Published online before print May 12, 2008, doi: 10.1161/CIRCULATIONAHA.107.738625
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(Circulation. 2008;117:2591-2598.)
© 2008 American Heart Association, Inc.
Coronary Heart Disease |
Independent Prognostic Importance of a Restrictive Left Ventricular Filling Pattern After Myocardial Infarction
An Individual Patient Meta-Analysis: Meta-Analysis Research Group in Echocardiography Acute Myocardial Infarction
Correspondence to Dr Gillian Whalley, PhD, Department of Medicine, Faculty of Medicine and Health Sciences, University of Auckland, Private Bag 92 019, Auckland, New Zealand. E-mail g.whalley{at}auckland.ac.nz
Received September 13, 2007; accepted February 11, 2008.
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Abstract |
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Background— Restrictive mitral filling pattern (RFP), the most severe form of diastolic dysfunction, is a predictor of outcome after acute myocardial infarction (AMI). Low power has precluded a definite conclusion on the independent importance of RFP, especially when overall systolic function is preserved. We undertook an individual patient meta-analysis to determine whether RFP is predictive of mortality independently of LV ejection fraction (LVEF), end-systolic volume index, and Killip class in patients after AMI.
Methods and Results— Twelve prospective studies (3396 patients) assessing the relationship between prognosis and Doppler echocardiographic LV filling pattern in patients after AMI were included. Individual patient data from each study were extracted and collated into a single database for analysis. RFP was associated with higher all-cause mortality (hazard ratio, 2.67; 95% CI, 2.23 to 3.20; P<0.001) and remained an independent predictor in multivariate analysis with age, gender, and LVEF. The overall prevalence of RFP was 20% but was highest (36%) in the quartile of patients with lowest LVEF (<39%) and lowest (9%) in patients with the highest LVEF (>53%; P<0.0001). RFP remained significant within each quartile of LVEF, and no interaction was found for RFP and LVEF (P=0.42). RFP also predicted mortality in patients with above- and below-median end-systolic volume index (1575 patients) and in different Killip classes (1746 patients). Importantly, when diabetes, current medication, and prior AMI were included in the model, RFP remained an independent predictor of outcome.
Conclusions— Restrictive filling is an important independent predictor of mortality after AMI regardless of LVEF, end-systolic volume index, and Killip class.
Key Words: diastole • echocardiography • meta-analysis • mortality • myocardial infarction
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Introduction |
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Acute myocardial infarction (AMI) is characterized by regional myocardial damage with a subsequent risk of left ventricular (LV) remodeling, local and systemic neurohormonal activation, and vascular dysfunction. LV remodeling and systolic dysfunction after AMI have been the focus of research for several decades and have been recognized as important markers of outcome.1 Many modern therapies have been developed to prevent or reverse this adverse remodeling. The mechanisms leading to systolic dysfunction also would be anticipated to alter the filling dynamics of the LV both by direct effects on the rate of myofibrillar crosslink detachment during ventricular relaxation and by alterations in ventricular stiffness. LV filling may be assessed noninvasively by pulsed-wave Doppler assessment of blood flow velocities across the mitral valve.2 With mitral valve opening, the early inflow velocity will be determined largely by ventricular suction and the pressure gradient between the left atrium and LV.3,4 The time taken for the velocity to return to zero, mitral deceleration time, typically is 140 to 240 milliseconds, but with high filling pressures and increased chamber stiffness, early mitral filling will terminate abruptly, and deceleration time will be abnormally short, a pattern called restrictive.3,4
Editorial 2570
Clinical Perspective p 2598
Several studies,5–10 although not all,11–14 have suggested that a restrictive filling pattern is an independent predictor of poor outcome after AMI. However, the conclusions of these studies have been limited by small sample sizes and low overall event rates. This has precluded a definite conclusion on the independent importance of a restrictive filling pattern, especially when overall LV systolic function is preserved. To address this, the Meta-Analysis Research Group in Echocardiography (MeRGE) was formed for the purpose of collating the available prognostic data on Doppler assessment of mitral filling after AMI into an individual patient meta-analysis. The prespecified aim of the present analysis was to determine the difference in mortality between patients with nonrestrictive and restrictive filling patterns and, in particular, to determine whether this is independent of LV systolic function, LV volumes, and Killip class.
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Methods |
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Study Selection and Data Collection
The present study was designed as an individual patient meta-analysis of observational data and as such followed the Meta-Analysis of Observational Studies in Epidemiology (MOOSE) convention for study selection, collation of data, and analysis.15 The detailed protocol for selection of relevant studies, data processing, and analysis has been described.16 Briefly, 12 studies are included in this meta-analysis.5–14,17,18 Five eligible studies were not included because the data were inaccessible,19–23 leaving 3739 included patients (90% of all potentially eligible patients). To be eligible, studies needed to be prospective, to enroll patients with a documented AMI, to include Doppler echocardiographic assessment of mitral filling and systolic function, and to report mortality. Each original study was approved by the host Ethics Committee. Individual databases were collated, variables were identified, measurements were verified, and comparisons with individual reports were made. The prespecified primary end point was all-cause mortality, which was available for all but 1 study, for which only cardiovascular mortality was available.9 For the purposes of these analyses, these deaths were treated as all-cause mortality. A total of 3739 patients were identified, of whom 3396 (91%) were included in the final analysis. Of the 343 patients excluded, 82 (2.2%) were excluded because of atrial fibrillation and 261 (6.9%) because of incomplete data.
Definition of Restrictive Filling Pattern
Conventional pulsed-wave Doppler echocardiography was performed in the apical window with the Doppler sample volume placed at the tips of mitral leaflets during diastole. Patients were classified at the time of their echocardiography as restrictive filling (based on high E:A and/or shortened deceleration time), or if not classified (n=1695) within the individual studies, deceleration time <140 ms was considered suggestive of restrictive filling. Patients were dichotomized according to restrictive or nonrestrictive filling.
Measurement of Ejection Fraction and LV Volumes
In all patients, an assessment of systolic function was available. LV ejection fraction (LVEF) was estimated with validated quantitative (single or biplane planimetry) or semiquantitative methods, including wall motion score index in 799 patients using a previously validated algorithm.24,25 In a subgroup of 1575 patients, LV volumes indexed to body surface area were available, and targeted subgroup analysis was performed to evaluate the independence of restrictive filling pattern and end-systolic volume index (ESVi).
Analyses
The influence of the restrictive filling pattern on survival was analyzed with the Kaplan-Meier method and was assessed with the log-rank test in the whole group and in the group divided into quartiles of EF. The I2 statistic and 
2 test were used to assess heterogeneity among individual hazard ratios for each included study.26 Univariate hazard ratios were used to investigate the association between restrictive filling pattern and all-cause mortality in the whole group, the 2 groups divided by median ESVi, and the 3 groups divided by Killip class (I, II and III/IV).
Multivariate analyses to investigate independent predictors of all-cause mortality (or cardiovascular death when all-cause death was unavailable) were performed with the Cox proportional-hazards model. Information on LVEF, age, gender, and the presence of restrictive filling was available on all subjects and thus formed the core group of potential predictors. Further analysis included interaction terms for age, gender, and LVEF with restrictive filling. We used age in 10-year and LVEF in 10% bands to make the results clinically applicable. Three additional multivariate models allowed inclusion of some limited clinical data (previous AMI, diabetes, and current angiotensin-converting enzyme inhibitor or β-blocker use), LV ESVi, and Killip class, respectively. For the Killip class analysis, Killip class I was used as the reference group.
Comparisons of continuous variables were made with the 2-sample Student t test or ANOVA as appropriate and of categorical variables with the 2 test. All analyses were performed within SAS version 9.1 (SAS Institute, Cary, NC).
The authors had full access to and take responsibility for the integrity of the data. All principal collaborators (see the Appendix) have read and agree to the manuscript as written.
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Results |
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The baseline characteristics of the group are shown in Table 1. Overall, the average age was 64 years; approximately three quarters were male; mean LVEF was 46% (SD, 11%); and restrictive filling was present in 670 patients (20%). Patients with restrictive filling were characterized by more frequent history of diabetes, prior AMI, hyperlipidemia, and higher Killip class during admission and were more likely to have sustained an anterior AMI (Table 1). Patients with restrictive filling also had larger LV volumes and lower LVEF. During follow-up, 192 patients (29%) with restrictive filling and 307 patients (11%) with nonrestrictive filling died (univariate hazard ratio, 2.67; 95% CI, 2.23 to 3.20; P<0.001; Figure 1). The 90% survival times were 39 days in the restrictive filling group and 802 days in the nonrestrictive group. Comparing the individual hazard ratios for each included study did not identify important heterogeneity (I2=0.042; P=0.06).
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When patients were divided into quartiles on the basis of LVEF, patients with the lowest LVEF were older and had prior AMI more frequently, a higher incidence of anterior AMI, a higher Killip class, and a larger LV volume (Table 2). In addition, the prevalence of restrictive filling increased with lower LVEF, and the overall death rate was higher with lower LVEF. However, the relationship between mortality and restrictive filling remained significant within each quartile of LVEF (Figure 2), and no significant interaction with LVEF was found for the risk of death associated with restrictive filling (P=0.42). The 90% survival times were shortest in the lowest LVEF group, but within each quartile, the time was markedly reduced when patients with restrictive filling were compared with nonrestrictive filling (quartile 1: restrictive, 10 days; nonrestrictive, 182 days; quartile 2: restrictive, 267 days; nonrestrictive, 736 days; quartile 3: restrictive, 284 days; nonrestrictive, 1080 days; and quartile 4: restrictive, 126 days; nonrestrictive, 1183 days).
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LV ESVi was available in 1575 patients. Restrictive filling pattern was seen most frequently in patients with LV ESVi greater than the median of 35 mL/m2 (287 patients [36%] versus 118 [15%]; P<0.0001). Regardless of LV ESVi, a restrictive filling pattern was a predictor of outcome (Figure 3, top). Patients with small LV volumes and nonrestrictive filling experienced the longest 90% survival times (1461 versus 472 days); patients with above-median volumes had shorter 90% survival times (225 and 916 days in the restrictive and nonrestrictive filling groups, respectively).
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In a subgroup of 1746 patients (51%), Killip class was recorded at admission and/or during hospitalization. In-hospital heart failure was seen in 204 patients (61%) with restrictive filling but in 425 (30%) with nonrestrictive filling (P<0.0001. A restrictive filling pattern was seen in 12%, 28%, and 45% of patients in Killip class I, II, and III or IV, respectively (P<0.0001). Regardless of Killip class, restrictive filling was a predictor of outcome (Figure 3, bottom) with no significant interaction (P=0.99). The lowest 90% survival time was observed in the group with Killip class III and IV: 2 days for the restrictive filling group and 4 days for the nonrestrictive group. In Killip class II, the 90% survival times were 46 days for restrictive and 182 days for nonrestrictive; in Killip class I, 90% survival times were 218 days for restrictive and 1335 days for nonrestrictive.
In multivariate analysis, which included age, gender, and LVEF, restrictive filling pattern remained an independent predictor of outcome (Table 3). No significant interaction with gender (P=0.90) or age (P=0.74) was found for the risk of death associated with restrictive filling. This was true when LVEF was entered in 10% increments and when used as a dichotomous variable (less than the median value). When clinical data were added to the model, restrictive filling remained a significant predictor of outcome, but the presence of diabetes also was associated with worse outcome, and current use of either angiotensin-converting enzyme inhibitors or β-blockers was associated with better mortality (Table 3). Previous AMI did not remain significant in the model.
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ESVi offered no additional prognostic information to the presence of restrictive filling in the multivariate model (Table 3). In a multivariate model that included Killip class, restrictive filling remained an independent predictor of all-cause mortality (Table 3).
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Discussion |
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This unique international collaboration, which compiled the largest data set ever to prospectively study the independent influence of restrictive LV filling in patients after AMI, has several important findings. First, this study has confirmed with considerably greater power than any previous study the important individual prognostic power of a restrictive filling pattern, with a nearly 3-fold unadjusted increase in the risk of death. Importantly, the present study demonstrates for the first time that restrictive filling is predictive of adverse outcome after AMI even in the presence of preserved LVEF. In light of the growing burden of patients with heart failure and apparently preserved LVEF, this observation could have important implications for our understanding of the development of heart failure in these patients. Finally, we demonstrate that a restrictive filling pattern provides incremental prognostic information to LV volumes and the presence and severity of in hospital heart failure. The 90% survival times associated with restrictive filling were consistently lower than those for nonrestrictive filling in the whole group and when divided by LVEF, LV volumes, and Killip class, supporting its prognostic power in a wide range of patients after AMI.
The transmitral inflow pattern is determined mainly by the interplay between left atrial pressure, LV relaxation, and LV compliance. In vitro experimental animal and human studies have suggested that with increasing LV chamber stiffness (low operating compliance), mitral deceleration time will be shortened.27–29 With low operating compliance, filling will occur on the steep portion of the diastolic pressure-volume relationship. Thus, the ventricle will fill only at very high pressures. This explains the high predictive value of a short deceleration time to detect increased filling pressure.30,31 This may also provide an important link between restrictive filling and poor outcome through several mechanisms. A low LV operating compliance and a high filling pressure are associated with increased risk of pulmonary congestion and may be associated with increased wall stress. This is in turn associated with poorer subendocardial perfusion, reduced energy production, and reduced risk of adverse LV remodeling. In agreement, several studies have demonstrated progressive ventricular dilatation in patients with restrictive filling9,14,22,23 even in the presence of a patent infarct-related coronary artery.32 Finally, low chamber compliance and increased filling pressures are closely associated with sympathetic and neurohormonal activation.33 In agreement with this, we found that restrictive filling predicted all-cause mortality independently of other known risk markers.
A pertinent question is why some patients develop a restrictive filling pattern whereas others do not despite infarcts of similar sizes as judged from regional wall motion analyses and global LVEF. Our data show that patients with restrictive filling are characterized by a higher risk of atherosclerotic risk factors. It could therefore be speculated that many patients who develop restrictive filling after AMI had abnormal ventricular filling before the index AMI resulting from vascular dysfunction and intrinsic abnormal myocardial function resulting from hypertrophy and fibrosis. This may also help explain why some patients with what seems to be a minor myocardial infarction develop a restrictive filling pattern.
Management of AMI usually includes a measure of infarct size and systolic function. The findings from the present study suggest that routine assessment should extend to assessment of diastolic filling. Although it remains clear that patients with dilated LV cavities and low LVEF have poor long-term survival, the present study suggests that it is possible to further differentiate within this group and to identify a high-risk group of patients within the group previously considered low risk: those without significant LV remodeling. This approach, which relies only on mitral inflow deceleration time, is simple and requires little in the way of advanced equipment or imaging.
The present study has limitations. Although all patients had documented AMI, different inclusion criteria were used. Thus, the true prevalence of restrictive filling in unselected patients with AMI cannot be assessed from the present data. The present result may be subject to publication bias. However, inspection of the funnel plot of the individual hazard ratios for each included study failed to identify important heterogeneity (I2=0.042, P=0.06). In addition, a small number of published studies were unable to be included (
10% of all patients reported in published studies). The timing of echocardiography was variable in the studies but was always within 2 weeks of the index AMI. Better differentiation of at-risk patients is achieved with longer time between the ischemic event and echocardiography.14 However, despite these factors, the different inclusion criteria, and major temporal changes in the management of AMI, the risk associated with restrictive filling was strikingly consistent. This study used very simple Doppler assessment of diastolic filling, and although significant results were obtained, the addition of more advanced diastolic parameters such as tissue Doppler and mitral flow propagation velocity may offer additional benefit, especially for identifying other diastolic filling patterns. Diastolic filling patterns can be challenging in an older population. However, the normal aging process seems to be associated with a lengthening rather than a shortening of the mitral deceleration time. We therefore do not believe that normal aging could account for the presence of a restrictive mitral filling pattern in our population, Furthermore, we included age in our multivariable models, and both age and restrictive filling pattern remained significant independent predictors of outcome.
Deceleration time is a proven technique that is easily measured and routinely available in most, if not all, echocardiography laboratories. Many clinical factors contribute to survival after AMI, and we have not been able to investigate the independence or relative contribution of these findings when all clinical factors are available. However, in our models, we have shown that restrictive filling is independent of LVEF, end-systolic volume, Killip class, diabetes, previous AMI, and current angiotensin-converting enzyme inhibitor or β-blacker use. Importantly, the hazard ratio associated with restrictive mitral filling was not affected by the introduction of these other parameters into the models. Finally, it should be noted that most of these studies collected data before the new definition of AMI and thus may not be applicable to all patients, especially those with unstable angina.
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Conclusions |
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On the basis of the present large study collating individual patient data from more than 90% of published data, we demonstrate that a restrictive filling pattern is an important predictor of adverse outcome after AMI regardless of LVEF, chamber size, and severity of in-hospital heart failure. Thus, the mitral filling pattern should be assessed routinely when the risk of AMI patients is being stratified.
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Appendix |
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MeRGE AMI Collaborators
MeRGE Coordinating Center
Cardiovascular Research Laboratory, University of Auckland, New Zealand: R.N. Doughty (co-principal investigator), G.D. Gamble (statistician), K.K. Poppe (statistician), J.B. Somaratne, G.A. Whalley (co-principal investigator).
Writing Committee
J.E. Møller (co-chair), G.A. Whalley (co-chair), F.L. Dini, R.N. Doughty, G.D. Gamble, A.L. Klein, M. Quintana, C.M. Yu, with review by all principal collaborators.
MeRGE Steering Committee
F.L. Dini (Santa Chiara Hospital, Pisa, Italy), R.N. Doughty (co-chair; University of Auckland, New Zealand), G.D. Gamble (University of Auckland, New Zealand), A.L. Klein (Cleveland Clinic Foundation, Ohio), J.E. Møller (Copenhagen University Hospital Rigshospitalet, Denmark), M. Quintana (Karolinska Institute, Huddinge, Sweden), G.A. Whalley (co-chair; University of Auckland, New Zealand), C.M. Yu (Prince of Wales Hospital, Chinese University of Hong Kong, HKSAR, China).
Principal Collaborators
MeRGE Steering Committee Members plus M.I. Burgess (England), G. Cerisano (Italy), M.S. Feinberg (Israel), G.S. Hillis (Scotland), E. Kinova (Bulgaria), K. Sakata (Japan), P.L. Temporelli (Italy).
Studies Included
Bulgaria: University Hospital Queen Joanna, Sofia: E. Kinova (principal collaborator), H. Kozhuharov; Denmark: Svendborg Hospital, Aarhus University Hospital, Svendborg and Skejby: K. Egstrup, J.E. Møller (principal collaborator), S.H. Poulsen, E. Søndergaard; England: Wythenshawe Hospital, Manchester: P. Atkinson, M.I. Burgess (principal collaborator), S.G. Ray; Israel: Chaim Sheba Medical Centre, Sheba Medical Centre, Rabin Medical Centre, Tel Hashomer, and Petach Tiqvah: S. Behar, R. Beinart, V. Boyko, M. Eldar, M.S. Feinberg (principal collaborator), H. Hod, R. Kuperstein, S. Matetzky, A. Sagie, E. Schwammenthal; Italy: Careggi Hospital, Florence: D. Antoniucci, L. Bolognese, P. Buonamici, G. Cerisano (principal collaborator); Japan: Kyorin University, Tokyo: S. Hirata, K. Ishikawa; S. Kashiro, K. Sakata (principal collaborator), A. Yanagisawa; Scotland: Aberdeen Royal Infirmary Aberdeen: K. Kruszewski, G.S. Hillis (principal collaborator). Multicenter clinical trials: the Carvedilol Post-Infarct Survival Control in LV Dysfunction (CAPRICORN) Echocardiography Substudy Investigators: R.N. Doughty (principal collaborator), J. Lopez-Sendon, D.N. Sharpe, G.A. Whalley (principal collaborator); the Attenuation by Adenosine of Cardiac Complications (ATTACC) trial: M. Edner, P. Hjemdahl, T. Kahan, N. Rehnqvist, A. Sollevi, M. Quintana (principal collaborator); Gruppo Italiano per lo Studio della Sopravvivenza nell’Infarcto Miocardico (GISSI-3) Echocardiography Substudy Investigators: M.G. Franzosi, F. Gentile, P. Giannuzzi, R. Latini, A.P. Maggioni, G.L. Nicolosi, L. Tavazzi, P.L. Temporelli (principal collaborator); the Optimal Therapy in Myocardial Infarction With the Angiotensin II Antagonist Losartan (OPTIMAAL) Echocardiographic Substudy Investigators: G.S. Andersen, U. Dahlström, K. Egstrup, O. Gøtzsche, A. Lahiri, J.E. Møller (principal collaborator), K. Skagen; the Bucindolol Evaluation in Acute Myocardial Infarction Trial (BEAT) participating hospitals: K. Egstrup, L. Køber, J.E. Møller (principal collaborator), O. Nyvad, S.H. Poulsen, C. Torp-Pedersen.
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Acknowledgments |
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Sources of Funding
This study was supported by research grants from the University of Auckland and the National Heart Foundation of New Zealand.
Disclosures
None.
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References |
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Footnotes |
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*The Appendix contains a list of the Meta-Analysis Research Group in Echocardiography Acute Myocardial Infarction (MeRGE AMI) Collaborators.
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