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European Heart Journal Advance Access originally published online on January 24, 2007
European Heart Journal 2007 28(3):326-333; doi:10.1093/eurheartj/ehl464
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© The European Society of Cardiology 2007. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org

Mitral regurgitation in myocardial infarction complicated by heart failure, left ventricular dysfunction, or both: prognostic significance and relation to ventricular size and function

Maria Amigoni1,*,{dagger}, Alessandra Meris1,{dagger}, Jens Jakob Thune1, Deepa Mangalat1, Hicham Skali1, Mikhail Bourgoun1, J. Wayne Warnica2, Stale Barvik3, J. Malcolm O. Arnold4, Eric J. Velazquez5, Frans Van de Werf6, Jalal Ghali7, John J.V. McMurray8, Lars Køber9, Marc A. Pfeffer1 and Scott D. Solomon1

1 Brigham and Women's Hospital, Boston, Massachusetts, USA
2 Foothills Hospital, Calgary, Canada
3 Central Hospital in Rogaland, Stavanger, Norway
4 London Health Sciences Center-Victoria Campus, East London, Canada
5 Duke University Medical Center, Durham, North Carolina, USA
6 Leuven Coordinating Center, Leuven, Belgium
7 Cardiac Centers of Louisiana, Shreveport, Louisiana, USA
8 Western Infirmary, Glasgow, Scotland
9 University of Copenhagen Rigshospitalet, Copenhagen, Denmark

Received 22 April 2006; revised 24 October 2006; accepted 14 December 2006; online publish-ahead-of-print 24 January 2007.

* Corresponding author. Tel: +39 328 4090281. E-mail address: maria_amigoni{at}libero.it


   Abstract
Top
 Abstract
Introduction
 Methods
 Results
 Discussion
 Acknowledgements
 References
 
Aims Mitral regurgitation (MR) confers independent risk in patients with acute myocardial infarction. We utilized data from the VALsartan In Acute myocardial iNfarcTion echo study to relate baseline MR to left ventricular (LV) size, shape, and function, and to assess the relationship between baseline MR and progression of MR and cardiovascular (CV) outcomes.

Methods and results We studied 496 patients with heart failure (HF) and/or systolic dysfunction after MI who underwent echocardiography at a median of 5 days after MI. MR severity, quantified as the regurgitant jet area/left atrial area ratio, was assessed at baseline, one and 20 months post-MI and related to LV size, shape, function, and clinical outcomes. Increased MR at baseline was associated with larger LV end-diastolic and end-systolic volumes, increased sphericity index, and reduced ejection fraction (P trend < 0.001). Moderate–severe MR was an independent predictor of total mortality [adjusted hazard ratio (HR) 2.4 (1.1–5.3)], CV mortality [adjusted HR 2.7 (1.2–6.1)], hospitalization for HF [adjusted HR 2.5 (1.1–5.5)], or death or HF hospitalization [adjusted HR 2.5 (1.4–4.6)]. Patients with progression of MR during the first post-MI month were substantially more likely to die or develop HF (adjusted HR per increased MR grade 3.0, 95% CI 1.8–4.9). Progression of MR over 20 months in survivors was associated with increased hospitalizations for HF (P < 0.001).

Conclusion Following high-risk myocardial infarction, baseline mitral regurgitant severity is associated with larger LV volumes and worse LV function. Both baseline MR severity and progression of MR are associated with an increased likelihood of adverse outcomes.

Key Words: VALsartan In Acute myocardial iNfarcTion • Echocardiography • Mitral regurgitation • Left ventricular shape and function • Prognosis


   Introduction
Top
 Abstract
 Introduction
Methods
 Results
 Discussion
 Acknowledgements
 References
 
Left ventricular (LV) remodelling after myocardial infarction (MI) can lead to apical and posterior displacement of the papillary muscles with resulting malcoaptation of the mitral leaflets and valvular insufficiency.1–4 Similar mechanisms appear to contribute to the functional mitral regurgitation (MR) seen often as a complication of systolic LV dysfunction (LVSD).5,6 In the acute and in the chronic phase after MI, MR has been shown to be associated with poor outcomes,4,7,8 as is the case in patients with LV systolic dysfunction of other etiologies.9,10

The VALsartan In Acute myocardial iNfarcTion (VALIANT) trial enrolled patients with acute myocardial infarction complicated by LVSD, heart failure (HF), or both.11 We studied patients in the VALIANT echocardiographic substudy to determine the incidence and prognostic implications of MR following high-risk myocardial infarction, and to study the prognostic significance of progression of MR after infarction.


   Methods
Top
 Abstract
 Introduction
 Methods
Results
 Discussion
 Acknowledgements
 References
 
Study population
The VALIANT study enrolled 14 703 patients with LVSD [ejection fraction (EF) < 35% on echocardiography or < 40% on contrast angiography], clinical signs of HF or both, and randomized these patients to receive valsartan (target dose, 160 mg twice daily), captopril (target dose, 50 mg three times daily), or a combination of valsartan and captopril (target dose, 80 mg twice daily and 50 mg three times daily, respectively).11 All patients gave their written informed consent, and the protocol was approved by the appropriate institutional review boards. The VALIANT Echo study was designed and powered prospectively to test the hypothesis that the angiotensin receptor blocker valsartan, either alone or combination with captopril, could attenuate progressive LV enlargement or improve LV function to a greater extent than captopril alone.12 Patients were eligible if they had a myocardial infarction and evidence of LVSD (EF < 35% on echocardiography or < 40% on contrast angiography), HF or both, identical criteria to those for the main VALIANT study. All clinical sites participating in the main VALIANT study were invited to participate in the VALIANT echocardiographic substudy, and all patients enrolled in the VALIANT trial at participating sites were eligible for inclusion in the echo study.

Patients enrolled in the echocardiographic substudy (n = 603) underwent two-dimensional echocardiography at a median of 5 (IQR 3–7) days after MI (prior to randomization). Assessment of MR by colourflow Doppler was possible in 496 patients, and not possible in 107 patients because of absence of colourflow Doppler or echocardiographic images of insufficient quality. Echocardiographic data were available in 419 patients at one month, and in 341 patients at 20 months.

Echocardiographic assessment
All two-dimensional echocardiograms were analysed by the core laboratory at the Brigham and Women's hospital. Echocardiograms from videotape were digitized and analyses were performed utilizing an offline analysis workstation. LV volumes and EFs were calculated in the usual fashion, as previously described.12 Infarct location was assessed by determining the location of hypokinesis, akinesis, or dyskinesis.

The LV sphericity index was calculated as the ratio of LV volume (end diastolic and end systolic) and the volume of a sphere with a diameter equal to the LV (end diastolic and end systolic) long axis (sphericity index = 6V/{pi}L3).13 Mitral annular diameter was measured in four and two-chambers views at end diastole and end systole from three separate cardiac cycles, and annular areas were calculated by using an ellipsoid assumption (annular area = d1 x d2 x {pi}/4).6,14 Mitral annular contraction was defined as mitral end-diastolic annular area – mitral end-systolic annular area/mitral end-diastolic annular area.

MR was categorized mapping jet expansion in the left atrium (LA) in four and two-chamber views at end systole from three separate cardiac cycles. MR was considered mild when the regurgitant jet area occupied > 5% and < 20% of the left atrial area, moderate when regurgitant jet area occupied > 20% and < 40%, and severe when regurgitant jet area occupied > 40% of the left atrial area.15,16 The grade of MR was increased by one degree (mild to moderate, moderate to severe) in the setting of an eccentric mitral regurgitant jet based on evidence of reduced colourflow jet areas due to loss of momentum in jets adjacent to chamber walls.17

LA volume was assessed by the biplane area-length method from apical 4- and 2-chamber views at end systole from the frame preceding mitral valve opening. LA volume index was calculated as LA volume/body surface area (mL/m2). Mitral flow velocity was assessed by transmitral pulsed wave Doppler study from the apical four chambers view with measurement of the E- and A-waves (in sinus rhythm) velocity, their ratio and the deceleration time of the E-wave.

Statistical methods
The intraobserver reproducibility of the MR measurement was assessed by the primary reader performing two sets of MR measurements in 15% of patients, randomly selected, in a blinded fashion. The Bland-Altman coefficient of repeatability was 1%.18 We used linear-regression analysis to examine trends in clinical and echocardiographic characteristics across three MR groups, considering MR as an ordinal variable. The median follow-up time was 24.7 months. Clinical outcomes were adjudicated by an independent Clinical Endpoints Committee. Event rates were calculated using survival time data and expressed as events per 100 patient-years. We evaluated the effect of MR severity on outcomes of interest using Cox-proportional hazard regression models, adjusting for the most powerful covariate predictors of mortality identified from the overall VALIANT study. These were selected using both forward stepwise and backwards variable selection techniques applied to 70 baseline covariates, and validated with bootstrap resampling,19 with the most important baseline demographic and echocardiographic baseline covariates included in the models [age, gender, heart rate, Killip class, percutaneous coronary intervention (PTCI) after MI, diabetes, history of HF, history of MI, renal insufficiency, EF, LV diastolic volume, left atrial volume]. A P-value < 0.05 was considered statistically significant.


   Results
Top
 Abstract
 Introduction
 Methods
 Results
Discussion
 Acknowledgements
 References
 
Baseline clinical characteristics
Baseline characteristics in the MR cohort and the remainder of the VALIANT cohort are shown in Table 1. Patients in the MR cohort differed minimally from the overall VALIANT cohort, and were similar with respect to gender, BMI, Killip class, history of myocardial infarction, hypertension, diabetes, HF, smoking, infarct location, infarct type (Q-wave or non-Q-wave), and thrombolytic therapy. The MR cohort had slightly lower age, systolic and diastolic blood pressures, slightly higher rate of PTCI, and slightly higher use of ACE inhibitors and beta-blockers pre-randomization.


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  		Table 1 Baseline characteristics of VALIANT patients not included in the echo cohort, and in patients included in the echo cohort with MR assessed

 
At baseline, MR was absent by colourflow Doppler echocardiography in 231 patients (46.6%), mild in 202 patients (40.7%), moderate in 49 (9.9%), and severe in 14 (2.8%). Patients with moderate and severe MR were grouped together because of small numbers in these groups (MR moderate–severe: n = 63, 12.7%). No patient had evidence of significant structural valvular disease.

MR severity at baseline was associated with older age, female sex, history of MI, hypertension, diabetes, HF, and a non-Q-wave infarction (Table 2). Anterior infarction was less prevalent with increasing MR. Baseline medication use was similar in the three groups.


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  		Table 2 Baseline characteristics of the study population divided according to the severity of MR

 
Echocardiographic characteristics
LV end-diastolic and end-systolic volumes were significantly increased, and EF significantly reduced, in patients with worse MR at baseline (Table 3). The LVs of patients with worse MR were significantly more spherical, and patients with worse MR had significant increases in diastolic and systolic mitral annular areas (MAAs), reduced annular contractility, and increased LA volume index. E-wave and E/A ratio were increased, and deceleration time was reduced in patients with worsening MR.


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  		Table 3 Echocardiographic characteristics of the study population divided according to the severity of MR

 
Relationship between baseline MR and clinicaloutcomes
In this cohort, 84 (16.9%) patients died [75 cardiovascular (CV)], 79 (15.9%) patients were hospitalized for HF, 134 (27%) patients either died or developed HF, and 50 (10.1%) patients had recurrent myocardial infarction. Any MR at baseline was associated with increased long-term mortality, CV death, hospitalization for HF, and death or HF hospitalization (Table 4). In a multivariable model adjusting for independent clinical and echocardiographic variables known to be predictive of outcome, the presence of any MR was found to be independently associated with long-term mortality [hazard ratio (HR) (95% CI), 1.81 (1.05–3.11), P = 0.03], CV mortality [HR (95% CI), 1.93 (1.08–3.45), P = 0.02], hospitalization for HF [HR (95% CI), 1.90 (1.08–3.34), P = 0.02], and death or HF hospitalization [HR (95% CI), 1.72 (1.12–2.64), P = 0.01]. An increased risk of adverse outcome was significantly associated with worsening MR grade (Figure 1 and 2, Table 5). Baseline MR degree was associated with an increased number of total episodes of HF (Figure 3, P trend < 0.001).


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  		Table 4 Multivariable analysis of variables predictive of all-cause mortality

 

Figure 4641
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  		Figure 1 Kaplan–Meier survival curves divided according to the severity of MR. P < 0.001 by Logrank test.

 

Figure 4642
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  		Figure 2 Kaplan–Meier curve for death or hospitalization for HF by severity of MR. P < 0.001 by Logrank test.

 

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  		Table 5 Moderate/severe MR and risk of adverse events

 

Figure 4643
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  		Figure 3 HF episodes (per patient-year) on follow-up by MR severity at baseline.

 
Progression of MR and outcomes
MR jet to LA area ratio increased from 7.6 ± 8.7% to 9.9 ± 9.9% in 419 patients whose MR could be evaluated at 1 month after MI. In 341 patients with completed echocardiographic follow-up at 20 months, MR jet to LA area ratio increased from 6.7 ± 7.8% at baseline to 9.1 ± 9.5% at 20 months. Progression of MR from baseline to 1 month was associated with a significantly increased risk of death or HF hospitalization (adjusted HR per unit increase in MR jet/LA area ratio: 1.04, 95% CI 1.02–1.07, P = 0.002; adjusted HR per increase in MR grade: 3.0, 95% CI, 1.8–4.9, P < 0.001; Table 6). In patients who survived and underwent a 20-month echocardiogram, MR progression was greater in those with one or more episodes of hospitalization for HF during that period than in patients who were event-free (MR jet/LA Area Ratio 7.8 ± 11.3 vs. 1.5 ± 7.7, P < 0.001). There were no differences in progression of MR at either one or 20-months based on treatment assignment.


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  		Table 6 Relationship between changes in MR from baseline to 1 month and subsequent death or development of HF

 

   Discussion
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
Acknowledgements
 References
 
In patients with LVSD, HF, or both after acute MI, the degree of MR at baseline is associated with worse LV function, greater LV enlargement and chamber distortion, increased MAA and worse mitral annular contraction. The presence and degree of MR at baseline was significantly and independently associated with mortality and other adverse clinical outcomes. Moreover, worsening of MR between baseline and 1 month was associated with an increased risk of adverse outcomes, and patients whose MR progressed over the 20-month follow-up period had increased hospitalizations for HF during that period.

MR has been shown to have independent prognostic value after acute and chronic MI.3,7,20,21 In the majority of patients with MR following MI, the MR is functional rather than due to inherent abnormalities of the mitral valve apparatus. In these individuals, the papillary muscles, chordae, and valve leaflets are normal, but distortion of ventricular geometry displaces the attachments of the mitral leaflets to the papillary muscles and annulus thereby restricting their ability to close effectively at the annular level, with resulting decrease in the LV-generated leaflet-closing force.22,23

In the present study, as previously shown, worse MR was more common in older people,3,4,7,20,24,25 women4,16,26, and in those with previous MI.3 In contrast to other studies, we observed no clear relationship between severity of MR and infarct location.27 Our data suggest that increased chamber sphericity may cause MR by lateral migration of the papillary muscles resulting in disadvantageous alignment of the papillary muscles apparatus relative to the mitral leaflets,28 and are consistent with recent studies in which the most important determinant for the development of MR in patients with acute MI and in patients with LVSD was local LV remodelling.6,29

Our data demonstrate that a higher degree of MR is independently associated with an increased risk of mortality, CV mortality, and hospitalization for HF, even after adjusting for the most important known covariates. The early separation of the survival curves suggests that a higher degree of MR is a predictor of early outcome, adding incremental prognostic value over the other known predictors of outcome, including echocardiographic measures, such as EF and ventricular volume.

Moreover, we found that progression of MR, even within the first month after infarction, was associated with an increased risk of adverse outcomes. Worsening of MR during this early period may be a sensitive marker of early changes in ventricular geometry that might predispose to adverse outcome. While long-term worsening of MR was associated with increased HF, these data are inherently limited by survivor bias, as many patients with the worst degree of MR at baseline and 1 month died prior to the 20-month echocardiogram. Nevertheless, our data underscore the importance of detecting and quantifying and following the presence of MR after MI in patients with signs or symptoms of LVSD. Whether acute pharmacologic, surgical, or even percutaneous interventions might influence the progression of MR is not known.30–33

Some limitations of this study should be noted. We graded MR by colourflow Doppler, mapping regurgitant jet expansion within the LA, a method that may have resulted in misclassification of MR in some patients. More rigorous evaluation of regurgitant mitral lesions is possible using volumetric-based techniques such as proximal isovelocity surface area (PISA) method, but the necessary images for this technically more challenging and less widely used technique were not available in VALIANT, an international, multicenter clinical trial. Nevertheless, in a direct comparison of techniques in a single centre, the mitral jet area to LA ratio correlated well with effective regurgitant orifice area determined by the PISA method.34 Finally, assessment of sphericity is limited by potential ventricular foreshortening.

In conclusion, we observed that even mild MR was associated with increased ventricular size, worse ventricular function, and alterations in ventricular geometry in patients with acute MI complicated by systolic dysfunction, HF, or both. Early post-infarct MR was an independent and important predictor of death or development of HF following MI, and progression of MR, even during the first month post-MI, was a potent predictor of subsequent outcome. Accurate assessment of MR and its progression following MI may help identify a particularly high-risk group who may benefit from aggressive adjunctive therapy.


   Acknowledgements
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 Acknowledgements
References
 
The VALIANT trial was funded by a grant from Novartis Pharmaceutical Corporation, East Hanover, New Jersey. W.W., S.B., J.M.O.A., E.J.V., F.V.de W., J.G., J.J.V.M., L.K., M.A.P., and S.D.S. received research support from Novartis Pharmaceuticals.

Conflict of interest: M.A., A.M., J.J.T., D.M., H.S., and M.B. have no conflicts of interest.


   Footnotes
 
{dagger} The first two others have contributed equally to this paper. Back

This paper was guest edited by Prof. Jeroen J. Bax, Leiden University Medical Center, Leiden, The Netherlands


   References
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 Acknowledgements
 References
 

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