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Archives of cardiovascular diseases
Volume 102, n° 8-9
pages 599-605 (août 2009)
Doi : 10.1016/j.acvd.2009.04.012
Received : 28 January 2009 ;  accepted : 28 April 2009
Different patterns of left ventricular enlargement and long-term prognosis after reperfused acute myocardial infarction
Différents modes de la dilatation du ventricule gauche et le pronostic à long terme après un infarctus du myocarde traité par reperfusion à la phase aiguë

Janusz Lipiecki a, , Nicolas Durel a, Laura Ernande a, Séverine Monzy a, Aurelien Muliez b, Jean Ponsonnaille a
a Department of Cardiology, Gabriel Montpied University Hospital, Clermont-Ferrand, rue Montalembert, 63003 Clermont-Ferrand, France 
b Department of Statistics, Gabriel Montpied University Hospital, Clermont-Ferrand, France 

Corresponding author.

Dilation of end-systolic and end-diastolic volumes (ESV, EDV) has been used to define left ventricular remodelling after acute myocardial infarction (MI), but the prognostic significance of different enlargement patterns has not been evaluated fully.


To analyse the evolution of left ventricular volumes and parameters of global and regional contractility and their correlations with long-term prognosis in patients treated by angioplasty in the acute phase of MI.


Seventy-four patients (mean age 56±13 years; 77% men), treated successfully by angioplasty in the acute phase of MI, were included prospectively. Significant enlargement of left ventricular volumes was defined as a greater than 20% increase between acute phase and 6-month control, assessed by contrast ventriculography. Clinical follow-up was obtained for all patients at 82±19months.


Four groups were identified based on volume evolution: Group I (n =29, 39%; no volume enlargement); Group II (n =8, 11%; isolated EDV enlargement); Group III (n =10, 14%; isolated ESV enlargement); Group IV (n =27, 36%; ESV plus EDV enlargement). Global left ventricular ejection fraction increased in Groups I (p =0.001) and II (p =0.037), but decreased in Groups III (p =0.0002) and IV (p =0.019). The 6-year event-free survival rate was significantly (p =0.0039) better in Groups I and II (100%) than in Groups III and IV (80 and 78%, respectively).


ESV enlargement in patients with reperfused acute MI impacts negatively on long-term prognosis, while isolated EDV enlargement does not.

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L’augmentation du volume télédiastolique et/ou du volume télésystolique du ventricule gauche est habituellement utilisée pour définir le remodelage ventriculaire après infarctus du myocarde Cependant, la valeur pronostique des différentes modalités de dilatation du ventricule gauche n’a pas été complètement évaluée.


Soixante-quatorze patients (âge moyen de 56±13ans, 77 % d’hommes) traités par angioplastie à la phase aiguë d’un infarctus du myocarde ont été prospectivement inclus. Une augmentation des volumes angiographiques était définie comme significative si elle était supérieure ou égale à 20 % entre la phase aiguë et le contrôle au sixième mois. Le suivi clinique a été obtenu pour tous les patients à 82±19mois.


Quatre groupes de patients ont été individualisés en fonction de l’évolution des volumes : groupe I (n =29, 39 %) sans dilatation ventriculaire, groupe II (n =8, 11 %) avec une augmentation isolée du volume télédiastolique, groupe III (n =10, 14 %) avec une augmentation isolée du volume télésystolique, et IV (n =27, 36 %) avec augmentation des volumes télédiastoliques et télésystoliques. La fraction d’éjection globale du ventricule gauche augmentait dans le groupe I (p =0,001) et II (p =0,037) alors qu’elle diminuait dans le groupe III (p =0,0002) et IV (p =0,019). À six ans, le taux de survie sans évènement était significativement supérieur dans les groupes I et II (100 %) par rapport aux groupes III et IV (80 et 78 % respectivement, p =0,0039).


Une augmentation du volume télésystolique après infarctus du myocarde chez des patients traités par angioplastie à la phase aiguë a un impact négatif sur leur pronostic à long terme, alors qu’une dilatation isolée du volume télédiastolique n’en a pas.

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Keywords : Acute myocardial infarction, Left ventricular remodeling, Long-term prognosis

Mots clés : Infarctus du myocarde aigu, Remodelage du ventricule gauche, Pronostic à long terme

Abbreviations : EDV, ESV, MI, LV, LVEF, RWMA


Myocardial infarction (MI) remains a leading cause of mortality and morbidity in western countries. Patients who have had an MI have a 7- to 10-fold greater risk of developing heart failure compared with the normal population [1]. The development of clinically significant heart failure is frequently delayed, preceded by an asymptomatic phase during which LV volume enlargement is associated with changes in its shape [2]. The changes in ventricular topography, occurring both acutely and chronically after MI, were attributed to postinfarct remodelling in the 1990s and were identified as an important prognostic variable [3]. The prevention or reversal of LV remodelling has become one of the surrogate endpoints in the analysis of the efficacy of different therapeutic approaches, including reperfusion techniques in the acute phase of MI, pharmacological treatment or, more recently, cell replacement therapy in the subacute or chronic phase of ischaemic heart disease [4, 5, 6, 7]. In different reports dealing with the problem of LV remodelling, several indicators of LV function have been analysed: LVEF, RWMA, sphericity index, ESV, EDV [4, 6, 8, 9, 10]. Currently, there is no consensus about the degree of LV enlargement necessary to define clinically significant remodelling, because of the different imaging techniques used for analysis, with their inherent reproducibilities. Although ESV seems to be the most powerful predictor of long-term prognosis [9, 11], the increase in EDV is used more frequently to define the remodelling [4, 12, 13, 14, 15, 16]. Moreover, discrepancies between changes in global ejection fraction and in LV volume evolution have been reported [15, 17].

We sought to analyse the evolution of LV volume and the parameters of global and regional contractility and their correlations with long-term prognosis in a subset of patients treated by angioplasty during the acute phase of MI.

Study population

Ninety consecutive patients with acute MI who were hospitalized in our department between March 1997 and March 2000 were included in this study. The inclusion criteria were as follows:

ongoing MI confirmed by typical chest pain for more than 20minutes associated with electrocardiogram changes (ST-segment elevation in at least two consecutive leads of greater than or equal to 1mm in limb leads or 2mm in precordial leads);
admission within the first 12hours after the onset of chest pain or within 24hours if the pain persisted; successful angioplasty procedure defined as residual stenosis less than 30% and TIMI flow score 2 or 3;
stable sinus rhythm;
absence of bundle branch block;
stable haemodynamic conditions, defined as Killip class less than 3.

Routine contrast digital ventriculography was performed immediately after the emergency angioplasty. According to the policy of our department, control coronary ventriculography was proposed at this stage to all patients treated by angioplasty in the acute phase of MI. The rationale for this approach was the search for occult restenosis of the culprit artery, which occurs frequently and can alter the functional recovery of partially infarcted myocardium [18]. Non-invasive tests for the detection of myocardial ischaemia produce disappointing results in this patient population [19, 20]. This study was conducted according to the principles outlined in the Declaration of Helsinki and informed consent was obtained from all patients.

Acquisition and analysis of contrast digital ventriculograms

Contrast digital ventriculography was obtained in the acute phase and at 6-month control under the same technical conditions. A 30mm steel sphere was placed on the lateral wall of the chest at the level of the tip of the “pig tail” catheter in the left lateral view and filmed in right oblique view at 30°. The non-ionic contrast dye was injected by a power injector (0.5mL/kg of body mass at the rate of 10mL/sec). Images were stored in digital form for offline analysis using dedicated software (Sanders Medical Data, San Francisco, CA, USA). The EDV and ESV were calculated using the area-length method and the RWMA index was calculated using the centerline method, as described by Sheehan et al. [21]. The software allows also the calculation of global LVEF and the contractility index in the wall opposite the necrosis. Significant enlargement of LV volume was defined as a greater than or equal to 20% increase between the acute phase and 6-month control, as proposed by Bolognese et al. [4].

Long-term clinical follow-up

Major cardiac adverse events were defined as cardiac death, heart transplantation and hospitalization for overt heart failure or life-threatening ventricular arrhythmias. After hospital discharge, patients were referred to their usual cardiologist and/or general practitioner. Follow-up data were collected by telephone interview with patients, their relatives and/or physicians.

Statistical analysis

Continuous variables are expressed as mean±standard deviation. Comparisons of numerical data within groups were carried out using Student’s t test for paired data. Comparisons between groups were performed using one-way analysis of variance and Newman-Keuls tests. Qualitative data were compared using the chi-square test with Yates’s correction or Fisher’s exact test. Event-free survival curves were constructed using the Kaplan-Meier method and statistical differences between curves were assessed by the log-rank test. All tests were two-tailed and a p -value less than 5% was considered to be significant. All computations were performed using the SAS statistical software package, release 8.02 (SAS Institute, Cary, NC, USA).


Of the 90 patients included in this study, 11 (12%) were excluded because of insufficient quality of angiographic images and five (5.5%) refused control coronary angiography. The final study population consisted of 74 patients, who were predominantly men (77%) and relatively young (mean age 56±13 years). Five patients had a history of previous MI and three had undergone another angioplasty procedure. The electrocardiogram location of the MI was anterior in 26 (35%) patients, inferior in 44 (59%) patients and lateral in four (6%) patients. Prehospital fibrinolysis was administered in seven (9%) patients and glycoprotein IIb/IIIa antagonists were used during or immediately after the angioplasty procedure in 12 (16%) patients. At hospital discharge, all patients received conventional treatment including aspirin and ticlopidine (100%), betablockers (93%), statins (57%) and angiotensin-converting enzyme inhibitors (42%).

The final study population of 74 patients were grouped as follows:

absence of LV volume enlargement (n =29, 39%; Group I);
isolated enlargement of EDV (n =8, 11%; Group II);
isolated enlargement of ESV (n =10, 14%; Group III);
increase in both EDV and ESV (n =27, 36%; Group IV).

All groups were similar in terms of their clinical variables except for the use of glycoprotein IIb/IIIa antagonists and the peak of creatine kinase release, which were borderline statistically significantly different (Table 1). Groups III and IV with ESV enlargement had a significantly higher peak creatine kinase release than Groups I and II without ESV enlargement (2995±1760 IU/L vs 2032±1440 IU/L, respectively; p =0.009) and a lower use of glycoprotein IIb/IIIa inhibitors (9% vs 33%, respectively; p =0.016).

Among the angiographic variables, total occlusion of infarct-related artery with TIMI flow grade 0–1 before angioplasty was seen more often in Groups III and IV with ESV dilation than in Groups I and II without ESV dilation (95% vs 76%, respectively; p <0.05), while the difference in minimal lumen diameter was of borderline significance (0.05±0.23mm vs 0.18±0.33mm, respectively; p =0.06). No difference was seen between angiographic variables immediately after angioplasty or at 6-month control except minimal luminal diameter of culprit lesion immediately after angioplasty, which was significantly higher in Group II compared with the other groups (p =0.048; Table 2). The 6-month restenosis rate was 25% in Group I, 0% in Group II, 10% in Group III and 24% in Group IV (p =0.50). All patients with restenosis greater than 50% were treated by another angioplasty during the control coronary angiography.

Evolution of LV volume and contractility between the acute phase and 6-month control

The evolution of LV volume and contractility between the acute phase and 6-month control is depicted in Figure 1. When Groups I and II without ESV dilation were compared with Groups III and IV with ESV dilation, there was a borderline difference in EDV in the acute phase (122±30mL vs 108±28mL, respectively; p =0.045), while at 6-month control this ratio was reversed, with a larger difference (124±30mL vs 148±39mL, respectively; p =0.005).

Figure 1

Figure 1. 

Six-month evolution of LV volumes (a and b), global LVEF (c), RWMA in the territory of infarct-related artery (d) and compensatory hyperkinesis in the territory opposite to the infarct (e). The basal EDV, global LVEF and compensatory hyperkinesis values were statistically different between groups (p =0.003, p =0.029 and p =0.01, respectively). The control EDV, ESV, RWMA and LVEF values were statistically different between groups (p =0.002, p <0.0001, p <0.0001, p <0.001, respectively).


Global LVEF increased in Group I (from 57±11% to 62±8%; p =0.001) and in Group II (from 49±13% to 63±9%; p =0.037), but decreased in Group III (from 65±11% to 52±9%; p =0.0002) and in Group IV (from 55±12% to 49±11%; p =0.019). Similar differences were observed when groups with and without ESV enlargement were compared.

RWMA indexes were similar in all groups in the acute phase. In contrast, at 6-month control, a significant recovery of RWMA was observed in Group I (from –2.90±1.42 S.D. to –1.32±1.25 S.D.; p 0.0001) and Group II (from –3.39±0.59 S.D. to –1.03±0.93 SD; p =0.0002) but not in Group III (from –2.37±1.04 S.D. to –2.67±1.03 S.D.; p =0.25) and Group IV (–3.01±1.14 S.D. to –2.92±1.02 S.D.; p =0.68). Compensatory hyperkinesis in the myocardial region opposite the infarction was statistically more important in the acute phase in Groups III and IV (2.45±1.08 S.D. and 2.06±1.47 S.D., respectively) compared with Groups I and II (1.15±1.43 S.D. and 0.87±1.23 S.D., respectively; p =0.001 between groups). This difference disappeared at 6-month control.

Long-term follow-up

Clinical follow-up was obtained for all patients at 82±19 months. The overall six-year clinical event rate was 30%. The total ischaemia-driven revascularization rate at 6-month control was 13.5% (14%, 13%, 0% and 15% in Groups I–IV, respectively; p =0.8). Three patients died from cancer during long-term follow-up (one each in Groups I, III and IV).

During long-term follow-up, eight (11%) patients experienced a predefined major adverse cardiac event. Four patients died from cardiac causes (three from progressive heart failure and one from sudden cardiac death); all presented with simultaneous enlargement of ESV and EDV at six months (Group IV). Another two patients from this group presented with ventricular arrhythmias and were implanted with an implantable defibrillator. Two patients from Group III were hospitalized for worsening of dyspnoea (New York Heart Association class IV); one was treated further by heart transplantation. At six years, the major adverse cardiac event-free survival rate was significantly better in Groups I and II (100%) than in Groups III and IV (80 and 78%, respectively, p =0.0039 vs Groups I and II). The difference in event-free survival between groups became statistically significant after three years of follow-up (Figure 2).

Figure 2

Figure 2. 

Kaplan-Meier plot of event-free survival. Log-rank analysis at three and six years. p =0.47 and 0.039, respectively.



LV remodelling can be considered to be both an adaptive and a maladaptive process, with the adaptive component enabling the heart to maintain function in response to myocardial insult in the acute phase of cardiac injury. To date, however, there are no data to indicate when the transition from possible adaptive to maladaptive remodelling occurs or how this might be evaluated in patients [22]. Our results suggest that visualization of isolated EDV enlargement between the acute phase and six months after a reperfusion could serve as an indicator of such an adaptive mechanism. In our study, patients with isolated EDV enlargement and those with no volume enlargement had a similar evolution pattern with regard to RWMA, contractility in the opposite wall to the infarction and global LVEF; patients with this pattern had small enzymatic infarct size and normalized global LVEF at six months, associated with the recovery of RWMA in the infarct territory. Similar findings with magnetic resonance imaging have been reported by Fieno et al. [23] in an animal model of MI and by Kramer et al. [17] in a clinical study of patients treated by angioplasty in the acute phase of MI. We have also shown that a relatively small initial EDV is predictive of further remodelling – a finding that has been observed previously in larger studies [4, 15]. However, in contrast to these two studies, we did not find a difference in the RWMA index in the acute phase between groups with and without remodelling; this could be related to the use of different techniques for its assessment (the semiquantitative score obtained by echocardiography and the quantitative centerline method used in our work).

More importantly, the long-term prognosis of patients with isolated EDV enlargement was excellent in our study. One explanation might be that the LV volume overload that occurs after MI increases end-diastolic stress which causes the laying down of new sarcomeres at the end of individual myocytes. Longer myocardial fibres result in increased LV end-diastolic chamber size. The resulting larger EDV can accommodate the volume overload with a smaller (or no) increase in end-diastolic pressure [24]. Unfortunately, only a few patients in our study (11%) showed such an isolated EDV enlargement. In contrast, ESV enlargement (isolated or associated with EDV enlargement), which was observed in 50% of patients in this study, is associated with a completely different evolution of regional and global LV contractility. ESV enlargement is associated at six months with a fall in global LVEF, absence of recovery of RWMA and a dramatic decrease in compensatory hyperkinesis in the opposite wall, particularly if both volumes dilate. The event-free survival at six years is significantly worse than in patients without ESV enlargement. ESV has been shown to be the variable that is most predictive of long-term prognosis, both in patients in the prereperfusion era [9] and in those treated by reperfusion therapy [4]. Moreover, significant ESV enlargement impedes functional recovery after bypass surgery, even in the presence of a substantial amount of viable myocardium [25]. A lack of recovery gives those patients a poor long-term prognosis [26]. Taken together, all these data indicate that ESV rather than EDV evolution should be used as a marker of ischaemic heart disease evolution and eventually serve as a surrogate endpoint for the comparison of different therapeutic approaches.

Despite the predominant inferior infarct location in this study, the observed LV volume enlargement rate is one of the highest compared with data published previously [4, 12, 15, 16]. This observation can be explained in part by the low rate of prescription of angiotensin-converting enzyme inhibitors at discharge from initial hospitalization in these supposedly low-risk patients. The 36% rate of simultaneous EDV and ESV enlargement is very similar to that observed in the echo substudy of the third Gruppo Italiano per lo Studio della Sopravvivenza nell’Infarto Miocardico study (GISSI-3) (19% for early dilation and 16% for late dilation), where the angiotensin-converting enzyme inhibitor lisinopril was used in 50% of patients. Additionally, our results suggest that LV remodelling should also be evaluated in patients with non-anterior infarct location.

Study limitations

The main limitation of our study was the small sample size, so our results need to be confirmed by a larger-scale study. Furthermore, functional patient assessment was not done during long-term follow-up, which could have given additional insights into their evolution. We did not perform a serial assessment of LV volumes and contractility, unlike Bolognese et al. [4] and Giannuzzi et al. [15]. Contrary to these two studies, in which echographic assessment of LV function was performed, our analysis was based on contrast ventriculography, which cannot be repeated serially due to its invasive character. Another limitation of our study was the use of contrast angiography for LV volume assessment. A magnetic resonance imaging approach would have been more precise but this technique was not at our disposal during the inclusion period of our study. Finally, the LV end-diastolic pressure was not recorded systematically during the acute phase intervention, so we were unable to analyse the eventual predictive character of this variable.


Our study stresses the long-term clinical impact of ESV dilation after acute MI. ESV enlargement of 20% or greater corresponds better to the definition of LV remodelling than EDV enlargement. EDV dilation can accompany ESV dilation or be a compensatory mechanism associated with the recovery of global and regional LV contractility.

Conflicts of interest



Glasser S.P. The time course of left ventricular remodeling after acute myocardial infarction Am J Cardiol 1997 ;  80 : 506-507
Sharpe N. Cardiac remodeling in coronary artery disease Am J Cardiol 2004 ;  93 : 17B-20B [cross-ref]
Opie L.H., Commerford P.J., Gersh B.J., and al. Controversies in ventricular remodelling Lancet 2006 ;  367 : 356-367 [cross-ref]
Bolognese L., Neskovic A.N., Parodi G., and al. Left ventricular remodeling after primary coronary angioplasty: patterns of left ventricular dilation and long-term prognostic implications Circulation 2002 ;  106 : 2351-2357 [cross-ref]
Britten M.B., Abolmaali N.D., Assmus B., and al. Infarct remodeling after intracoronary progenitor cell treatment in patients with acute myocardial infarction (TOPCARE-AMI): mechanistic insights from serial contrast-enhanced magnetic resonance imaging Circulation 2003 ;  108 : 2212-2218 [cross-ref]
St John Sutton M., Pfeffer M.A., Moye L., and al. Cardiovascular death and left ventricular remodeling two years after myocardial infarction: baseline predictors and impact of long-term use of captopril: information from the Survival and Ventricular Enlargement (SAVE) trial Circulation 1997 ;  96 : 3294-3299
Warda H.M., Bax J.J., Bosch J.G., and al. Effect of intracoronary aqueous oxygen on left ventricular remodeling after anterior wall ST-elevation acute myocardial infarction Am J Cardiol 2005 ;  96 : 22-24 [cross-ref]
Neumann F.J., Blasini R., Schmitt C., and al. Effect of glycoprotein IIb/IIIa receptor blockade on recovery of coronary flow and left ventricular function after the placement of coronary-artery stents in acute myocardial infarction Circulation 1998 ;  98 : 2695-2701
White H.D., Norris R.M., Brown M.A., and al. Left ventricular end-systolic volume as the major determinant of survival after recovery from myocardial infarction Circulation 1987 ;  76 : 44-51
Wong S.P., French J.K., Lydon A.M., and al. Relation of left ventricular sphericity to 10-year survival after acute myocardial infarction Am J Cardiol 2004 ;  94 : 1270-1275 [cross-ref]
Pfeffer M.A., Pfeffer J.M. Ventricular enlargement and reduced survival after myocardial infarction Circulation 1987 ;  75 : IV93-IV97
Araszkiewicz A., Grajek S., Lesiak M., and al. Effect of impaired myocardial reperfusion on left ventricular remodeling in patients with anterior wall acute myocardial infarction treated with primary coronary intervention Am J Cardiol 2006 ;  98 : 725-728 [cross-ref]
Cerisano G., Pucci P.D., Valenti R., and al. Comparison of the usefulness of Doppler-derived deceleration time versus plasma brain natriuretic peptide to predict left ventricular remodeling after mechanical revascularization in patients with ST-elevation acute myocardial infarction and left ventricular systolic dysfunction Am J Cardiol 2005 ;  95 : 930-934 [cross-ref]
Gaudron P., Eilles C., Kugler I., and al. Progressive left ventricular dysfunction and remodeling after myocardial infarction. Potential mechanisms and early predictors Circulation 1993 ;  87 : 755-763
Giannuzzi P., Temporelli P.L., Bosimini E., and al. Heterogeneity of left ventricular remodeling after acute myocardial infarction: results of the Gruppo Italiano per lo Studio della Sopravvivenza nell’Infarto Miocardico-3 Echo Substudy Am Heart J 2001 ;  141 : 131-138 [cross-ref]
Savoye C., Equine O., Tricot O., and al. Left ventricular remodeling after anterior wall acute myocardial infarction in modern clinical practice (from the REmodelage VEntriculaire [REVE] Study Group) Am J Cardiol 2006 ;  98 : 1144-1149 [cross-ref]
Kramer C.M., Rogers W.J., Theobald T.M., and al. Dissociation between changes in intramyocardial function and left ventricular volumes in the eight weeks after first anterior myocardial infarction J Am Coll Cardiol 1997 ;  30 : 1625-1632 [cross-ref]
Bauters C., Delomez M., Van Belle E., and al. Angiographically documented late reocclusion after successful coronary angioplasty of an infarct-related lesion is a powerful predictor of long-term mortality Circulation 1999 ;  99 : 2243-2250
Desmet W., De Scheerder I., Piessens J. Limited value of exercise testing in the detection of silent restenosis after successful coronary angioplasty Am Heart J 1995 ;  129 : 452-459 [cross-ref]
Miller T.D., Gersh B.J., Christian T.F., and al. Limited prognostic value of thallium-201 exercise treadmill testing early after myocardial infarction in patients treated with thrombolysis Am Heart J 1995 ;  130 : 259-266 [cross-ref]
Sheehan F.H., Bolson E.L., Dodge H.T., and al. Advantages and applications of the centerline method for characterizing regional ventricular function Circulation 1986 ;  74 : 293-305
Cohn J.N., Ferrari R., Sharpe N. Cardiac remodeling-concepts and clinical implications: a consensus paper from an international forum on cardiac remodeling. Behalf of an International Forum on Cardiac Remodeling J Am Coll Cardiol 2000 ;  35 : 569-582 [cross-ref]
Fieno D.S., Hillenbrand H.B., Rehwald W.G., and al. Infarct resorption, compensatory hypertrophy, and differing patterns of ventricular remodeling following myocardial infarctions of varying size J Am Coll Cardiol 2004 ;  43 : 2124-2131 [cross-ref]
Grossman W., Lorell B.H. Hemodynamic aspects of left ventricular remodeling after myocardial infarction Circulation 1993 ;  87 : VII28-30
Schinkel A.F., Poldermans D., Rizzello V., and al. Why do patients with ischemic cardiomyopathy and a substantial amount of viable myocardium not always recover in function after revascularization? J Thorac Cardiovasc Surg 2004 ;  127 : 385-390 [cross-ref]
Bax J.J., Schinkel A.F., Boersma E., and al. Extensive left ventricular remodeling does not allow viable myocardium to improve in left ventricular ejection fraction after revascularization and is associated with worse long-term prognosis Circulation 2004 ;  110 : II18-22

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