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Mitral valve prolapse (MVP) is an important clinical entity. In most patients, the condition remains either undiagnosed or inconsequential whereas, for others, MVP confers significant morbidity and even mortality.
Since we have gained a greater understanding of cardiac structure and the limitations of echocardiography, the definition of MVP has been refined. In the 1980s, MVP was over-diagnosed with prevalence over 35 per cent. Modern thinking has revised this figure to around 2-3 per cent.
The most common cause of MVP is myxomatous degeneration, which, in addition to causing valve thickening, makes the chordae over-extensible and prone to rupture.
In the absence of myxomatous degeneration, causes include excessively long chordae, a small left ventricle and autosomal dominant inheritance. MVP may also co-exist with a secundum atrial septal defect.
In most instances, MVP is an isolated finding. It may be associated with a number of conditions including collagen disorders such as Ehlers-Danlos, pseudoxanthoma elasticum, and Marfan's syndrome.
One may suspect MVP either by history or examination. It then needs to be confirmed on echocardiography. In many instances, it is an incidental finding when echocardiography is performed for other reasons.
Clinical features
While many textbooks teach that patients with MVP often present with breathlessness, atypical chest pain and anxiety disorder, data from Framingham do not support this.1
Some reports have commented on the link between anxiety and MVP being no more than coincidence.2 Other reported associated symptoms include palpitations, which may reflect ectopic beats or supravent- ricular tachycardia, and fatigue.
General clinical examination may reveal features of mitral valve 'syndrome' such as pectus excavatum, scoliosis and small anterior-posterior chest diameter. Marfanoid features may be noted rarely.
Cardiac auscultation demonstrates a high-pitched mid-systolic click (loudest over the mitral area) as the valves prolapse beyond the plane of the mitral annulus into the left atrium. This may be followed by a murmur of mitral regurgitation.
Squatting, which increases left ventricular end diastolic volume, delays the systolic click. The converse is true on standing and performing the valsalva manoeuvre.
Investigations
ECG is neither specific nor sensitive and is frequently normal in patients with MVP. Non-specific ST segment or inferior T wave changes may be seen. Patients may be subjected to unnecessary invasive procedures after a false positive exercise tolerance test.
Echocardiography is the investigation of choice. Either or both of the mitral valve leaflets are required to prolapse ≥2mm beyond the mitral annular plane in the echocardiographic long-axis view before a diagnosis can be made.
If prolapse is seen in the four-chamber view but not the long-axis view, a diagnosis cannot be made.
The echocardiographer should also comment on the thickness of the valve leaflets as this has prognostic significance. A thickness of ≥5mm is termed 'classic MVP' and has an increased risk of endocarditis, mitral regurgitation and sudden cardiac death compared with 'non-classic' disease.
Other important prognostic features on echocardiography include the presence and severity of mitral regurgitation and left ventricular systolic dysfunction (LVSD). A dilated left atrium increases the risk of AF.
Complications
Complications of MVP are more common in men but affect fewer than one in 50 people a year and include AF, LVSD, chordal rupture, endocarditis, arrhythmias, mitral regurgitation, embolic disease, pulmonary hypertension and cardiac death.
The key to managing MVP is to identify and monitor those at risk of significant morbidity.
Patients without symptoms or those with non-progressive symptoms and findings are at lowest risk and may be reviewed every three years.
Patients with classic MVP have a 14-fold risk of embolic disease, infective endocarditis and sudden cardiac death. Other predictors of these complications include age over 45, LVSD, moderate-to-severe mitral regurgitation and increased left atrium size.
LVSD and moderate-to-severe mitral regurgitation confer a 78 per cent 10-year risk of complications. At-risk patients should be reviewed annually. Patients with new symptoms or symptoms or examination findings suggestive of complications, such as mitral regurgitation or progressive symptoms, require repeat echocardiography.
Management
Patients with tachyarrthymias and adrenergic symptoms may benefit from drugs including beta-blockers.
The presence of mitral regurgitation, which may only be exertional, is an indication for antibiotic prophylaxis against endocarditis. Men over 45 years of age with classic MVP, those with LVSD and patients with a previous history of endocarditis are also at higher risk of endocarditis. Aspirin may be recommended to high-risk patients and anticoagulation may be offered to those with a history of embolic stroke or if in AF.
Men have an increased risk compared with women of requiring surgery for MVP with severe mitral regurgitation. Age, classic MVP, left ventricular dilation, hypertension and obesity are also risk factors for requiring surgery.
- Dr Thakkar is a GP in Wooburn Green, Buckinghamshire
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References
1. Mitral valve prolapse. Lancet 2005; 365: 507-18.
2. Current management of mitral valve prolapse. Am Fam Physician 2000; 61: 3,343-50.
