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COMMENTARY
Year : 2016  |  Volume : 9  |  Issue : 5  |  Page : 615-616  

Prognostic significance of mitral regurgitation after myocardial infarction: An echocardiography-based study


1 Department of Cardiology, 5 Air Force Hospital, Jorhat, Assam, India
2 Department of Cardiology, Army College of Medical Sciences, New  Delhi, India

Date of Web Publication13-Oct-2016

Correspondence Address:
Anil Kumar
5 Air Force Hospital, Jorhat - 785  005, Assam
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0975-2870.192140

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How to cite this article:
Kumar A, Mahesh N K. Prognostic significance of mitral regurgitation after myocardial infarction: An echocardiography-based study. Med J DY Patil Univ 2016;9:615-6

How to cite this URL:
Kumar A, Mahesh N K. Prognostic significance of mitral regurgitation after myocardial infarction: An echocardiography-based study. Med J DY Patil Univ [serial online] 2016 [cited 2024 Mar 29];9:615-6. Available from: https://journals.lww.com/mjdy/pages/default.aspx/text.asp?2016/9/5/615/192140



Mitral regurgitation (MR) is a frequent complication during and after the acute phase of myocardial infarction (MI), with reported incidences ranging from 3.4% to 35%.[1],[2] It has been proved to be a predictor of the long-term cardiovascular mortality after an acute myocardial infarction (AMI).

When present, it may exhibit a broad range of severity, from clinically evident and hemodynamically obvious to clinically silent and detected only as an incidental finding on catheterization or Doppler echocardiography. Indeed, when it is sought by Doppler,[3] MR has been reported to occur in up to 39% of patients with MI. Papillary muscle dysfunction and associated dysfunction of the underlying ventricular wall are thought to be the most common cause of MR in post-AMI patients,[4],[5] and MR has generally been identified as a more frequent complication of inferior than anterior infarction. Although severe MR may place an additional hemodynamic stress on the left ventricle (LV), its prognostic significance independent of LV function has been controversial.[5] Barzilai et al.[3] found that AMI patients with a murmur suggestive of MR had a 12-month mortality of 36% compared with 15% for patients without an MR murmur. However, correction for differences in baseline variables indicated that the presence of an MR murmur was not an independent predictor of outcome. In contrast, Lehmann et al.[1] found that MR present on left ventriculography within 7 h of MI was an independent predictor of survival at 1 year. Tcheng et al.[6] also found that moderately severe to severe MR appeared to be the likely independent predictor of impaired survival.

Mittal et al.[4] speculated that papillary muscle dysfunction alone is insufficient to cause MR after MI and that an underlying wall motion abnormality is needed. Others have supported this hypothesis [5] by reporting that in dogs, hypokinesia of the ventricular segment overlying the papillary muscle, which leads to retraction of the mitral leaflets toward the apex, is a sufficient condition to produce MR. Earlier studies have emphasized that MR in ischemic heart disease is most prominent in patients with inferior or inferoposterior infarctions.[7] This has been postulated to be due to the particular vulnerability of the posterior papillary muscle to its blood supply.

It has been seen in studies that patients having MR are more likely to have multivessel disease as compared to patients not having MR who have commonly single-vessel disease.

The importance of mild MR could be addressed in the SAVE study because SAVE entry criteria excluded patients with severe MR. Furthermore, extensive additional data were available regarding demographics, clinical care during hospitalization, physical findings, coronary anatomy, and most importantly, LV volumes and geometry. Univariate analyses revealed that patients with MR had larger LV volumes, more spherical LV chambers, and more severe coronary disease than patients without MR. A multivariate analysis that included coronary anatomy, LVEF, and extent of coronary disease found MR to be an independent predictor of cardiovascular mortality.

There are several potential reasons why mild MR is an independent predictor of cardiovascular outcome. The present study convincingly demonstrates that patients with larger, more geometrically abnormal LVs are more likely to have MR despite similar systolic function as defined by LVEF. Mild MR is a marker of these geometric abnormalities. Thus, although mild MR may not present a severe hemodynamic load due to simple valvular regurgitation, the noninfarcted myocardium of these ventricles is laboring under a severe hemodynamic load because of the marked geometric abnormalities present in MR patients. There also may be additional abnormalities of LV function or geometry that were undetected by the present single-plane analyses, for which MR, therefore, is a marker.

Acute pharmacological or mechanical reperfusion therapy has been reported to reverse acute severe MR.[8] Thus, detecting MR with echocardiography in patients with AMI helps in the management of such cases as they may require early intervention and aggressive treatment.

 
  References Top

1.
Lehmann KG, Francis CK, Dodge HT. Mitral regurgitation in early myocardial infarction. Incidence, clinical detection, and prognostic implications. TIMI Study Group. Ann Intern Med 1992;117:10-7.  Back to cited text no. 1
    
2.
Lamas GA, Mitchell GF, Flaker GC, Smith SC Jr., Gersh BJ, Basta L, et al. Clinical significance of mitral regurgitation after acute myocardial infarction. Survival and Ventricular Enlargement Investigators. Circulation 1997;96:827-33.  Back to cited text no. 2
    
3.
Barzilai B, Gessler C Jr., Pérez JE, Schaab C, Jaffe AS. Significance of Doppler-detected mitral regurgitation in acute myocardial infarction. Am J Cardiol 1988;61:220-3.  Back to cited text no. 3
    
4.
Mittal AK, Langston M Jr., Cohn KE, Selzer A, Kerth WJ. Combined papillary muscle and left ventricular wall dysfunction as a cause of mitral regurgitation. An experimental study. Circulation 1971;44:174-80.  Back to cited text no. 4
    
5.
Kono T, Sabbah HN, Rosman H, Alam M, Jafri S, Stein PD, et al. Mechanism of functional mitral regurgitation during acute myocardial ischemia. J Am Coll Cardiol 1992;19:1101-5.  Back to cited text no. 5
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6.
Tcheng JE, Jackman JD Jr., Nelson CL, Gardner LH, Smith LR, Rankin JS, et al. Outcome of patients sustaining acute ischemic mitral regurgitation during myocardial infarction. Ann Intern Med 1992;117:18-24.  Back to cited text no. 6
    
7.
Estes EH Jr., Dalton FM, Entman ML, Dixon HB 2nd, Hackel DB. The anatomy and blood supply of the papillary muscles of the left ventricle. Am Heart J 1966;71:356-62.  Back to cited text no. 7
    
8.
Leor J, Feinberg MS, Vered Z, Hod H, Kaplinsky E, Goldbourt U, et al. Effect of thrombolytic therapy on the evolution of significant mitral regurgitation in patients with a first inferior myocardial infarction. J Am Coll Cardiol 1993;21:1661-6.  Back to cited text no. 8
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