Skip Navigation

European Heart Journal 2004 25(3):224-231; doi:10.1016/j.ehj.2003.10.029
Copyright © 2004 by the European Society of Cardiology.
This Article
Right arrow Abstract Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow E-letters: Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when E-letters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (1)
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Cortadellas, J.
Right arrow Articles by Soler Soler, J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Cortadellas, J.
Right arrow Articles by Soler Soler, J.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Clinical review

ST segment elevation at 72 hours in patients with a first anterior myocardial infarction best correlates with pre-discharge and 1-year regional contractility and ventricular dilatation

Josefa Cortadellasa,*, Jaume Figuerasa, Mario Missoricia, Enric Domingoa, Josep Rodésa, Joan Castellb and Jordi Soler Solera

a Unitat Coronària–Secció d'Hemodinàmica, Servei de Cardiologia, Hospital General Vall d'Hebron, Barcelona, Spain
b Servei de Medicina Nuclear, Hospital General Vall d'Hebron, Barcelona, Spain

* Correspondence to: Josefa Cortadellas, M.D., Unitat Coronària, Servei de Cardiologia, Hospital General Vall d'Hebron, P. Vall d'Hebron 119-129, 08035 Barcelona, Spain. Tel: +34 932 746 134; fax +34 932 746002
E-mail address: jcortade{at}cs.vhebron.es

Received 14 March 2003; revised 20 October 2003; accepted 23 October 2003

Abstract

Aims To analyse the relationship between the in-hospital course of ST segment elevation (STE) and negative T wave (NTW) with ejection fraction, regional contractility and left ventricular end-diastolic volume at pre-discharge and at 1 year in patients with a first anterior STE acute myocardial infarction (AMI).

Methods and results ECG changes were measured during hospitalization and at 1 year whereas ejection fraction, regional contractility score and end-diastolic volume index were measured by isotopic ventriculography at pre-discharge and at 1 year. At 72h but not earlier patients with {Sigma}STE >0.6mV (group A, n: 35) had a lower ejection fraction (P<0.001), a higher regional contractility score (P<0.001) and a larger end-diastolic volume index (P<0.001) at discharge than those with 0.6mV (group B, n: 26). Negative T wave did not provide additional information. At 1 year, group A continued to show a more impaired ejection fraction and regional contractility than group B and a larger end-diastolic volume.

Conclusion Although reportedly changes in STE within the first hours correlate with coronary reperfusion our findings indicate that additional assessment of STE as early as at 72h correlates with wall motion, ejection fraction and ventricular dilatation at discharge and at 1 year.

Key Words: Myocardial infarction • Ejection fraction • Ventricular dilatation • Regional contractility

1. Introduction

Early coronary reperfusion is known to have salutary effects on global and regional contractility1and to prevent left ventricular dilatation.2,3On the other hand, analysis of ST segment elevation (STE) in the first hours of an acute myocardial infarction (AMI), particularly following fibrinolytic therapy or primary coronary angioplasty, may be an efficacious method to assess myocardial reperfusion.4–7During the first days, however, there may be dynamic changes in STE before a more stable pattern is established8–10but there are only few studies that have analysed the course of STE beyond the acute phase and its relationship with ejection fraction (EF), regional contractility score (RCS) or ventricular dilatation before hospital discharge in the fibrinolytic era.11–13Furthermore, even though the relationship betweenevolutionary changes in the T wave and the ventricular function have been analysed,12–19its possible relationship with left ventricular dilatation before discharge15or during the follow-up18remain ill-defined. Therefore, the goal of this study was to investigate the relationship between sequential changes in STE and negative T waves (NTW) with EF, RCS and end diastolic volume in patients with a first anterior STE AMI and to define the earliest time of hospitalization where the status of STE and T waves would identify those patients with an impaired left ventricular function and/or ventricular dilatation at discharge and at 1 year of follow-up.



View larger version (19K):
[in this window]
[in a new window]
  		Fig. 1 Course of the sum of ST elevation and maximum negative T wave from the admission until 1 year. MNTW=maximum negative T wave; {Sigma}STE=sum of ST elevation.

 
2. Methods

2.1. Patients
The 61 patients included met the following criteria: anginal pain >30min unresponsive to nitroglycerin, associated with STE >0.2mV in =>2 anterior leads (V1–V6) and elevated MB creatine kinase activity (>20IU/l, twice the upper normal level). Patients with a previous myocardial infarction, coronary revascularization procedures, left bundle branch block, cardiogenic shock or other associated cardiac diseases were excluded.

2.2. Protocol
A 12-lead ECG was taken on admission, daily during at least the first 3 days, shortly before discharge, and at 6 and at 12 months. ST-segment elevation was measured at 0.08s after the J point in eight leads (DI, aVL, and V1–V6) and reported as their sum ({Sigma}STE) and the maximum STE in a single lead (MSTE). Magnitude of NTW in the same leads was also analysed and reported as their sum in mV ({Sigma}NTW) and its maximum value in a single lead (MNTW). These electrocardiographic changes were measured in all patients on admission, at 24h, 72h, and at 6 and 12 months, whereas in 54 they were also analysed at the 5th day and at pre-discharge. The protocol was approved by the Human Research Committee of our hospital and informed consent was obtained prior to entering the study.

2.3. Isotopic ventriculography
An isotopic left ventriculography was performed prior to hospital discharge and at 12 months with red blood cells tagged with Tc99m. Image detection was performed in the left and right anterior oblique projections. Information was presented as a histogram using synchronization with the R wave of the ECG and stored in a computer in studies of 32 images/cardiac cycle in left anterior oblique projection with a minimum of 200?000 counts/image or 300 cycles, in 64x64 matrix. All cardiac cycles differing by >10% from the average cycle were rejected. Ejection fraction and left ventricular volumes were calculated using the geometric Massardo's method.20Visual assessment of regional contractility was performed using a rapid sequential cine analysis by two independent observers. A 15-colour scale with a resolution of 24°/colour and 5–6°/element was used for phase analysis and phase histogram. Segments without phase or amplitude were considered akinetics, those with a reduced amplitude and a delayed phase (width at the base of the ventricular peak of the histogram between 72° and 96°) were considered hypokinetics, and those with a reduced amplitude and a marked delay (base width of the ventricular peak >96°) were considered dyskinetics.

Regional contractility score was assessed in anterobasal, anteromedial and apical segments in right anterior oblique projection, and in septal and lateral segments in left anterior oblique projection, and was graded as 0 for normal contractility, 1 for hypokinesia, 2 for akinesia and 3 for dyskinesia. According to previous studies,21an end-diastolic volume index =>70cc/m2was categorized as a dilated ventricle. A >10% variation in end-diastolic volume index or >6% in EF were considered significant. Also, a =>1 point change in regional contractility score was judged as significant.

Performance of a coronary angiography in 44 patients during hospitalization was in part left to the discretion of the attending physician. The presence of significant stenoses (>70%) of =>1 major coronary artery and of collateral circulation were assessed (0: absence; 1: partial; or 2: adequate filling).

All patients were followed in the outpatient clinic at 6 and 12 months. One of the left ventriculograms could not be performed in two patients, whereas adequate left ventricular volumes or RCS could not be obtained in seven and 12 patients,respectively.


View this table:
[in this window]
[in a new window]
  		Table 1 Correlations between electrocardiographic and functional parameters (in-hospital)

 
2.4. Statistical analysis
The relationship between the electrocardiographic parameters ({Sigma}STE, MSTE, {Sigma}NTW and MNTW) measured at the different time intervals and the variables related to left ventricular function (EF, RCS and end-diastolic volume index) were investigated by using the Pearson coefficient correlation analysis. Subsequently, an analysis of the different cut-off points of the electrocardiographic parameters that best correlated with the functional variables at the earliest interval was performed as an attempt to define the point that would best separate patients with an impaired from those with a preserved left ventricular function. The Chi-square test or the Fisher exact test were used to compare categoric variables. The intragroup and intergroup (interaction term) differences for continuous variables were assessed using analysis of two-way repeated measures ANOVA. The Student t test for unpaired samples was used for intergroup differences between one time measurements. Data were expressed as mean±SD.

3. Results

3.1. STE, NTW and left ventricular function during hospitalization
ST-segment elevation was highest on admission and declined thereafter while NTW reached a main peak at 72h and an additional one at discharge (8–10 days). At 6 months STE and NTW had markedly fallen and were similar than at 12 months (Fig. 1). Overall, the correlation coefficients between STE and each of the three variables related to left ventricular function were higher than with NTW (Table 1). Moreover, the ECG at 72h was the earliest ECG where STE was significantly correlated with the three functional variables (Table 1). Correlation between {Sigma}STE and MSTE was high (0.902, P<0.001). Looking at different cut off points of STE at 72h it was found that {Sigma}STE 0.6mV would best separate patients with an impaired (>0.6mV, group A) from those with a preserved left ventricular function (=<0.6mV, group B, Fig. 2). Indeed, most patients with EF <40% (20/22, 91%) and end-diastolic volume index =>70cc/m2(17/23, 74%) belong to group A. The two groups, however, showed similar clinical characteristics except for a higher peak of CK MB in group A (Table 2). With respect to the relationship between NTW and the functional variables it was found that although the correlation between MNTW and {Sigma}NTW was also high (0.922, P<0.001), the best cut-off point was for MNTW (<0.5mV) at 72h (Table 3).



View larger version (23K):
[in this window]
[in a new window]
  		Fig. 2 Analysis of patients with sum of ST elevation ≤0.6mV and >0.6mV in the ECG of admission, 24h, 72h, 5 days and 8 days and their relation with ejection fraction, end-diastolic volume index and regional contractility score at discharge. d=days; EF=ejection fraction; EDVI=end-diastolic volume index; h=hours; RCS=regional contractility score; {Sigma}STE=sum of ST elevation.

 

View this table:
[in this window]
[in a new window]
  		Table 2 Baseline patient characteristics

 

View this table:
[in this window]
[in a new window]
  		Table 3 Relation between maximum negative T wave at the 72h ECG and infarct size, ejection fraction, regional contractility and end-diastolic volume at dischargea

 
Severity of coronary stenosis did not correlate with the magnitude of {Sigma}STE or MNTW (Table 4).


View this table:
[in this window]
[in a new window]
  		Table 4 Coronary angiographya

 
3.2. STE, NTW and left ventricular function at 1 year
As during the in-hospital evaluation correlation coefficients between STE and each of the three variables related to left ventricular function were higher than with NTW (Table 1). Moreover, the ECG at 72h was again the earliest ECG where STE was significantly correlated with the three functional variables (Table 5). We observed a significant improvement in ventricular function at 1 year in the two groups (Fig. 3). In fact, EF improved in 58% of patients from group A and in 52% from group B, and, particularly, in 68% of those with a severely depressed EF (<40%). Similarly, RCS improved significantly in 41% of patients from group A and in 45% from group B, whereas end-diastolic volume index decreased significantly in 33% and 45%, respectively. Moreover, a substantial number of patients with a dilated left ventricle at discharge (14/23, 61%) experienced a reduction of end-diastolic volume index to the extent that in 10 (43%) it returned to normal values. Overall, however, patients from group A continued to display a more deteriorated EF at 1 year (45±12% vs 55±12%, P<0.001) and RCS (3.10±1.82 vs 1.2±1.1, P<0.001) than those from group B, and a larger end-diastolic volume index (69±24 vs 59±12cc/m2, P<0.05), (Fig. 3). Also, patients with MNTW at 72h <0.5mV showed the same trend of changes in the different parameters than those from group A, whereas changes in patients with MNTW 0.5mV at 72h were similar to those from group B. Among patients with high {Sigma}STE, however, there was a small subset of six patients with deep NTW, 0.5mV, who presented a better EF (56±8% vs 36±11%, P<0.001) and a trend towards a better RCS and a smaller end-diastolic volume.


View this table:
[in this window]
[in a new window]
  		Table 5 Correlations between electrocardiographic and functional parameters (at 1 year)

 


View larger version (11K):
[in this window]
[in a new window]
  		Fig. 3 Evolutionary changes in regional contractility score, end diastolic volume index and ejection fraction during the first year in patients from group A: sum of ST elevation >0.6mV, and group B: sum of ST elevation ≤0.6mV. In both groups, there was a significant improvement in the ejection fraction and in the group with sum of ST elevation ≤0.6mV the regional contractility score also improved significantly. EF=ejection fraction; EDVI=end-diastolic volume index; RCS=regional contractility score.

 
3.3. Left ventricular dilatation at 1 year
At 1 year, 16 patients showed a dilated left ventricle (=>70cc/m2) and 12 belong to group A (75%). Thirteen (81%), however, had already a dilated left ventricle at hospital discharge, and four of them had experienced a further dilatation. Thus, of the 54 patients with volume measurements, only seven showed a progressive dilatation at 12 months (13%) and five belonged to group A (71%). Patients with a dilated left ventricle at 1 year were older and had a higher {Sigma}STE at 72h than those with a dilated ventricle at discharge but not at 1 year (Table 6).


View this table:
[in this window]
[in a new window]
  		Table 6 Patients with end-diastolic volume index ≥70cc/m2at discharge. Comparison between patients who normalized the end-diastolic volume index and those with persistent dilatation at 1 yeara

 
4. Discussion

We have documented that in patients with a first anterior STE AMI the 12-lead ECG performed at 72h was helpful in identifying those with a more deteriorated ventricular function and a dilated left ventricle both at hospital discharge and at 1 year. Thus, most patients with EF <40% (91%) and end-diastolic volume index =>70cc/m2(74%) presented a {Sigma}STE >0.6mV at 72h and 75% of those who would present a dilated left ventricle at 1 year and 71% of those who would experience further dilatation also belong to this group.

4.1. STE, infarct size and left ventricular function
Studies on the relationship between magnitude of STE and infarct size in the pre-fibrinolytic era had shown controversial results.24–27Resolution of STE during the first 3h after a primary coronary angioplasty22,23or thrombolysis,2,28on the other hand, has been successfully correlated with a reduction in infarct size and a variable preservation of ventricular function. In some patients, however, resolution of STE may be delayed or STE may reappear after an initial reduction. In the reperfusion era little information is available with respect to the prognostic implications of the course of STE beyond the initial phase regarding the status of EF, RCS or end-diastolic volume index.11,29In our study, a {Sigma}STE >0.6mV at 72h permitted identification of patients with large infarcts, a depressed ventricular function and an enlarged end-diastolic volume index at hospital discharge. In part, these findings differ from those reported by Nixdorff29who found that in patients treated with streptokinase, a marked STE ({Sigma}STE >1.0mV) already on admission was associated with extensive AMI and large hypokinetic areas. Indeed, we encountered that {Sigma}STE in the admission ECG was less consistent in predicting RCS than in the ECG at 72h. Thus, our results would be more in agreement with those from Bodí et al.11who reported that patients with a >0.1mV STE in =>2Q leads at 1 week had more severe regional dysfunction than those with a lesser STE. In our study, however, the discriminant ECG was an earlier one, at 72h, and the correlation with ventricular function was extended to a 12 months follow-up.

It is worth to emphasize, however, that an important proportion of patients from the two groups experienced an improvement in left ventricular function along the first year. It is conceivable then, that both, small and extensive infarctions had relevant areas of stunned myocardium that recovered progressively in contradistinction with the lack of recovery generally reported in the pre-fibrinolytic period.30Despite this improvement, patients from group A continued to exhibit a greater functional impairment at 1 year than those from group B.

4.2. STE and left ventricular dilatation
The relationship between STE and left ventricular dilatation has received less attention and results of preceding analysis have been inconclusive.11,29As others,29,31–35we found that most patients with ventricular dilatation at hospital discharge had large infarctions and belong to group A. We also observed, however, that there was a remarkable rate of reduction in end-diastolic volume index at 1 year, to the extent that 43% of dilated ventricles regained normal values. In this regard, our results are somewhat different from those ofNixdorff et al.29for they found that patients with high STE on admission exhibited a progressive ventricular enlargement at 6 months. Indeed, we encountered that although STE on admission was similarly predictable of increased EDVI than at 72h, a sizable number of patients with persistent STE did not evolve to dilatation at 1 year. More consistent with our findings, therefore, are those from Bodí who reported no significant change in end-diastolic volume index for the whole group of patients studied.11Unfortunately, however, they did not perform subgroup analysis. In our patients improvement in end-diastolic volume index was associated with a significant improvement in RCS indicating that, at least in part, it reflected recovery of stunned myocardium.

At 1 year, left ventricular dilatation was present in only 30% of our patients and a similar figure has been recently reported.35Most of these patients (75%), however, belong to group A and had initiated this process during the hospital course, as previously suggested.31Moreover, 71% of patients who presented a progressive dilatation at 1 year also belong to group A. These patients were older and had a greater STE than those who had a dilated ventricle at discharge but not at 1 year although they showed a similar enzymatic infarct size. Hence, these findings would be in line with observations made in elderly patients that suggest a particularly impaired microvascular reperfusion perhaps related to a pre-existing endothelial dysfunction.36In keeping with this, impaired microcirculation within the infarcted area has been claimed to unfavourably influence postinfarctional remodelling.1–3We may add, according to our findings, that among patients with a comparable infarct size those with a greater STE would present a more transmural necrosis and, thus, a lesser amount of viable tissue in the epicardial zone which could facilitate a progressive ventricular dilatation.

4.3. NTW, infarct size, and left ventricular function and dilatation
The functional significance of NTW following an AMI has not been investigated in depth although several authors have indicated that patients with greater NTW during the first days have smaller infarcts and a better ventricular function than those with NTW of lesser magnitude.15–17Nevertheless, most of these studies do not report concurrent changes in the ST segment and hence, it is unclear whether T wave changes provide any additional useful information. In our study and with respect to infarct size and global left ventricular function, the information derived NTW at 72h was comparable to that of {Sigma}STE. In contrast, NTW were of no help in identifying differences in RCS and end-diastolic volume index before discharge, or in recognising those patients who would undergo a subsequent left ventricular dilatation.

4.4. Limitations
Two potential drawbacks of our study are the reduced number of patients included and the lack of angiography in some of them. Also, the fact that coronary angiography was not performed in the first 72h in most patients does not allow a strict on-time correlation with the ECG findings. However, patency of the artery responsible for AMI can not be always correlated with existence of adequate perfusion in the corresponding myocardial region.1–3In fact, and as it has been suggested,32absence of viable myocardium in the infarcted territory is likely to account for ventricular dilatation in patients with open arteries. Another limitation is that because of technical difficulties, analysis of RCS and end-diastolic volume could not be performed in all patients. Notwithstanding these drawbacks, a definite correlation could be established between the course of STE and the status of leftventricular function and end-diastolic volume.

4.5. Implications
Our data provide evidence that as early as at 72h a relevant STE ({Sigma}STE >0.6mV) in patients with an anterior AMI is a useful marker of an impaired EF and RCS at pre-discharge and at 1 year. This is of practical interest for it would be complementary to the informationderived from STE analysis within the first hours for assessment of coronary reperfusion.22,23,28According to our findings, therefore, re-evaluation of STE at 72h would allow a further stratification of these patients. In fact, most of those with a severely impaired systolic left ventricular function or a dilated ventricle at hospital discharge and/or at 1-year follow-up would identified by an {Sigma}STE >0.6mV at 72h. In these patients one might be inclined to provide not only afterload reduction, particularly with ACE inhibitors, but also to consider the convenience of coronary revascularization to reduce subsequent remodelling and improve systolic function.37–39In fact, it is likely that very early reperfusion therapy would avoid the persistence of STE and its negative consequence in a sizable proportion of these patients.

References

  1. Ito H, Tomooka T, Sakai N et al. Lack of myocardial perfusion immediately after successful thrombolysis. A predictor of poor recovery of left ventricular function in anterior myocardial infarction. Circulation. 1992;85:1699–1705.[Abstract/Free Full Text]
  2. Ito H, Maruyama A, Iwakura K et al. Clinical implications of the ‘no reflow’ phenomenon. A predictor of complicating and left remodeling in reperfused anterior wall myocardial infarction. Circulation. 1996;93:223–228.[Abstract/Free Full Text]
  3. Destro G, Marino P, Barbieri E et al. Postinfarctional remodeling: increased dye intensity in the myocardial risk area after angioplasty of infarct-related coronary artery is associated with reduction of ventricular volumes. J Am Coll Cardiol. 2001;37:1239–1245.[Abstract/Free Full Text]
  4. Clemmensen P, Ohman EM, Sevilla D et al. Changes in standard electrocardiographic ST-segment elevation predictive of successful reperfusion in acute myocardial infarction. Am J Cardiol. 1990;66:1407–1411.[CrossRef][Web of Science][Medline]
  5. Schröder R, Wegscheider K, Schroder K, for the INJECT Trial Group et al. Extent of early ST segment elevation resolution: a strong predictor of outcome in patients with acute myocardial infarction and a sensitive measure to compare thrombolytic regimens. A substudy of the International joint efficacy comparison of thrombolytics (INJECT) trial. J Am Coll Cardiol. 1995;26:1657–1664.[Abstract]
  6. Santoro GM, Valentí R, Buonamici P et al. Relation between ST segment changes and myocardial perfusion evaluated by myocardial contrast echocardiography in patients with acute myocardial infarction treated with direct angioplasty. Am J Cardiol. 1998;82:932–937.[CrossRef][Web of Science][Medline]
  7. Watanabe J, Nakamura S, Sugiura T et al. Early identification of impaired myocardial reperfusion with serial assessment of ST segments after percutaneus transluminal coronary angioplasty during acute myocardial infarction. Am J Cardiol. 2001;88:956–959.[CrossRef][Web of Science][Medline]
  8. Zmyslinski RW, Akiyama T, Biddle T et al. Natural course of the ST segment and QRS complex in patients with acute myocardial infarction. Am J Cardiol. 1979;43:29–34.[CrossRef][Web of Science][Medline]
  9. Kwon K, Freedman B, Wilcox I et al. The unstable ST segment early after thrombolysis for acute myocardial infarction and its usefulness as a marker of recurrent coronary occlusion. Am J Cardiol. 1991;67:109–115.[CrossRef][Web of Science][Medline]
  10. Sagie A, Strasberg B, Imbar S et al. Value of the electrocardiogram for prediction of left ventricular thrombus in anterior wall myocardial infarction. Am J Cardiol. 1991;68:957–959.[CrossRef][Web of Science][Medline]
  11. Bodí V, Sanchís J, Llácer A et al. ST segment elevation on Q leads at rest and during exercise: relation with myocardial viability and left ventricular remodeling within the first 6 months after infarction. Am Heart J. 1999;137:1107–1115.[CrossRef][Web of Science][Medline]
  12. Kusniek J, Solodky A, Strasberg B et al. The relationship between the electrocardiographic pattern with TIMI flow class and fraction in patients with a first acute myocardial infarction. Eur Heart J. 1997;18:420–425.[Abstract/Free Full Text]
  13. Adler Y, Zafrir N, Ben-Gal T et al. Relation between evolutionary ST segment and T-wave direction and electrocardiographic prediction of myocardial infarct size and left ventricular function among patients with anterior q-wave acute myocardial infarction who received reperfusion therapy. Am J Cardiol. 2000;85:927–933.[CrossRef][Web of Science][Medline]
  14. Matetzky SH, Barabash GI, Shahar A et al. Early T wave inversion after thrombolytic therapy predicts better coronary perfusion: clinical and angiographic study. J Am Coll Cardiol. 1994;24:378–383.[Abstract]
  15. Kosuge M, Kimura K, Shimizu T et al. Clinician significance of inverted T-waves during the acute phase of myocardial infarction in patients with myocardial reperfusion. J Cardiol. 1995;25:69–74.[Medline]
  16. Nakajima T, Kagoshima J, Fujimoto S et al. The deeper the negativity of the T waves recorded, the greater is the effectiveness of reperfusion of the myocardium. Cardiology. 1996;87:91–97.[CrossRef][Web of Science][Medline]
  17. Merchan A, Millan V, Lopez JR et al. The appearance of giant negative T waves in anterior acute myocardial infarct with a Q wave is associated with minor myocardial damage and minor extension of coronary disease. Rev Esp Cardiol. 1999;52:294–300.[Web of Science][Medline]
  18. Bosimini E, Giannuzzi P, Temporelli PL et al. Electrocardiographic evolutionary changes and left ventricular remodeling after acute myocardial infarction. Results of the GISSI-3 substudy. J Am Coll Cardiol. 2000;35:127–135.[Abstract/Free Full Text]
  19. Birnbaum Y, Strasberg B. The predischarge electrocardiographic pattern in anterior acute myocardial infarction:relation between evolutionary ST segment ant T wave configuration and prediction of myocardial infarct size and left ventricular systolic function by the QRS Selvester score. J Electrocardiol. 2000;33(Suppl):73–80.
  20. Massardo T, Gal RA, Grenier RP et al. Left ventricular volume calculation using a count-based ratio method applied to multigated radionuclide angiography. J Nucl Med. 1990;31:450–456.[Abstract/Free Full Text]
  21. Castell Conesa J. Ventricular volume measurement. Candell J, Ortega D. Nuclear cardiology in everyday practice. Dordrecht: Kluwer Academic Publishers; 1994. p. 158–172.
  22. Van't Hof AW, Liem A, de Boer MJ, for the Zwolle Myocardial Infarction Study Group et al. Clinical value of 12-lead electrocardiogram after successful reperfusion therapy for acute myocardial infarction. Lancet. 1997;350:615–619.[CrossRef][Web of Science][Medline]
  23. Matetzky SH, Novikov M, Gruberg L et al. The significance of persistent ST elevation versus early resolution of ST segment elevation after primary PTCA. J Am Coll Cardiol. 1999;34:1932–1938.[Abstract/Free Full Text]
  24. Mills R, Young E, Gorlin R et al. Natural history of S-T segment elevation after acute myocardial infarction. Am J Cardiol. 1975;35:609–614.[CrossRef][Web of Science][Medline]
  25. Yusuf S, Lopez R, Maddison A et al. Value of electrocardiogram in predicting and estimating infarct size in man. Br Heart J. 1979;42:286–293.[Abstract/Free Full Text]
  26. Norris RM, Barratt-Boyes C, Heng MK et al. Failure of ST segment elevation to predict severity of acute myocardial infarction. Br Heart J. 1976;38:85–92.[Abstract/Free Full Text]
  27. Thompson PL, Katavatis V. Acute myocardial infarction: evaluation of precordial ST segment mapping. Br Heart J. 1976;38:1020–1024.[Abstract/Free Full Text]
  28. Matetzky SH, Freimark D, Chouraqui P et al. The distinction between coronary myocardial reperfusion after thrombolytic therapy by clinical markers of reperfusion. J Am Coll Cardiol. 1998;32:1326–1330.[Abstract/Free Full Text]
  29. Nixdorff U, Erbel R, Rupprecht HJ et al. Sum of ST-segment elevations on admission electrocardiograms in acute myocardial infarction predicts left ventricular dilation. Am J Cardiol. 1996;77:1237–1241.[CrossRef][Web of Science][Medline]
  30. Borer JS, Rosing DR, Miller RH et al. Natural history of left ventricular function during 1 year after acute myocardial infarction: comparison with clinical, electrocardiographic and biochemical determinants. Am J Cardiol. 1980;46:1–12.[CrossRef][Web of Science][Medline]
  31. Jeremy RW, Allman K, Bautovitch G et al. Patterns of left ventricular dilation during the six months after myocardial infarction. J Am Coll Cardiol. 1989;13:304–310.[Abstract]
  32. Bolognese L, Cerisano G, Buonamici P et al. Influence of infarct-zone viability on left ventricular remodeling after acute myocardial infarction. Circulation. 1997;96:3353–3359.[Abstract/Free Full Text]
  33. Sanchís J, Bodí V, Insa LD et al. Predictors of early and late ventricular remodeling after acute myocardial infarction. Clin Cardiol. 1999;22:581–586.[Web of Science][Medline]
  34. Gaudron P, Eiles CH, Kugler I et al. Progressive left ventricular dysfunction and remodeling after myocardial infarction. Potential mechanisms and early predictors. Circulation. 1993;87:755–763.[Abstract/Free Full Text]
  35. Zaman A, Helft G, Worthley S et al. Ventricular dilation after anterior ST-elevation myocardial infarction in the thrombolytic era. Am Heart J. 2000;140:611–616.[CrossRef][Web of Science][Medline]
  36. Claeys MJ, Bosmans J, Veenstra L et al. Determinants and prognostic implications of persistent ST-segment elevation after primary angioplasty for acute myocardial infarction. Importance of Microvascular Reperfusion Injury on clinical outcome. Circulation. 1999;99:1972–1977.[Abstract/Free Full Text]
  37. Pizzetti G, Belotti G, Margonato A et al. Coronary recanalization by elective angioplasty prevents ventricular dilation after anterior myocardial infarction. J Am Coll Cardiol. 1996;28:837–845.[Abstract]
  38. Assman P, Aengevaeren W, Tijssen J et al. Early identification of patients at risk for significant left ventricular dilation one year after myocardial infarction. J Am Soc Echocardiogr. 1995;8:175–184.[CrossRef][Medline]
  39. Nidorf SM, Siu SC, Galambos G et al. Benefit of late coronary reperfusion on ventricular morphology and function after myocardial infarction. J Am Coll Cardiol. 1993;21:683–691.[Abstract]

Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?



This Article
Right arrow Abstract Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow E-letters: Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when E-letters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (1)
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Cortadellas, J.
Right arrow Articles by Soler Soler, J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Cortadellas, J.
Right arrow Articles by Soler Soler, J.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?