Collateral-Dependent‚ÄàIschemic Mitral Regurgitation

ABSTRACT: There is much debate on the pathogenesis of ischemic mitral regurgitation (MR), usually related to global or regional left ventricular dysfunction or remodeling secondary to chronic ischemic changes, altering the tethering and closing forces on the mitral apparatus. There is a paucity of literature describing MR in the setting of acute ischemia. We describe a case in which the MR was dynamic and directly related to changes in coronary collateral flow. 

J INVASIVE CARDIOL 2014;26(3):E27-E28

 Key words: ischemia, mitral regurgitation, coronary collaterals

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Case Report. A 69-year-old woman with chronic lung disease and dyspnea was hospitalized for acute coronary syndrome with pulmonary congestion. Physical examination revealed signs of left and right heart failure. Electrocardiography showed sinus rhythm with non-specific ST-T changes.

Echocardiography (echo) demonstrated severe left ventricular (LV) dysfunction. The interventricular septum was deviated to the left (“D-sign”). As shown in Figure 1A, there was severe mitral regurgitation (MR). In addition, there was a moderate degree of tricuspid regurgitation (TR) with evidence of severe pulmonary hypertension (69 mm Hg), and hypokinesis of the right ventricle (RV). These findings were in sharp contrast to an echo performed 2 months previously, which showed mild LV dysfunction, mild MR, no TR or pulmonary hypertension, and normal RV function.

Coronary angiography was performed, revealing mild irregularities in the left main and left anterior descending (LAD) arteries, an occluded proximal circumflex (CX) artery (Figure 2) and a 70% stenosis in the mid-portion of the right coronary artery (RCA). There was very faint collateral filling of the distal CX artery from the LAD.

Bearing in mind the coronary anatomy, reduced LV function, and the presence of severe MR, it was decided to consider referring her for cardiac surgery.

Prior to surgery, a repeat echo was performed because of a marked clinical improvement. This demonstrated moderate to severe LV dysfunction, only very mild MR (Figure 1B), minimal TR, pulmonary pressure of 30 mm Hg, and a persistently hypokinetic RV.

Because of the greatly improved MR and the amenability of the CX to percutaneous coronary intervention, the patient was recatheterized. Initial angiography demonstrated well-developed collaterals to the CX from the RCA that were absent previously (Figure 3). A stent was successfully inserted into the CX.

A few days later, a MIBI SPECT isotope study was performed, demonstrating no ischemia, but a small fixed posterobasal and posterolateral defect, eliminating the need for intervention to the RCA. Of interest, the global LV ejection fraction was 58%.

Four months after PCI, she was still asymptomatic and a repeat echo demonstrated mild LV systolic dysfunction and mild MR. 

Discussion. Ischemic MR refers to functional MR (as opposed to organic damage to the valve apparatus), appearing as a result of LV remodeling due to ischemic heart disease (IHD).¹ The functional changes to the valve mechanism may also, in the long run, cause structural changes in the leaflets.² Ischemic MR results from an imbalance between increased tethering forces caused by alterations in the LV geometry as a result of infarction and reduced closing forces (due to decreased LV contractility, change in systolic annular contraction and reduced synchrony between the papillary muscles).¹ Although the term ischemic MR is used, it is usually a result of chronic changes brought about by IHD and generally speaking, no active ischemia is involved.

Ischemic MR, when present in chronic IHD, worsens the prognosis.³ As a result, its presence is essential to be addressed in addition to the coronary disease when planning therapy. The treatment modalities available include conservative medical therapy, cardiac resynchronization therapy (CRT), PCI, coronary artery bypass grafting (CABG), or CABG combined with MV repair or replacement. Newer modes of therapy have recently appeared (such as the MitraClip) that seem to be appropriate in specific cases.

CABG alone usually does not correct MR⁴ and even relatively mild or moderate residual MR is related to a greater mortality risk.⁵ Combined mitral repair and CABG improves functional class, LV function, and pulmonary artery pressure,⁶ but only recently has been proven to have a favorable effect on survival⁷ compared to PCI.

Regarding PCI for MR, the severity of the regurgitation may improve,⁸ but this has not been shown in all studies.⁹ Survival may also improve, although to a lesser extent than combined CABG and mitral annuloplasty.⁷

Very little has been published on PCI in acute ischemic MR. Heuser et al¹⁰ described 3 patients presenting with acute myocardial infarction (AMI) together with severe MR. In all cases, there was significant improvement clinically and in MR severity after successful PCI. Shawl et al¹¹ presented 5 patients with moderate or severe MR in the context of AMI. All underwent successful PCI (in 3 patients to a dominant CX and the others to a dominant RCA), with marked clinical and hemodynamic improvement and resolution of the MR.

Movahed et al¹² described a patient with an acute coronary syndrome who was found to have a stenotic CX artery. No-reflow developed during PCI, causing hemodynamic collapse and acute severe MR. Once the no-reflow phenomenon resolved, the patient made a swift clinical and hemodynamic recovery, including disappearance of the severe MR.

The patient we described is the first in the literature who developed severe MR as a result of an acute coronary syndrome due to CX occlusion, in whom significant  improvement in MR was observed due to greatly improved collateral flow to the occluded vessel, thereby obviating the need for surgery.

 References

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From the Cardiology Department, Soroka Medical Center and Ben-Gurion University of the Negev, Beer-Sheva, Israel.

Disclosure: The authors have completed and returned the ICMJE Form for Disclosure of Potential Conflicts of Interest. The authors report no conflicts of interest regarding the content herein.

Manuscript submitted August 15, 2013 and accepted September 30, 2013.

Address for correspondence: Reuben Ilia, MD, Director, Cardiology Department, Soroka University Medical Center, PO Box 151, Beer-Sheva, Israel. Email: iliar@bgu.ac.il