The mitral valve is a bicuspid valve that separates the left atrium (LA) and left ventricle (LV). The fibrous mitral annulus sits at the left atrio-ventricular junction and serves as an insertion point for the anterior and posterior leaflets.

The valve leaflets open into the left ventricle, tethered by papillary muscles on the wall of the LV that extend chordae tendineae attachments to the leaflets. The anterolateral papillary muscle attaches chordae tendineae to the anterior leaflet while the posteromedial papillary muscle attaches chordae tendineae to the posterior leaflet.

During diastole, the mitral valve is open allowing for LV filling. The mitral valve closes during systole due to increased pressure of the LV, blocking blood flow back into the left atrium. Complete mitral valve closure ensures the unidirectional flow of blood from the LV to the aorta.

The mitral valve closure is associated with the S1 sound.

Mitral Valve Regurgitation (MR) occurs when the mitral valve becomes incompetent as a result of compromised or structurally disrupted components of the valve apparatus. This renders gaps in leaflet apposition, allowing for insufficiency, or regurgitation, from the left ventricle back into the left atrium during systole.

There are two main types MR: Chronic and Acute.

Chronic MR results from progressive deterioration of the mitral valve apparatus with increasing insufficiency over the course of many years. The defect may be within the valve itself, referred to as organic, or may appear secondary to pathology within the ventricles without coexisting structural change of the valve, called Functional MR [1, 2].

As a result of any defect, increased volumes within the left side of the heart lead to compensatory dilatation of the left atrium and left ventricle. The resulting increase in LV end-diastolic volume allows for an increased ejection fraction (0.5–0.6), while the enlarged atrial cavity better accommodates the regurgitant volume of blood. These compensations abate the symptoms of MR: pulmonary congestion and forward failure.

Over the course of 6–10 years, however, the prolonged burden to volume overload causes LV dysfunction and the emergence of MR symptoms [3].

Acute MR is the result of an acute impairment of the mitral valve apparatus without time to establish sufficient compensatory mechanisms. The left atrium and left ventricle experience a sudden volume overload as a result of dramatic backflow of blood coupled with decreased stroke volume and cardiac output. The regurgitant volume increases intra-atrial pressure, preventing flow of blood from the pulmonary circulation into the left atrium and resulting in pulmonary congestion. In acute MR, therefore, the patient experiences reduced forward output, or even shock, along with congestion of the pulmonary vasculature [3].

MR occurs due to a defect to any part of the mitral valve apparatus – the leaflets, chordae tendineae, papillary muscles, or mitral annulus. The location and extent of damage to the apparatus determines whether the pathology presents as Acute or Chronic MR.

Infectious endocarditis is most frequently affects mitral valve structures [4]. It may lead to rupture of the chordae tendineae and/or enlargement of the posterior portion of the mitral annulus [1].

Myocardial infarction/Coronary Artery Disease– Prolonged ischemia and/or infarction to the region of the tensor apparatus weakens the papillary muscles and results in an inability to sufficiently tether the corresponding leaflet to the left ventricle. An alternate hypothesis suggests that an infarct near the base of the papillary muscle may cause disorganized muscle contraction, shifting the position of the leaflet during ventricular contraction and precluding appropriate closure [5]. Others argue that MR results from displacement of papillary muscles as a result of left ventricular remodeling rather than an intrinsic defect with the muscle itself [1]. Regardless of the exact mechanism, MR in the setting of ischemic disease is rarely organic or acute, but is rather Functional MR as a result of left ventricular or papillary muscle pathology [1]. Note: Occlusion in the right coronary artery will affect the posteromedial structures, whereas left anterior descending or circumflex artery occlusion will compromise the anteromedial structures. Due to its single blood supply, posteromedial rupture is more common.

Myxomatous degeneration of mitral leaflet(s): Pathological weakening of the valve connective tissues renders the mitral leaflets floppy and redundant, resulting in mitral valve insufficiency. Degenerative MR is usually associated with mitral valve prolapse. Myxomatous degeneration is the most frequent cause of surgical MR [4].

Rheumatic Fever: Acquired during childhood, Rheumatic Fever (RF) induces a slow progression of scarring and retraction of the valvular leaflets that manifests as MR and mitral stenosis with fusion of the commissures in middle age. These cardiac sequelae are no longer common in the United States, but are still a frequent cause of MR in countries where RF remains endemic [1].

Mitral annular calcification: More common in elderly, mitral annular calcification is usually of little clinical significance; however, it may result in MR due to impairment of contraction of the valve annulus and deformation of valve leaflets. Often associated with conditions such as hypertension, aortic stenosis, diabetes and end stage renal disease [4].

Depending on the cause, time course of valvular degeneration/destruction, and severity of valvular pathology, MR may remain asymptomatic or lead to severely debilitating symptoms.

Symptoms of chronic MR include:

Acute MR – Symptoms of acute MR are markedly more severe than those of chronic MR, as the LA and LV have not been able to adapt to the regurgitant blood flow. An immediate and unabated increase in pressure within the LA and LV coupled with a dramatic reduction in cardiac output results in rapid onset of the following symptoms:

MR is among the most common valve disease in developed countries, representing nearly one-third of acquired left-sided valve pathology [2].

Moderate to severe mitral regurgitation affects 1.7 % of the general population with equal gender distribution and increases in prevalence with age, from .1 % among 45–50 year-olds to 9.3 % in those ≥75 years [6].

The Framingham Heart Study demonstrates that, including mild MR, this condition is found in 19.0 % and 19.1 % in men and women, respectively [7].

The classical holosystolic murmur, commencing immediately after S1 and continuing up to S2. It is most often “blowing” and high pitched in quality.

Murmur is heard best over the apex.

The likelihood of auscultating a murmur is proportionately related to the grade of severity of MR on echocardogram. Murmur prevalence increases from 40 % to nearly 90 % with increasing severity of MR to grade 1 through grade 4, respectively [8]. See Figs. 9.4 and 9.5.

Presence of S3 gallop.

No S4 gallop heard in chronic MR, due to an enlarged, poorly contractile left atrium.

Auscultation Examples of Mitral Regurgitation.

An apical systolic murmur with early- and mid- systolic crescendo-decrescendo. The diminishment of the late systolic sound is thought to be due to building atrial pressures that soon equalize that of the LV [9, 10].

Murmur best heard along the left sternal border.

Prominent S4 gallop: Caused by normal-sized, vigorously contracting left atrium following exaggerated expansion during systole. It is suggestive of acute onset of regurgitation due to the rupture of the chordae tendineae that anchor the valvular leaflets [11].