Mechanisms and predictors of mitral regurgitation after high-risk myocardial infarction.
BACKGROUND
Mitral regurgitation (MR) has been associated with adverse outcomes after myocardial infarction (MI). Without structural valve disease, functional MR has been related to left ventricular (LV) remodeling and geometric deformation of the mitral apparatus. The aims of this study were to elucidate the mechanistic components of MR after high-risk MI and to identify predictors of MR progression during follow-up.


METHODS
The Valsartan in Acute Myocardial Infarction Echo substudy prospectively enrolled 610 patients with LV dysfunction, heart failure, or both after MI. MR at baseline, 1 month, and 20 months was quantified by mapping jet expansion in the left atrium in 341 patients with good-quality echocardiograms. Indices of LV remodeling, left atrial size, and diastolic function and parameters of mitral valve deformation, including tenting area, coaptation depth, anterior leaflet concavity, annular diameters, and contractility, were assessed and related to baseline MR. The progression of MR was further analyzed, and predictors of worsening among the baseline characteristics were identified.


RESULTS
Tenting area, coaptation depth, annular dilatation, and left atrial size were all associated with the degree of baseline MR. Tenting area was the only significant and independent predictor of worsening MR; a tenting area of 4 cm(2) was a useful cutoff to identify worsening of MR after MI and moderate to severe MR after 20 months.


CONCLUSIONS
Increased mitral tenting and larger mitral annular area are determinants of MR degree at baseline, and tenting area is an independent predictor of progression of MR after MI. Although LV remodeling itself contributes to ischemic MR, this influence is directly dependent on alterations in mitral geometry.
Cardiovascular Division, Brigham and Women's Hospital, Boston, Massachusetts 02115, USA.
Alessandra
A
Meris
Maria
M
Amigoni
Anil
A
Verma
Jens Jakob
JJ
Thune
Lars
L
Køber
Eric
E
Velazquez
John J V
JJ
McMurray
Marc A
MA
Pfeffer
Robert
R
Califf
Robert A
RA
Levine
Scott D
SD
Solomon
D000328:Adult; D000367:Age Factors; D000368:Aged; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use*; D002216:Captopril / Q000627:therapeutic use; D018450:Disease Progression; D018618:Echocardiography, Doppler, Color / Q000379:methods*; D004562:Electrocardiography / Q000379:methods; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D008297:Male; D008875:Middle Aged; D008944:Mitral Valve Insufficiency / Q000000981:diagnostic imaging* / Q000453:epidemiology / Q000209:etiology; D008991:Monitoring, Physiologic / Q000379:methods; D015999:Multivariate Analysis; D009203:Myocardial Infarction / Q000150:complications* / Q000175:diagnosis / Q000188:drug therapy*; D011237:Predictive Value of Tests; D011446:Prospective Studies; D012372:ROC Curve; D012016:Reference Values; D015203:Reproducibility of Results; D018570:Risk Assessment; D012720:Severity of Illness Index; D012737:Sex Factors; D018709:Statistics, Nonparametric; D013318:Stroke Volume / Q000502:physiology; D013777:Tetrazoles / Q000627:therapeutic use; D013997:Time Factors; D014633:Valine / Q000031:analogs & derivatives / Q000627:therapeutic use; D000068756:Valsartan; D018487:Ventricular Dysfunction, Left / Q000000981:diagnostic imaging / Q000453:epidemiology / Q000209:etiology; D020257:Ventricular Remodeling / Q000502:physiology
D000806:Angiotensin-Converting Enzyme Inhibitors; D013777:Tetrazoles; D000068756:Valsartan; D002216:Captopril; D014633:Valine