Ischemic Mitral Regurgitation

Marc Katz, MD and D. Scott Lim, MD

1Medical University of South Carolina, Charleston, SC 29425, USA

2University of Virginia Health System, Charlottesville, VA, USA

Introduction

A 57-year-old man reported experiencing dyspnea after walking 100 feet that has been progressing despite medical therapy. He has two-pillow orthopnea and occasional nighttime dyspnea but no angina. He had an anterior myocardial infarction 5 years previously but did not seek medical care until 2 days after the event. Viability studies demonstrated only limited anterior wall viability.

– Electrocardiogram: sinus rhythm with left bundle branch block.

– Medications: furosemide, 120 mg twice daily;metolazone, 5 mg every other day; carvedilol,25 mg twice daily; lisinopril, 40 mg daily; spironolactone, 25 mg daily.

– Creatinine 2.2 mg/dL, blood urea nitrogen 76 mg/dL, B-type natriuretic peptide 1567 ng/L.

–PE: P 64: blood pressure 90/70 mmHg.

– Estimated central venous pressure 10 cm H2O.

– Chest: bilateral basilar rales.

– COR: S3; grade 1/6 holosystolic apical murmur.

–EXT: 1=ankle edema.

– Echocardiogram: anterior akinesis; ejection fraction 25%. Tethered anterior mitral lea flet; severe mitral regurgitation (MR).

– Tricuspid jet 4.1 m/s.

The patient underwent biventricular cardiac resynchronization therapy with modest improvement but again worsened symptomatically in 3 months.Echocardiography still demonstrates severe MR.

This patient demonstrates classic signs and symptoms of congestive heart failure with poor end organ perfusion, secondary to ischemic cardiomyopathy, following a completed anterior myocardial infarction. The insult, presumably an occlusion of the left anterior descending artery, has led to limited anterior wall viability and its subsequent akinesis.Given the relative hypotension and ejection fraction of 0.25, he likely has poor cardiac output. The anterior infarct also likely damaged the anterolateral papillary muscle and led to ventricular dilation with resultant tethering of the anterior mitral valve lea flet, leading to poor coaptation and severe MR.

This description paints a clear picture of secondary (or functional) MR. In secondary MR the lea flets are structurally intact, unlike in primary(or degenerative) MR, where the disorder is abnormality of the lea flets due to myxomatous changes,infection, or loss of support (chordal elongation or rupture). Secondary MR is a disease of the ventricle and/or annulus.

Ischemic or nonischemic cardiomyopathy leads to ventricular dilation and papillary muscle displacement, which causes lea flet tethering.Cardiomyopathy and atrial fibrillation can also cause annular dilation, distracting the zones of apposition at the lea flet edges. In the case of cardiomyopathies,poor ventricular systolic function also leads to lowered valve closing forces. The combination of one or more of these factors secondarily leads to poor mitral valve lea flet coaptation and regurgitation.

In the case of symmetric annular dilatation, the jet would likely be central (Carpentier type I). If one lea flet is tethered or an asymmetric area of remodeling is present, the jet would be directed anterior or posterior (Carpentier type IIIb) [1].

Post–myocardial infarction ischemic MR is an independent predictor of death, with death rates up to 40% [2, 3].

Diagnosis

Diagnosis primarily relies on echocardiography,both transthoracic and transesophageal. The transthoracic echocardiogram is the ideal measurement of the severity of functional MR, as the transesophageal echocardiogram can underestimate it, because of changes in loading conditions related to dehydration and sedation. The transesophageal echocardiogram is the ideal test for determination of the mechanism of the MR, and therefore potential therapeutic options. For consideration of surgical intervention as well as novel transcatheter options,cardiac computed tomography can also be helpful, particularly for determination of the extent and distribution of mitral annular calci fication. Cardiac magnetic resonance imaging can also be used to determine MR severity when echocardiography findings are not clear. Left-sided heart catheterization is useful in ischemic patients.

Treatment

Medical

Guideline-directed medical therapy (GDMT) is the first-line therapy for patients with secondary MR,with evidence supporting its survival bene fit [4].Therefore patients should be optimized with dosages of a beta blocker and neurohormonal antagonists, with reassessment of the severity of MR and symptoms after maximally tolerated doses have been reached. Some patients will have reduction in their degree of MR after undergoing GDMT.

Cardiac resynchronization therapy is a documented therapy for heart failure [5], although its utility in treating secondary MR is variable [6].

Surgery

Surgical options for secondary MR include valve repair, which encompasses a variety of potential techniques, and valve replacement. Historically,repair has been favored over replacement because of lower perioperative morbidity and mortality and preservation of the subvalvar apparatus with its presumed bene fit in maintenance of ventricular function [7]. The repair procedure most commonly performed is an undersized annuloplasty.

Two-year follow-up from the Cardiothoracic Surgical Trials Network randomized trial revealed that overall mortality was similar between repair and chordal sparing replacement. This trial also showed a very marked difference in the rate of recurrent MR, 59% in the repair group versus 4%in the replacement group over 2 years [8]. A basal aneurysm was present in 62% of the repair failures versus 20% without recurrent leak [9].

Chordal sparing mitral valve replacement provided a more durable correction in the setting of ischemic MR, which may have an effect on longterm outcomes [8].

Despite a poor prognosis with GDMT, most ischemic heart failure patients with secondary MR do not undergo surgery. Given the uncertain riskbene fit ratio, mitral valve surgery is uncommon in patients not requiring revascularization [10].

Transcatheter Devices

The MitraClip device was developed as a percutaneous means of recreating the edge-to-edge mitral valve repair as introduced by Al fieri et al. [11].

The EVEREST II trial compared surgical mitral valve repair with MitraClip in low surgical risk patients, finding that although MitraClip was safer, it was not as effective at reducing regurgitation as surgery. Only 27% of the patients in this trial had secondary MR, with the remaining having degenerative disease. In the 4-year follow-up study it was noted that although primary MR was treated more effectively with surgical repair, the outcomes for secondary MR were comparable with those for MitraClip [12]. Indeed, since its approval in Europe, more than 66% of MitraClip implants have been for secondary MR. From this standpoint, the multicenter COAPT trial was initiated to evaluate the role of MitraClip in patients with secondary MR in whom GDMT had failed:the trial recently completed enrollment and is in follow-up at present, with anticipated data release in 2019.

A variety of new devices that will enable transcatheter replacement of the mitral valve are currently beginning clinical trials. Other devices in various stages of development are focused on annuloplasty, and placement of neochordae.

Ischemic secondary MR is a complex process requiring the input of a multidisciplinary team that includes heart failure specialists, electrophysiologists, structural cardiologists, and cardiac surgeons. With the advent of newer technologies,hope is available for patients such as the one presented.

REFERENCES

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