boon and Bloomfield, 2002).
If the disease is an active process common to atherosclerosis it may be hastened by the additional stress placed on the abnormal valve. Lipid deposition and inflammation may occur, and in approximately 50% of patients with calcific aortic stenosis there will be coronary artery disease (Boon and Bloomfield, 2002).
The consequences of aortic stenosis are serious, and in severe stenosis death may occur without the patient previously reporting any symptoms. As the stenosis limits the volume of blood leaving the left ventricle, the ventricle works harder to overcome the pressure gradient. This causes hypertrophy and, crucially, coronary blood flow may be affected, causing angina even in the absence of coronary artery disease.
The heart is unable to increase cardiac output in response to exercise and hypotension, and syncope may occur. Eventually left ventricular failure will happen. Patients may feel well and have relatively few symptoms, but once they are reported there can be rapid deterioration, and death can occur within three to five years (Bonow et al, 1998). Medical treatment can relieve symptoms, but surgery should be considered at an early stage.
Boon and Bloomfield (2002) offer a summary of medical treatments for heart valve disease (Table 1). Care should always be taken in the administration of common cardiac drugs to patients with heart valve disease, as the altered physiology will differ, depending on the underlying cause of the disease.
Indications for and timing of surgery - Surgery is advised for all symptomatic patients with severe aortic stenosis. If the patient has left ventricular dysfunction, valve replacement would be indicated.
Prognosis of untreated patients is poor. The average survival is two to three years for those with angina and syncope and one to two years for those with cardiac failure (Swanton, 2003).
Early detection, with regular follow-up using non-invasive and sometimes invasive cardiac investigations, should monitor the progress of the condition.
Aortic regurgitation is the leakage of blood from the aorta back into the left ventricle. The valve fails to close properly owing to damage to the leaflets or changes in the valve annulus (Blackburn and Bookless, 2002). It can be acute or chronic. The most common causes of acute aortic regurgitation are infective endocarditis and prosthetic valve dysfunction. Other causes include aortic dissection, systemic hypertension and trauma.
Chronic regurgitation is commonly caused by a dilated aortic root or valve annulus. Rheumatic fever, bicuspid aortic valve and other degenerative or inflammatory processes can cause regurgitation (Keon and Masters, 2000; Blackburn and Bookless, 2002).
Aortic regurgitation leads to volume overload of the left ventricle. In acute regurgitation the ventricle will begin to fail rapidly, but in chronic cases the ventricle can compensate for the increased volume by adaptive modelling processes, and the patient may be unaware that anything is wrong. Eventually the compensatory mechanisms fail and the ventricle will no longer cope with the increased volume.
Symptoms of dyspnoea, particularly on exertion or when lying flat, and fatigue may be reported. Medical management will be aimed at relieving symptoms and preserving left ventricular function, which may delay the need for surgery.
Indications for and timing of surgery
Chronic aortic regurgitation can be better tolerated than aortic stenosis if compensatory mechanisms occur (Swanton, 2003). However, the condition is unlikely to improve in the long term, and surgery should be performed before left ventricular dysfunction occurs (Keon and Masters, 2000).
With acute aortic regurgitation, surgery may be needed urgently or as an emergency. This would be the case in aortic dissection or a ruptured sinus of valsalva (Keon and Masters, 2002; Swanton, 2003).
Mitral valve disease
Mitral stenosis is the narrowing of the valve orifice which reduces blood flow leaving the left atrium and entering the left ventricle. Left atrial pressure rises, the left atrium enlarges and pulmonary congestion occurs. Left ventricular filling becomes more dependent on left atrial contraction.
Where diastole is shortened - for example, with increased heart rate on exertion - the left atrium does not empty properly, compounding the problem further. Atrial fibrillation is very common, as it is caused by the enlargement of the atrium (Boon and Bloomfield, 2002).
Mitral stenosis is almost always caused by rheumatic fever (Swanton, 2003). Although this is less common in the developed world, health-care professionals should be alert for the possibility that patients may have been exposed to the disease if they have visited developing countries. The consequences of mitral stenosis can severely impair quality of life.
Indications for and timing of surgery
Surgery is the only treatment option for mitral stenosis. Medical therapy may help to control symptoms, and antibiotic prophylaxis can reduce the risk of further streptococcal infection which leads to rheumatic damage (Boon and Bloomfield 2002, Swanton 2003).
Surgery is recommended for all patients with severe mitral stenosis and all patients with a history of thromboembolism. It is also recommended for asymptomatic patients who have pulmonary artery hypertension, episodic pulmonary oedema or atrial fibrillation.
Mitral regurgitation is the back flow of blood from the left ventricle to the left atrium through an incompetent valve (Otto, 2003). Examples of primary mitral regurgitation include rheumatic disease, which causes leaflet stiffness and chordal shortening, and endocarditis, which leads to leaflet deformation and destruction.
An example of secondary mitral regurgitation would be ischaemic heart disease, which can affect the function of the papillary muscles and underlying left ventricular wall (Otto, 2003). Untreated mitral regurgitation has a poor prognosis. Left ventricular failure will develop and deterioration can be rapid.
Indications for and timing of surgery
Medical treatment for mitral regurgitation is aimed at reducing symptoms, preventing endocarditis and recurrent rheumatic fever. Otto (2003) emphasises that surgery for those patients who have additional coronary heart disease carries a higher risk, so secondary prevention for coronary risk factors should be initiated. Atrial fibrillation and the associated risk of thromboembolism should be managed with cardioversion or rate control and anticoagulation therapy.
Patients requiring surgery may be suitable for either a mitral valve replacement or mitral valve repair which confers some advantages to the patient. Long-term anticoagulation can be avoided, and there will be preservation of the continuity between the mitral annulus and papillary muscles (Otto, 2003). The risk of operative mortality is lower for mitral valve repair than mitral valve replacement (Otto, 2003).
Timing of surgery is determined by physiological indicators, including left ventricular size and systolic function, left atrial size, pulmonary artery pressures and atrial fibrillation. Where patients have relatively few symptoms, the decision to operate can be difficult. It is important to give due attention to this when preparing patients for surgery.
Types and choice of prosthetic valve
Prosthetic heart valves fall into two categories - mechanical and biological. Some studies have been performed to compare mechanical and biological valves, but as the population ages, different criteria may need to be applied to choice of valves (Bloomfield, 2002; Taylor, 2003). For patients in their sixties and seventies, a biological valve that avoids the need for anticoagulation may be the best choice, but as individuals live longer the need for re-operation is more likely. This carries increased operative risk, so perhaps more consideration should be given to the use of mechanical valves for this group (Hanania, 2003)
Mechanical prostheses have better durability than biological prostheses but require long-term anticoagulation therapy. There are three main types of mechanical valve (Bloomfield, 2002):
- Ball valves are made from a silastic ball that sits in a sewing ring and is enclosed by a metal cage. The ball is pushed forward as the pressure of blood behind it rises
- Disc valves are made from a single graphite disc coated with pyrolite carbon. This tilts between two struts of housing made of stainless steel or titanium. Modifications of this type of valve have been made over the years, but concern has been raised about their durability and function (Bloomfield, 2002)
- Bileaflet valves have two semicircular leaflets that open and close, allowing blood to flow through three openings (Bloomfield, 2002).
Biological or tissue valves
Biological valves avoid the need for long-term anticoagulation therapy, but are less durable than mechanical valves and more likely to need replacing within 10 years. Several types are in use:
- Autologous valves can be constructed from the patient’s own pericardium
- Autograft valves are used in the Ross procedure, where the diseased aortic valve of the patient is removed and replaced with their pulmonary valve. This is then replaced by a homograft valve
- Homograft valves are taken from human cadavers and can be used for aortic valve replacement in addition to their use in the Ross procedure. The donated valves are treated with antibiotics and cryopreserved before use
- Porcine heterograft (or xenograft) valves are made from porcine tissue that has been specially treated. These valves can be stentless or mounted on a stent (Bloomfield, 2002).
Special considerations for nursing care
The principles of nursing care for this group of patients are similar to those undergoing other forms of cardiac surgery, and Margereson and Riley (2003) provide a comprehensive overview of pre- and postoperative care.
There are special considerations for patients who may already have chronic arrhythmias, altered left ventricular function and pulmonary hypertension. Great care is required with fluid management and haemodynamic monitoring. Ricci et al (2000) and Donias and Karamanoukian (2000) describe the main complications of aortic and mitral valve surgery, which are summarised in Box 1.
Nurses can help patients understand the nature of their disease and the risks and benefits of surgery. While medical treatment may provide symptomatic control and surgery can offer improved long-term outcomes, there is an important role for secondary prevention for these patients who may not be perceived as having the same risks as those with coronary artery disease.
Nurses can provide support for patients as they adapt to living with a prosthetic valve. Those with a mechanical prosthesis will start long-term anticoagulation therapy that will demand changes in lifestyle and self-management. The risks of native and prosthetic valve endocarditis should be raised with patients who are waiting for or who have had valve surgery; education about prophylactic antibiotic therapy for dental and other invasive procedures should be discussed.
Hospital-acquired infection plays a greater role in infective endocarditis than has previously been emphasised. Good infection control practices in hospital can reinforce education messages given to valve patients who are learning to reduce the risk of developing infective endocarditis (Ekyn, 2001; Sparacino, 1999).
Those undergoing surgical intervention require specialist support throughout their diagnosis and treatment. Surgery can affect the long-term outcomes for these patients, but quality of life and benefit from surgery is likely to be enhanced by effective patient education and by encouraging patients to be involved in decision-making.
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