Mitral Regurgitation - Questions And Answers

A 50-year-old woman who had an “innocent” murmur diagnosed in childhood presents with dyspnea on exertion, orthopnea, and paroxysmal nocturnal dyspnea of several months' duration. On questioning, she describes a 1-year history of fatigue and exhaustion that has limited her daily activities. She has not seen a physician in years.
On physical examination, her blood pressure is 110/70 mm Hg. Her jugular venous pressure is normal and she has mildly diminished arterial pulse amplitude with a normal arterial upstroke. Her lungs are clear to percussion and auscultation. There is a laterally displaced apex impulse and a palpable third heart sound that is easily heard. The first heart sound is soft and there is a widely split second heart sound with normal respiratory splitting. A grade 3/4 blowing, high-pitched systolic murmur is heard at the apex and radiates to the axilla and left infrascapular area. There is trace edema but no clubbing or cyanosis.

1. What is the valvular lesion in this patient?
2. What is the most common underlying cause of severe mitral regurgitation in the adult U.S. population?
3. Does medical therapy prevent progression of mitral regurgitation?
4. When should surgery be considered for patients with severe mitral regurgitation?
5. What are the choices for mitral valve surgery?

Answers :


1. What is the valvular lesion in this patient?
Chronic mitral regurgitation, the most insidious of all left-sided valvular lesions, is the most likely diagnosis in this patient. Severe left ventricular dysfunction is not uncommon at presentation in this disorder. The holosystolic apical murmur is characteristic of chronic mitral regurgitation.
The third heart sound suggests that the mitral regurgitation is severe, and is a reflection of the large volume of blood crossing the mitral valve in early diastole. How ever, the third heart sound does not necessarily imply HF. In chronic mitral regurgitation, the large regurgitant volume entering the left
atrium results in left atrial enlargement w ith the left atrium often touching the spine. The murmur is transmitted to the spine through the left atrium, accounting for its radiation to the subscapular area.

The murmur described is typical for chronic mitral regurgitation, but must be distinguished from such murmurs as tricuspid regurgitation, aortic stenosis, and VSD.

The murmur characteristic of aortic stenosis is distinguished by its quality (crescendo–decrescendo), location, and radiation,

A tricuspid insufficiency murmur is usually well localized to the left sternal border with little radiation, and has the characteristic feature of an increase in intensity with inspiration.

The murmur characteristic of VSD is typically heard best at the left sternal border, often has a harsh quality, and does not change w ith respiration. The murmur of VSD is rarely heard in adults because most congenital VSDs are detected in childhood and resolve spontaneously or are surgically corrected. A VSD is a rare complication of acute MI in adults.

2. What is the most common underlying cause of severe mitral regurgitation in the adult U.S. population?
Myxomatous mitral valve disease, usually as an isolated lesion or sometimes associated with other connective tissue disorders (e.g., Marfan's and Ehlers-Danlos syndromes), constitutes the most common cause of severe mitral regurgitation necessitating mitral valve replacement or repair in the United States, especially in younger people.
A smaller number of cases are due to rheumatic heart disease, infective endocarditis, or spontaneously ruptured chordae tendineae.
In older people, severe mitral regurgitation often accompanies left ventricular enlargement and dysfunction due to CAD and MI.
The mitral regurgitation is not due to an abnormality of the valve leaflets but due to a combination of abnormalities of the supporting structures of the valve including stretching of the mitral annulus along with papillary muscle dysfunction and w all motion abnormalities.

3. Does medical therapy prevent progression of mitral regurgitation?
There are no clinical trials demonstrating benefits of any medical therapy for chronic mitral regurgitation that is due to a primary abnormality of the mitral valve.
If mitral regurgitation is due to left ventricular enlargement with dysfunction of the mitral valve apparatus, ACE inhibitors and β-blockers are indicated to improve ventricular function. If ventricular function improves in patients with mitral regurgitation due to ventricular dysfunction, the mitral
regurgitation will improve as the valve apparatus becomes more functional.

4. When should surgery be considered for patients with severe mitral regurgitation?
Mitral regurgitation results in a chronic volume overload on the left ventricle and ultimately results in left ventricular contractile dysfunction. Mitral valve surgery should be performed before ventricular dysfunction occurs, but there is no method to precisely predict the onset of ventricular dysfunction. Serial Doppler echocardiography studies should be performed to evaluate left ventricular size and function and assess pulmonary pressures.
Surgery is recommended in the asymptomatic patient if the EF falls below 60%, or when the left ventricular end-diastolic dimension exceeds 45 mm, or if pulmonary hypertension or atrial fibrillation develops. Surgery is recommended for patients with symptoms of HF due to mitral regurgitation unless they have severe left ventricular dysfunction or other contraindications to surgery.

5. What are the choices for mitral valve surgery?
Mitral valve replacement with mechanical or bioprosthetic valves and, more recently, mitral valve repair constitute the surgical treatments available for severe mitral regurgitation due to a primary valve abnormality.
Mitral valve repair is associated with a lower surgical mortality rate and a better longterm outcome than mitral valve replacement, and is the preferred procedure when repair is possible.
Mitral valve surgery is generally not indicated if the mitral regurgitation is due to left ventricular dysfunction without a primary valve abnormality.