Mitral regurgitation (MR) refers to when the mitral valve closes incompletely during systole, causing blood to flow back from the left ventricle into the left atrium. It’s a common valvular heart disease.

MR can be primary, due to direct involvement of the valve itself or the chorda tendinae, or secondary, due to changes in the dimensions of the left ventricle, making it impossible for the anatomically normal mitral valve to close properly. It can also be either acute or chronic.

In acute MR, increased left ventricular end-diastolic volume causes backward congestion, causing pulmonary congestion or oedema.

In chronic MR, the heart compensates the increased LV end-diastolic volume by eccentric hypertrophy, dilating the chamber. However, over time, this compensatory mechanism leads to myocardial dysfunction and too large chamber, leading to heart failure.

Etiology

Pathophysiology

Mitral regurgitation causes a backward pressure increase to the left atricle and from there to the pulmonary vasculature, which causes the dyspnoea. The lungs respond by increasing pulmonary vascular resistance, which in turn increases the afterload of the right ventricle, which may cause dilation of the right ventricle.

The pressure load on the left atrium may also cause it to dilate, which may trigger atrial fibrillation. AFib may worsen the symptoms as they suddenly lose the atrial contraction needed to fill the left ventricle in diastole.

Clinical features

In acute MR, acute dyspnoea develops. In chronic MR, chronic heart failure develops. In case of acute MR, no murmur is typical, but in chronic MR there’s a holosystolic murmur with a “blowing” characteristic at the site of the apex. This murmur radiates to the left axilla.

Atrial fibrillation is common in chronic MR.

Diagnosis and evaluation

Echocardiography allows for assessment of the mitral valve motion during systole, and it can visualise regurgitated blood flow. Coronary angiography can be used to assess the degree of coronary artery disease if valvular surgery is indicated.

Coronary catheterisation used to be the gold standard for evaluation of mitral valve disease, as one can directly measure the pressure in the right heart, left atrium, and pulmonary vasculature, but nowadays echocardiography can estimate these well enough that catheterisation is rarely necessary.

If the left ventricle has dilated, a wide and bifid P-wave may be seen on the ECG.

Treatment

Surgery, either valve repair or replacement, is the definitive treatment for MR. In case of acute primary MR, urgent surgery is indicated. In case of chronic primary MR, surgery is indicated if the LVEF is decreased or the patient is symptomatic. However, if the LVEF is severely decreased (<30%), surgery is not recommended due to high mortality rate and low likelihood of improvement.

While waiting for surgery, pharmacological therapy for heart failure is required, if present. Even if there is no overt heart failure, RAAS inhibitors may decrease peripheral vascular resistance and therefore improve symptoms.