Mitral regurgitation refers to an incompetence of the valve that may occur due to abnormalities to the valve leaflets, subvalvular apparatus or left ventricle.
Regurgitation refers to a ‘leaking’ of blood through the valve during ventricular systole. It can be classified as primary or secondary:
It may also be classified into acute and chronic disease based on the speed of onset and severity of regurgitation. Mitral regurgitation is the second most common indication for valvular surgery (the most common being aortic stenosis).
The mitral valve is termed (somewhat erroneously) a bicuspid valve and sits between the left atrium and ventricle.
The term atrioventricular valve complex refers to the entirety of the valve and its supporting apparatus. It consists of the orifice, valve leaflets, chordae tendineae, papillary muscles and the ventricle itself.
There are two valve leaflets, anterior and posterior. The posterior leaflet is divided by indentations into three scallops (P1, P2, P3). The corresponding areas on the anterior leaflet may also be divided to reflect the posterior scallops (A1, A2, A3). The normal cross-sectional area of the mitral valve orifice is 4-6 cm2.
Each leaflet is attached to chordae tendineae, which are string-like structures that connect leaflets to papillary muscles. Two papillary muscles support the mitral valve and arise from the ventricular wall.
Pathology affecting any of these structures may lead to valvular dysfunction. In normal physiology the mitral valve opens to allow left ventricular filling and closes during ventricular contraction.
The cause of MR may be divided into acute and chronic cases.
Trivial MR is a relatively common finding on echocardiogram. In those with more significant incompetence heart failure can result and surgical intervention may be needed.
Primary MR: degenerative valve disease is the most common cause. Other causes include:
Secondary MR: ischaemic MR may result in chronic MR following a myocardial infarction (more commonly than acute ischaemic MR). The ischaemic insult leads to left ventriclar remodelling and dysfunction impairing the valves ability to close. Other causes include cardiomyopathy (dilated and hypertrophic).
Acute disease typically results from primary forms of MR. It can occur following myocardial ischaemia/infarction with secondary papillary muscle rupture and valvular incompetence.
Non-ischaemic forms include ruptured chordae tendineae and valvular disease secondary to infective endocarditis and rheumatic heart disease.
The pathophysiology of acute and chronic MR differ as in chronic disease compensatory mechanisms have time to develop.
MR results in a backflow of blood during ventricular systole from the left ventricle into the left atrium. This reduces the ejection fraction as part is flowing backwards and raises the atrial pressure.
In chronic MR there is gradual worsening of the regurgitant fraction that initially allows for compensatory mechanisms to occur. Eventually failure may result and the patient enters a decompensated state:
In acute MR there are fast and significant changes to flow without time for any adaptation or remodelling to occur as is seen in chronic MR.
The new regurgitation causes increased pressure within a non-compliant left atrium. As result of the lack of compliance this is reflected in rises in pressure in the pulmonary circulation. This pulmonary hypertension may cause pulmonary oedema to develop.
The ejection fraction falls precipitously as blood is ejected back across the regurgitant valve instead of forward though the aortic valve. A tachycardic response may be raised to help compensate for the reduced ejection fraction in an attempt to return the cardiac output to normal. This is rarely sufficient and cardiogenic shock can occur.
The clinical features of MR include the signs and symptoms of heart failure and a pansystolic murmur.
Acute MR: characterised by the rapid development of heart failure with inadequate cardiac output and flash pulmonary oedema. Patients may be shocked and breathless, the condition is potentially life-threatening, and can necessitate emergency surgery.
Chronic MR: may be asymptomatic for many years until heart failure results in symptoms developing. Symptoms tend to involve dyspnoea and orthopnoea that results from pulmonary hypertension. Fatigue and malaise are common. As right-sided heart failure develops patients may notice swelling of their ankles (peripheral oedema).
Echocardiogram allows for the confirmation of an incompetent valve, assessment of the severity and identification the underlying cause.
In chronic MR evidence of left atrial and ventricular enlargement is often seen. In acute MR cardiomegaly is normally absent (unless there was pre-existing pathology) and signs of pulmonary oedema are seen. On the CXR left atrial enlargement can be seen with the tell-tale sign of a 'double right heart border' cause by the large left atrium.
In acute MR the ECG may be entirely normal or reflect a recent myocardial infarction. In chronic MR changes can include p-mitrale - a broad, notched p-wave with a negative component in V1 - (reflecting left atrial enlargement) and signs of left ventricular hypertrophy. Arrhythmia's, most commonly atrial fibrillation, are sometimes present.
Echo is the diagnostic modality of choice. Allows visualisation of the incompetent valve and can confirm the underlying aetiology. Left atrial and ventricular enlargement may be seen in chronic MR.
A number of additional investigations may be ordered depending on the clinical context.
Primary MR may be managed with medical therapies or surgical intervention.
Patients with acute MR are normally profoundly unwell - the condition characterised by shock and flash pulmonary oedema. Management follows two stages:
In secondary MR there is less conclusive evidence showing improved survival following mitral valve intervention.
Secondary MR is associated with increased mortality though at present there is less evidence showing surgical intervention improves outcomes. The management should be guided by MDT with key input from both heart failure and electrophysiology specialists. Medical therapy should follow heart failure management. CRT should be considered when appropriate.
The indications for surgery are complex and in some cases have a relatively limited evidence base. In patients undergoing CABG with LVEF > 30% with severe secondary MR, it should be considered. It is also discussed with patients with ongoing symptoms despite optimal medical therapy (including CRT if indicated).
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