Skip Navigation

European Journal of Heart Failure 2004 6(5):555-560; doi:10.1016/j.ejheart.2003.11.012
This Article
Right arrow Abstract Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow Alert me when this article is cited
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 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 arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Cochet, A.
Right arrow Articles by Brunotte, F.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Cochet, A.
Right arrow Articles by Brunotte, F.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© 2004 European Society of Cardiology

The extent of myocardial damage assessed by contrast-enhanced MRI is a major determinant of N-BNP concentration after myocardial infarction

Alexandre Cocheta, Marianne Zellerb, Yves Cottinb,*, Clothilde Robert-Vallaa, Alain Lalandea, Isabelle L'Huilllierb, Alexandre Comtea, Paul M. Walkera, Jean Desgresc, Jean-Eric Wolfb and François Brunottea

a Unité d'IRM, CHU Hopital d'enfants, Bd Mal de Lattre de Tassigny 21034 Dijon Cedex, France
b Service de Cardiologie, CHU Bocage, 2, Bd Mal de Lattre de Tassigny 21034 Dijon Cedex, France
c Laboratoire de Biochimie, CHU Hopital d'enfants, Bd Mal de Lattre de Tassigny 21034 Dijon Cedex, France

* Corresponding author. Tel.: +33-3-80-29-33-11; Fax: +33-3-80-29-33-33. E-mail address: yves.cottin{at}chu-dijon.fr


   Abstract
Top
 Abstract
1. Introduction
 2. Methods
 3. Results
 4. Discussion
 References
 
Aims: To evaluate the relationship between N-terminal Pro-Brain Natriuretic Peptide (N-BNP) level and contrast-enhanced MRI in patients after acute myocardial infarction (MI).

Methods: Eighty-two patients were studied. Venous blood samples were obtained 3 days after MI and MRI was performed from 2 to 7 days after MI, with determination of left ventricular function and acquisition of perfusion data after injection of gadolinium-DTPA. First-pass images (FPI) and Delayed contrast-enhanced (CE) images were analyzed using a 17-segment model, and the extent of transmurality was determined by a visual score.

Results: Univariate analysis showed that age (P<0.001), sex (P<0.02), Left Ventricular Ejection Fraction (LVEF) <45% (P<0.002), creatinine (P<0.05) and delayed CE-MR images (P<0.006) were predictors of a supramedian N-BNP level. FPI was not a predictor in this univariate analysis (P<0.078). In a multivariate model, only age, LVEF <45% and delayed CE-MRI were associated with an increased N-BNP level.

Conclusion: After MI, high N-BNP levels are dependent on the LVEF but also on the myocardial infarct size derived from the delayed CE-MR images.

Key Words: Brain natriuretic peptide • Myocardial infarction • Magnetic resonance imaging (MRI) • Delayed CE-MRI

Received May 7, 2003; Revised October 16, 2003; Accepted November 30, 2003


   1. Introduction
Top
 Abstract
 1. Introduction
2. Methods
 3. Results
 4. Discussion
 References
 
Reperfusion therapy has significantly improved survival after acute myocardial infarction, but it is clinically difficult to evaluate the efficacy of reperfusion, and thus the extent of non-viable myocardial tissue. In most of cases, myocardial perfusion and metabolism are abnormal despite restoration of a TIMI 3 flow [1]. The extent of non-viable myocardial tissue could play a major role in long-term morbidity and mortality after myocardial infarction (MI).

Brain natriuretic peptide (BNP) and the N-terminal fragment of its prohormone, N-terminal pro-brain natriuretic peptide (N-BNP), have provided valuable prognostic information on short and long term mortality in patients with acute coronary syndrome [2,3]. A recent work has suggested that the BNP level could also be linked to coronary artery disease and the extent of myocardium at risk [4].

Contrast-enhanced magnetic resonance imaging (CE-MRI) with a gadolinium-based contrast agent can quantitatively assess the extent of myocardial necrosis with transmural resolution, first pass perfusion providing assessment of the extent of microvascular damage. The objective of the present study was to examine the relationship between N-BNP level and the extent of myocardial damage assessed by contrast-enhanced MRI in patients after acute MI.


   2. Methods
Top
 Abstract
 1. Introduction
 2. Methods
3. Results
 4. Discussion
 References
 
2.1. Patient population
We studied 82 patients (57 men and 25 women, mean age 59±14 years), hospitalized in our department for a first acute myocardial infarction (MI), diagnosed by increased serum MB fraction of creatine kinase (CK-MB) level or troponin (I or T, typical rise and gradual fall) at least twice that of the normal laboratory level, acute chest pain, characteristic electrocardiographic changes (pathologic Q waves, or ST segment elevation or depression, on at least two derivations), and angiographically demonstrated partial or complete occlusion of the related artery (TIMI 0 or 1) with restoration of a TIMI 3 flow. These criteria are in line with the new redefinition of MI by the European Society of Cardiology and the American College of Cardiology [5]. To be included, patients had to be hemodynamically stable and have no contraindication to MRI. The Ethics Committee approved the study protocol and all participants gave written consent before entering the study.

2.2. Data collection
Demographic data, cardiovascular risk factors and history were collected as well as admission data (killip class, ECG and hemodynamic parameters).

2.3. Laboratory analysis
Blood samples were collected in EDTA (ethylenediamine-tetraacetic acid) containing tubes at 3 days after admission and stored at –20 °C until analysis (<3 days). Plasma N-BNP was determined using Elecsys N-BNP sandwich immunoassay on an Elecsys 2010 (Roche). The inter and intra assay coefficients of variation were <3.1% and the sensitivity of the assay was found to be 0.6 pmol/l. The cross reactivity with other natriuretic peptides (BNP, ANP and CNP) was <0.01%. The minimum and maximum quantities detectable ranged from 2.4 to 4130 pmol/l

2.4. MRI protocol
All patients were explored 2–7 days after MI. MRI was performed on a 1.5 T whole-body MR imager (Siemens, Magnetom Vision, GmbH, Erlangen, Germany), using a breath-hold technique and a phased array body coil. Coronal and left ventricular (LV) long-axis scout images were obtained to determine the orientation of the LV short axis imaging plane.

For LV function evaluation, cine-MRI was performed using an ECG-gated gradient echo sequence, with the following acquisition parameters; repetition time (TR) 9 ms, echo time (TE) 4.4 ms, pulse flip angle 15°, nine lines per segment, field of view (FOV) of 350–470 mm (Fig. 1). The acquisition matrix varied from 108x256, (12 cardiac cycles), to 144x256, (16 cardiac cycles), depending on the ability of patient to hold his breath [6]. A series of short-axis slices (5-mm thick, 15 mm apart) was defined from the base of the heart to the apex. The position of the heart was taken into account at end-systole and end-diastole times. A temporal resolution of 50 ms was obtained with the ‘view-sharing’ technique [7].


Figure 1
View larger version (79K):
[in this window]
[in a new window]
[Download PowerPoint slide]
  		Fig. 1 Cine-MR short-axis images at mid-ventricular level from a patient with a large anterior myocardial infarction. (a) end-diastolic slice; (b) end-systolic slice.

 
For LV perfusion evaluation, a first-pass ECG-gated gradient echo sequence was performed (turboFLASH sequence in T1-weighting), after manual injection of a bolus of gadolinium-DTPA (Magnevist) in a brachial vein at 0.1 mmol/kg with the following parameters; inversion time (TI) 400 ms, repetition time (TR) 3.5 ms, echo time (TE) 1.7 ms, FOV 400–470 mm, and matrix 96x128. A time delay buffer at the end of the sequence was adjusted in order to acquire one image every two cardiac cycles (Fig. 2). Three to five short-axis slices (12-mm thick, 3 mm apart) are obtained from the base of the heart to the apex [8].


Figure 2
View larger version (136K):
[in this window]
[in a new window]
[Download PowerPoint slide]
  		Fig. 2 Short-axis gradient-echo MR image at mid-ventricular level, during first pass of a bolus of gadolinium-DTPA, showing a localized no-reflow in the infero-lateral segment.

 
Ten minutes after bolus injection, delayed images were acquired using a segmented T1-weighted inversion-recovery turboFLASH sequence (Fig. 3) [9], with a variable TI delay adjusted for each studied patient [10]. The TI was adjusted to obtain an optimal myocardial nulling by varying the TI from 250 to 400 ms. The chosen TI ranged between 250 and 350 ms.


Figure 3
View larger version (90K):
[in this window]
[in a new window]
[Download PowerPoint slide]
  		Fig. 3 Vertical long axis (a) and short axis mid-ventricular (b) segmented Inversion Recovery gradient echo MR images 10 min after bolus injection of Gadolinium-DTPA, showing a large region of hyperenhancement in the anterior territory.

 
2.5. MRI data analysis
A 17-segment model was used for data analysis of cine-MRI and perfusion studies [11]. Left ventricular end-diastolic volume (EDV) and end-systolic volume (ESV) were calculated from short-axis views [6]. Left ventricular ejection fraction (LVEF) was calculated with the following formula: LVEF=(EDV–ESV)/EDV.

For each patient, perfusion data were analyzed and a visual score was attributed by two observers. Two scores were also given based on the signal intensity observed on early images (First-pass images: FPI) for 16 segments (the apical segment was not evaluated on early images, because no long axis slices were obtained) and late images (delayed perfusion CE images, 10 min after injection) for each of the 17 segments (vertical and horizontal long-axis slices allows the evaluation of the apical segment). Early regional hypoenhancement and late regional hyperenhancement were scored independently of wall motion with a scheme based on the transmural extent of contrast-enhanced tissue within each segment (0=no hypo or hyperenhancement; 1=1–25% hypo or hyperenhancement; 2=26–50% hypo or hyperenhancement; 3=51–75% hypo or hyperenhancement; 4=76–100% hypo or hyperenhancement). The two scores, FPI and delayed CE images, were determined by the sum of the scores of all the segments (16 for FPI, 17 for CE). Thus, the scores ranged from 0 to 64 for FPI, and from 0 to 68 for CE images.

2.6. Statistical analysis
Continuous data were expressed as mean values±S.D. and dichotomous data as percentages. Quantitative parameters were compared by the Kruskal–Wallis one-way analysis of variance on ranks. To analyse the relation between N-BNP levels and other parameters, patients were subdivided according to the median value of N-BNP [2]. The logistic regression model was chosen to assess the univariate relation between the variables. The test variables were: age, sex, Killip class >1, creatinine level, troponin level, creatine kinase (CK) and CK-MB level, end systolic volume, end diastolic volume, left ventricular ejection fraction, sum of the first pass image score and sum of the delayed contrast-enhanced image score. Multivariate analysis was performed and matched for sex and age, when univariate analysis showed a P<0.05. A P value <0.05 was considered to be significant.


   3. Results
Top
 Abstract
 1. Introduction
 2. Methods
 3. Results
4. Discussion
 References
 
Median plasma level of N-BNP was 142 pmol/l. The characteristics of the patients, subdivided according to this median level, are listed in Table 1.


View this table:
[in this window]
[in a new window]

  		Table 1 Patient characteristics, MRI values and biochemical data

 
The infarct localization was anterior in 39 cases (mean N-BNP=426±460), inferior in 38 cases (mean N-BNP=162±160) and lateral in five cases (mean N-BNP=308±266).

In an univariate logistic regression model (Table 2), predictors of N-BNP level >median value were age (P<0.001), sex (P<0.001), LVEF<45% (P<0.01), killip class >1, creatinine (P<0.05), troponin (P<0.05) and delayed CE-MR images (P<0.01). FPI score had no statistical significance.


View this table:
[in this window]
[in a new window]

  		Table 2 Univariate analysis of predictors for high N-BNP (supra-median) levels

 
Multiple logistic regression was undertaken to test for independent prediction of high N-BNP level. In this multivariate model, after adjusting for age and LVEF, delayed CE-MRI was still associated with an increased pro-BNP-level (Table 3).


View this table:
[in this window]
[in a new window]

  		Table 3 Multivariate analysis of predictors for high N-BNP (supra-median) levels

 

   4. Discussion
Top
 Abstract
 1. Introduction
 2. Methods
 3. Results
 4. Discussion
References
 
The major finding of the present study is that N-BNP level following MI appears associated not only with LVEF impairment but also with the extent of myocardial damage as assessed by CE-MRI.

Since its initial description by Sudoh et al., most studies have reported the role of BNP, and later, N-BNP as prognosis markers after MI, according to there relation with LVEF and LV remodeling [2,12]. Our data are in agreement with previous studies, concerning several known determinants of BNP levels such as LVEF, age and sex [13–20].

After acute coronary syndrome, global hemodynamic changes seem to be involved in increased BNP secretion as well as increased regional ventricular wall stretch [13]. These modulations could appear even in the case of minor myocardial damage and some authors recently suggested that the magnitude of the increase in N-BNP may also reflect the extent of the ischemic territory [2,21–23]. Talwar et al. demonstrated a significant difference in N-BNP levels between anterior and inferior MI, and a strong relation between N-BNP and echocardiographic assessment of wall motion index early after MI [21].

Our study clearly demonstrates a relationship between N-BNP and delayed CE-MR images, which accordingly has a strong correlation with myocardial infarct size, even early after MI (2–7 days in our study) [10,24].

Extra-cellular contrast-agents accumulate in the myocardium due to increased capillary permeability causing oedema, increased extracellular space and slower kinetics in infarcted regions [25–27]. As a consequence, delayed CE images early after MI reflect the sum of necrosis and a border zone of injured myocytes surrounding the acute infarct. Whatever the precise mechanism of contrast accumulation, using electron probe X-ray analysis in the rabbit, it has been shown that regional myocardial elevation in contrast agent is associated with irreversible ischemic injury [24,28]. According to the correlation between N-BNP and CE-MRI in our study, the extent of the myocardial damage depicted by CE-MRI could have a direct role in prognosis, even early after myocardial infarction.

The results of the present study demonstrate that hyperenhancement, but not early hypoenhancement, is a predictor of N-BNP level, although early hypoenhancement has been shown to predict late irreversibility and bad prognosis [29–31].

The poorer accuracy of early hypoenhancement may be due to the underestimation of the amount of irreversibly dysfunctional myocardium [31].

Among the limitations of this study, it should be noted that LVEF is a global marker of left ventricular dysfunction and does not reflect the heterogeneity of the regional impairment of the left ventricle in a manner comparable to the gadolinium perfusion scores. Unfortunately, no widely accepted single index reflecting contraction heterogeneity is available to be compared with N-BNP level. Further studies should attempt to define such an index in order to make comparisons possible with perfusion indices.

In conclusion, this study demonstrates the value of delayed CE-MRI studies in initial evaluation of MI, recently after the symptom onset. The ability to combine direct measurement of infarct extent and the study of other prognosis factors (microvascular obstruction, LVEF and left ventricular volumes) illustrate the potential of MRI to define high-risk patients, in combination with N-BNP and clinical factors.


   Acknowledgements
 
This work was supported by the Association de Cardiologie de Bourgogne and by grants from University Hospital of Dijon.


   References
Top
 Abstract
 1. Introduction
 2. Methods
 3. Results
 4. Discussion
 References
 

  1. Grines C.L., Browne K.F., Marco J., Rothbaum D., Stone G.W., O'Keefe J., et al. A comparison of immediate angioplasty with thrombolytic therapy for acute myocardial infarction. The primary angioplasty in myocardial infarction study group. N Engl J Med (1993) 328:673–679.[Abstract/Free Full Text]
  2. Omland T., Persson A., Ng L., O'Brien R., Karlsson T., Herlitz J., et al. N-terminal pro-B-type natriuretic peptide and long-term mortality in acute coronary syndromes. Circulation (2002) 106:2913–2918.[Abstract/Free Full Text]
  3. Richards A.M., Nicholls M.G., Yandle T.G., Frampton C., Espiner E.A., Turner J.G., et al. Plasma N-terminal pro-brain natriuretic peptide and adrenomedullin: new neurohormonal predictors of left ventricular function and prognosis after myocardial infarction. Circulation (1998) 97:1921–1929.[Abstract/Free Full Text]
  4. Kikuta K., Yasue H., Yoshimura M., Morita E., Sumida H., Kato H., et al. Increased plasma levels of B-type natriuretic peptide in patients with unstable angina. Am Heart J (1996) 132:101–107.[CrossRef][Web of Science][Medline]
  5. Alpert J.S., Thygesen K., Antman E., Bassand J.P. Myocardial infarction redefined—a consensus document of The European Society of Cardiology/American Society of Cardiology Committee for the redefiniton of myocardial infarction. J Am Coll Cardiol (2000) 36:959–969.[Free Full Text]
  6. Cottin Y., Touzery C., Guy F., Lalande A., Ressencourt O., Roy S., et al. MR imaging of the heart after myocardial infarction: effect of increasing intersection gap on measurement of left ventricular volume, ejection fraction, and wall-thickness. Radiology (1999) 213:513–520.[Abstract/Free Full Text]
  7. Foo T.K.F., Bernstein M.A., Aisen A.M., Hernandez R.J., Collick B.D., Bernstein T. Improved ejection fraction and flow velocity estimates with use of view-sharing and uniform repetition time excitation with fast cardiac techniques. Radiology (1995) 195:471–478.[Abstract/Free Full Text]
  8. Lauerma K., Virtanen K.S., Sipila L.M., Hekali P., Aronen H.J. Multislice MRI in assessment of myocardial perfusion in patients with single-vessel proximal left anterior descending coronary artery disease before and after revascularization. Circulation (1997) 96:2859–2867.[Abstract/Free Full Text]
  9. Kim R.J., Fieno D.S., Parrish T.B., Harris K., Chen E.L., Simonetti O., et al. Relationship of MRI delayed contrast enhancement to irreversible injury, infarct age, and contractile function. Circulation (1999) 100:1992–2002.[Abstract/Free Full Text]
  10. Simonetti O., Kim R.J., Fieno D.S., Hillenbrand H.B., Wu E., Bundy J.M., et al. An improved MR Imaging technique for the visualisation of myocardial infarction. Radiology (2001) 218:215–223.[Abstract/Free Full Text]
  11. Cerqueira M.D., Weissman N.J., Dilsizian V., Jacobs A.K., Kaul S., Laskey W.K., et al. Standardized myocardial segmentation and nomenclature for tomographic imaging of the heart. Circulation (2002) 105:539–542.[Free Full Text]
  12. Sudoh T., Kangawa K., Minamino N., Matsuo H. A new natriuretic peptide in porcine brain. Nature (1988) 332:78–81.[CrossRef][Medline]
  13. Richards A.M., Nicholls M.G., Yandle T.G., Ikram H., Espiner E.A., Turner J.G., et al. Neuroendocrine prediction of left ventricular function and heart failure after acute myocardial infarction. The Christchurch Cardioendocrine research group. Heart (1999) 81:114–120.[Abstract/Free Full Text]
  14. Groenning B.A., Nilsson J.C., Sondergaard L., Pedersen F., Trawinski J., Baumann M., et al. Detection of left ventricular enlargement and impaired systolic function with plasma N-terminal pro brain natriuretic peptide concentrations. Am Heart J (2002) 143:923–929.[CrossRef][Web of Science][Medline]
  15. Redfield M.M., Rodeheffer R.J., Jacobsen S.J., Mahoney D.W., Bailey K.R., Burnett J.C. Jr. Plasma brain natriuretic peptide concentration: impact of age and gender. J Am Coll Cardiol (2002) 40:976–982.[Abstract/Free Full Text]
  16. Sayama H., Nakamura Y., Saito N., Kinoshita M. Why is the concentration of plasma brain natriuretic peptide in elderly patients greater than normal? Coronary Artery Dis (1999) 10:537–540.[Web of Science][Medline]
  17. Nageh T., Chin D., Cooke J.C., Meehan N., Monaghan M.J., Sherwood R.A. Interpretation of plasma brain natriuretic peptide concentrations may require adjustement for patient's age. Ann Clin Biochem (2002) 39:151–153.[Abstract/Free Full Text]
  18. Wang T.J., Larson M.G., Levy D., Leip E.P., Benjamin E.J., Wilson P.W.F., et al. Impact of age and sex on plasma natriuretic peptide levels in healthy adults. Am J Cardiol (2002) 90:254–258.[CrossRef][Web of Science][Medline]
  19. Inoue T., Sakuma M., Yaguchi I., Mizoguchi K., Uchida T., Takayanagi K., et al. Early recanalization and plasma brain natriuretic peptide as an indicator of left ventricular function after acute myocardial infarction. Am Heart J (2002) 143:790–796.[CrossRef][Web of Science][Medline]
  20. Groenning B.A., Nilsson J.C., Sondergaard L., Kjaer A., Larsson H.B., Hildebrandt P. Evaluation of impaired left ventricular ejection fraction and increased dimensions by multiple neurohumoral plasma concentrations. Eur J Heart Fail (2001) 3:699–708.[Abstract/Free Full Text]
  21. Talwar S., Squire I.B., Downie P.F., McCullough A.M., Campton M.C., Davies J.E., et al. Profile of plasma N-terminal proBNP following acute myocardial infarction. Eur Heart J (2000) 21:1514–1521.[Abstract/Free Full Text]
  22. De Lemos J.A., Morrow D.A., Bentley J.H., Omland T., Sabatine M.S., McCabe C.H., et al. The prognostic value of B-type natriuretic peptide in patients with acute coronary syndromes. N Engl J Med (2001) 345(14):1014–1021.[Abstract/Free Full Text]
  23. Crilley J.G., Farrer M. Left ventricular remodeling and brain natriuretic peptide after first myocardial infarction. Heart (2001) 86:638–642.[Abstract/Free Full Text]
  24. Kim R.J., Chen E.L., Lima J.A., Judd R.M. Myocardial Gd-DTPA kinetics determine MRI contrast enhancement and reflect the extent and severity of myocardial injury after acute reperfused infarction. Circulation (1996) 94:3318–3326.[Abstract/Free Full Text]
  25. Dauber I.M., Van Benthuysen K.M., McMurtry I.F., Wheeler G.S., Lesnefsky E.J., Horwitz L.D., et al. Functional coronary microvascular injury evident as increased permeability due to brief ischemia and reperfusion. Circ Res (1990) 66:986–998.[Abstract/Free Full Text]
  26. Saeed M., Wendland M.F., Masui T., Higgins C.B. Reperfused myocardial infarctions on T1- and susceptibility-enhanced MRI: evidence for loss of compartmentalization of contrast media. Magn Reson Med (1994) 31:31–39.[Web of Science][Medline]
  27. Lima J.A.C., Judd R.M., Bazille A., Schulman S.P., Atalar E., Zerhouni E.A. Regional heterogeneity of human myocardial infarcts demonstrated by contrast-enhanced MRI. Potential mechanisms. Circulation (1995) 92:1117–1125.[Abstract/Free Full Text]
  28. Rehwald W.G., Fieno D.S., Chen E.L., Kim R.J., Judd R.M. Myocardial magnetic resonance imaging contrast agent concentrations after reversible and irreversible ischemic injury. Circulation (2002) 105:224–229.[Abstract/Free Full Text]
  29. Rogers W.J., Kramer C.M., Geskin G., Hu Y.L., Theobald T.M., Vido D.A., et al. Early contrast-enhanced MRI predicts late functional recovery after reperfused myocardial infarction. Circulation (1999) 99:744–750.[Abstract/Free Full Text]
  30. Wu K.C., Zerhouni E.A., Judd R.M., Lugo-Olivieri C.H., Barouch L.A., Schulman S.P., et al. Prognostic significance of microvascular obstruction by magnetic resonance imaging in patients with acute myocardial infarction. Circulation (1998) 97:765–772.[Abstract/Free Full Text]
  31. Gerber B.L., Garot J., Bluemke D.A., Wu K.C., Lima J.A.C. Accuracy of contrast-enhanced magnetic resonance imaging in predicting improvement of regional myocardial function in patients after acute myocardial infarction. Circulation (2002) 106:1083–1089.[Abstract/Free Full Text]

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


This article has been cited by other articles:


Home page
 Eur Heart JHome page
B. Verges, M. Zeller, J. Desgres, G. Dentan, Y. Laurent, L. Janin-Manificat, I. L'Huillier, G. Rioufol, J.-C. Beer, H. Makki, et al.
High plasma N-terminal pro-brain natriuretic peptide level found in diabetic patients after myocardial infarction is associated with an increased risk of in-hospital mortality and cardiogenic shock
Eur. Heart J., September 1, 2005; 26(17): 1734 - 1741.
[Abstract] [Full Text] [PDF]

This Article
Right arrow Abstract Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow Alert me when this article is cited
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 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 arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Cochet, A.
Right arrow Articles by Brunotte, F.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Cochet, A.
Right arrow Articles by Brunotte, F.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?