A. Primary Mitral Regurgitation
The degree of LV enlargement reflects the severity and chronicity of regurgitation. LV volume overload may ultimately lead to LV failure and reduced cardiac output. LA enlargement may be considerable in chronic mitral regurgitation and a large amount of mitral regurgitation regurgitant volume may be tolerated. Patients with chronic lesions may thus remain asymptomatic for many years. Surgery is necessary when symptoms develop or when there is evidence for LV dysfunction, since progressive and irreversible deterioration of LV function can occur prior to the onset of symptoms. Early surgery is indicated even in asymptomatic patients with a reduced EF (less than 60%) or marked LV dilation with reduced contractility (end-systolic dimension greater than 4.0 cm) (Figure 10–2). The 2017 update of the valvular guidelines has added a IIa indication for mitral valve surgery when the LVEF is greater than 60% and the LV end-systolic dimension is still less than 4.0 cm. The newer guidelines suggest that mitral valve replacement should be done if serial imaging reveals a progressive increase in the LV end-systolic dimension or a serial decrease in the EF. This latter recommendation is based on information that LV function is more likely to return to normal when the LVEF is greater than 64% and the LV end-systolic dimension is less than 3.7 cm. Calcification of the mitral valve is less common than in pure mitral stenosis. In some institutions, the calculation of an effective regurgitant orifice area by echocardiogram has proven useful in helping decide the severity of the mitral regurgitation. Regurgitant orifice areas greater than 40 mm2 are considered severe. This value may not be reproducible in different laboratories, however. The 2014 AHA/ACC valvular guidelines review echocardiography/Doppler criteria for defining mitral regurgitation severity. Pulmonary hypertension development suggests the mitral regurgitation is severe and should prompt intervention.
The 2017 focused update of the AHA/ACC guidelines for intervention in mitral regurgitation. (Reproduced, with permission, from Nishimura RA et al. 2017 AHA/ACC focused update of the 2014 AHA/ACC guideline for the management of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Circulation. 2017 Jun 20;135(25):e1159–95. © 2017 American Heart Association, Inc.)
Acute mitral regurgitation may develop abruptly, such as with papillary muscle dysfunction following MI, valve perforation in infective endocarditis, in patients with hypertrophic cardiomyopathy, or when there are ruptured chordae tendineae in patients with mitral valve prolapse. Emergency surgery may be required.
Some patients may become hemodynamically unstable and require treatment with vasodilators or intra-aortic balloon counterpulsation that reduce the amount of retrograde regurgitant flow by lowering systemic vascular resistance and improving forward stroke volume. There is controversy regarding the role of afterload reduction in chronic mitral regurgitation, since the lesion inherently results in a reduction in afterload, and there are no data that chronic afterload reduction is effective in avoiding LV dysfunction or surgical intervention. A heightened sympathetic state has led some experts to suggest that beta-blockade be considered routinely, though this also remains speculative. The mitral regurgitation in patients with tachycardia-related cardiomyopathy may improve with normalization of the heart rate.
B. Myocardial Disease and Mitral Regurgitation
When mitral regurgitation is due to papillary dysfunction, it may subside as the infarction heals or LV dilation diminishes. The cause of the regurgitation in most of these situations is displacement of the papillary muscles and an enlarged mitral annulus rather than papillary muscle ischemia. The fundamental problem is the lack of leaflet coaptation during systole (due to either leaflet prolapse or retraction). In acute MI, rupture of the papillary muscle may occur with catastrophic results. Transient—but sometimes severe—mitral regurgitation may occur during episodes of myocardial ischemia and contribute to flash pulmonary edema. Patients with dilated cardiomyopathies of any origin may have secondary mitral regurgitation due to the papillary muscle displacement or dilation of the mitral annulus, or both. In patients with ischemic cardiomyopathy, ventricular reconstructive surgery to restore the mitral apparatus anatomy and reshape the ventricle (Dor procedure) has had limited success and is rarely performed. If mitral valve replacement is performed, preservation of the chordae to the native valve helps prevent further ventricular dilation following surgery. Initially, several groups reported good results with mitral valve repair in patients with LVEF less than 30% and secondary mitral regurgitation. The 2014 AHA/ACC guidelines advise that mitral valve repair/replacement can be attempted in severe mitral regurgitation patients with an EF less than 30% or an LV end-systolic dimension greater than 5.5 cm, or both, as long as repair and preservation of the chordae are possible. The 2017 update (Figure 10–2) suggests the latest data favor mitral valve replacement with chordal preservation over mitral valve repair in patients with chronic ischemic cardiomyopathy. There may also be a role for cardiac resynchronization therapy with biventricular pacemaker insertion, which has been found to reduce mitral regurgitation related to cardiomyopathy in many patients. Guidelines recommend biventricular pacing prior to surgical repair in symptomatic patients who have functional mitral regurgitation as long as other criteria (eg, a QRS of greater than 150 msec or left bundle branch block or both) are present.
There are several ongoing trials of percutaneous approaches to reducing mitral regurgitation. These approaches include the use of a mitral clip (MitraClip) device to create a double orifice mitral valve, various coronary catheter devices to reduce the mitral annular area, and devices to reduce the septal-lateral ventricular size and consequent mitral orifice size. Of these devices, the most success has been noted with the MitraClip. Two major trials addressing the advantage of the percutaneous MitraClip reported findings in 2018. In the COAPT (Clinical Outcomes Assessment of MitraClip) trial among patients with heart failure and moderate-to-severe or severe secondary mitral regurgitation who remained symptomatic despite the use of maximum doses of guideline-directed medical therapy, transcatheter mitral-valve repair resulted in a lower rate of hospitalization for heart failure and lower all-cause mortality within 24 months of follow-up than medical therapy alone. The absolute risk reduction in all-cause mortality in patients receiving the MitraClip in the COAPT trial was 17%, which translated to a number needed to treat (NNT) of 6 to prevent 1 death over 2 years. This rather remarkably positive result, however, was tempered by another MitraClip randomized trial in a similar population that had a rather neutral result, the MITRA-FR (Percutaneous Repair with MitraClip Device for Severe Functional/Secondary Mitral Regurgitation) study, in which the MitraClip therapy failed to show any survival benefit over medical therapy during the 1-year follow-up period. One suggestion to reconcile the differences in outcome has been suggested wherein the MitraClip is ineffective if the echocardiographic regurgitant orifice size is consistent with the size of the dilated LV, but the device is effective if the regurgitant orifice size is large compared to the size of the LV. This seemed to be verified by the results of the two trials. The acceptance of the results from the COAPT trial is awaiting further confirmation.
In addition, vascular plugging and occluder devices are being used in selected patients to occlude perivalvular leaks around prosthetic mitral valves. A transcatheter stented valve, which is used as a transcatheter aortic valve replacement (TAVR) device, can be used to open a degenerated mitral bioprosthetic valve in any position (aortic, mitral, tricuspid, or pulmonary). Transcatheter valve replacement has also been attempted in small series to repair mitral regurgitation following mitral valve repair with mixed results. Finally, the first cases of a stented mitral valve prosthesis to replace the entire mitral valve have been reported. Abbott has initiated the SUMMIT trial, a US-based pivotal trial utilizing the Tendyne percutaneous mitral valve replacement device.