Overview of Mitral Regurgitation
Can be caused by rheumatic fever (usually associated with mitral stenosis), dilated cardiomyopathy, LV dilation from chronic ischemic heart disease, papillary muscle dysfunction or chordae tendineae rupture. Etiology is a major determinant of outcome in cardiac surgical patients.
Medical and Surgical Treatment
Medical treatment may include digoxin, diuretics, and/or vasodilators—including ACE inhibitors. Afterload reduction key
Surgical treatment is usually reserved for patients with moderate to severe symptoms (i.e. regurgitant fraction > 30%). Valvuloplasty is preferred over replacement. Whenever possible, valve repair is preferred to replacement, as it avoids long-term anticoagulation and, all other things being equal, affords a better long term prognosis. Posterior leaflet and small anterior leaflet lesions are often amenable to repair, whereas large anterior leaflet lesions and those involving the mitral annulus often require replacement.
Acute MR presents differently: volume overload of the LA and LV, increased filling pressures (because compliance hasn’t had time to change), decreased cardiac output, and pulmonary edema secondary to back-pressure.
Effect on cardiac anatomy
The inciting pathology is a reduction in forward stroke volume as the LV begins pumping blood into the LA – this results in increased end-diastolic volume (and increased LV compliance), which allows the heart to maintain adequate cardiac output. Compensatory changes also include atrial chamber enlargement, increased ventricular wall thickness, and increased blood volume. Early in the disease (before contractility is affected) the EF will actually be increased, as afterload is reduced. As the disease progresses and the heart becomes less efficient, EF will eventually start to decrease. Eventually, these patients develop eccentric left ventricular hypertrophy and worsened contractility. EF can fall below 50% and regurgitant volume can exceed forward volume in severe MR. Note that afterload is limited by the regurgitation, thus many patients will not be symptomatic (it is impossible to generate large LV pressures).
The regurgitant volume depends on the size of the mitral valve orifice, the heart rate, and the LV-LA pressure gradient during systole (which is determined by the balance between SVR and left atrial compliance). Atrial compliance also determines the predominant clinical manifestations, as it affects the amount of flow transmitted back to the lungs. Patients with normal or reduced atrial compliance (ex. acute regurgitation) will exhibit pulmonary vascular congestion and edema, whereas those with increased atrial compliance (ex. long-standing MR) primarily show signs of a low cardiac output. Most patients exhibit symptoms of both. Regurgitant fractions less than 30% of total stroke volume are mildly symptomatic, 30–60% is moderate, and fractions greater than 60% cause severe disease.
Mitral Regurgitation in Non-Cardiac Surgery
Pulmonary artery catheters are useful in patients with symptomatic disease (ie regurgitant fraction > 30%), and in fact MR can be recognized on the PA wedge waveform as a large v wave and a rapid y descent. Note, however, that the v wave may not be prominent in patients with chronic mitral regurgitation (except during deterioration) because their LA has adapted. Very large v waves can often be seen on the PA pressure waveform even without wedging the catheter. Afterload reduction with a vasodilator requires arterial monitoring. Color-flow Doppler TEE can help guide the severity of the regurgitation and detect blood flow reversal in the pulmonary veins.
Echocardiography is extremely useful. Mitral valve leaflet motion can be described as normal, excessive or prolapsing (movement of a leaflet beyond the plane of the mitral valve and into the left atrium), or restrictive. Eccentric regurgitant jets on color-flow Doppler echocardiography are typical of a prolapsing valve, whereas central jets are more typical of regurgitation with normal or restricted valve motion.
Major goals are relative tachycardia and reduced afterload. Slow heart rates (long diastole and thus regurgitation) and increases in afterload should be avoided. During bradycardia, the LV overfills, further distending the annulus, thus the heart rate should be kept between 80 and 100 beats/min. Acute increases in left ventricular afterload, such as following endotracheal intubation and surgical stimulation, should be treated rapidly but without excessive myocardial depression. Excessive volume expansion can also worsen the regurgitation by dilating the left ventricle.
Patients with well-preserved ventricular function can tolerate both general and central neuraxial anesthesia as long as bradycardia is avoided. Those with moderate (~ 30-60% regurgitation) to severe (> 60% regurgitation) impairment can be highly sensitive to volatile agents, and an opiate-based anesthetic may be preferable. Pancuronium may help maintain a slightly elevated heart rate.
Mitral Regurgitation in Cardiac Surgery
Post-Repair / Bypass
Repair will immediately increase LV afterload, and decrease LV preload, both of which make it appear that LV function has decreased (because EF falls). Additional preload (and sometimes ionotropes) may be necessary to separate from bypass. Furthermore, the additional load placed on the LV can “unmask” a dysfunction which was previously hidden due to the significantly lowered afterload.
While relative tachycardia and decreased afterload are generally advantageous, occasionally mitral repair (not replacement) patients will deteriorate due to a HOCM-like syndrome with SAM of the anterior leaflet, caused by the anatomic nature of the repair.
Note that while severe MR is generally defined as regurgitant volume > 60 mL or EROA > 40 mm2, in ischemic MR less regurgitation may still be considered severe – this is based on data suggesting that regurgitant volume > 30 mL or EROA > 20 mm2 are associated with increased mortality [Grigioni F et al. Circulation 103: 1759, 2001]
Echocardiographic Assessment of Mitral Regurgitation
The ASE lists 9 parameters that can be used to evaluate mitral regurgitation echocardiographically. Notable among them are the vena contracta width (notable for its relative load-independence and ability to accurately assess eccentric flow), effective regurgitant orifice area (i.e. EROA, either by PISA or PW flow quantification), peak mitral E velocity (if less than A wave velocity, severe MR can be excluded), and pulmonary vein flow (reversal of which suggests severe MR).
ASE Parameters for MR Quantification 1. Vena Contracta Width (> 0.6 to 0.8 cm severe MR) 2. Effective regurgitant orifice area (EROA) A. PISA (> 0.4 cm2 severe) B. PW flow quantification (> 0.4 cm2 severe) 3. Peak mitral E wave velocity (A > E rules out severe MR) 4. Pulmonary vein flow (reversal implies severe MR)
For complete recommendations and commentary, see the ASE Guidelines