Troponin release following endurance exercise: is inflammation the cause? a cardiovascular magnetic resonance study
© O'Hanlon et al; licensee BioMed Central Ltd. 2010
Received: 22 June 2010
Accepted: 2 July 2010
Published: 2 July 2010
The aetiology and clinical significance of troponin release following endurance exercise is unclear but may be due to transient myocardial inflammation. Cardiovascular magnetic resonance (CMR) affords us the opportunity to evaluate the presence of myocardial inflammation and focal fibrosis and is the ideal imaging modality to study this hypothesis. We sought to correlate the relationship between acute bouts of ultra endurance exercise leading to cardiac biomarkers elevation and the presence of myocardial inflammation and fibrosis using CMR.
17 recreation athletes (33.5 +/- 6.5 years) were studied before and after a marathon run with troponin, NTproBNP, and CMR. Specific imaging parameters to look for inflammation included T2 weighted images, and T1 weighted spin-echo images before and after an intravenous gadolinium-DTPA to detect myocardial hyperemia secondary to inflammation. Late gadolinium imaging was performed (LGE) to detect any focal regions of replacement fibrosis.
Eleven of the 17 participant had elevations of TnI above levels of cut off for myocardial infarction 6 hrs after the marathon (0.075 +/- 0.02, p = 0.007). Left ventricular volumes were reduced post marathon and a small increase in ejection fraction was noted (64+/- 1% pre, 67+/- 1.2% post, P = 0.014). Right ventricular volumes, stroke volume, and ejection fraction were unchanged post marathon. No athlete fulfilled criteria for myocardial inflammation based on current criteria. No regions of focal fibrosis were seen in any of the participants.
Exercise induced cardiac biomarker release is not associated with any functional changes by CMR or any detectable myocardial inflammation or fibrosis.
Acute bouts of ultra-endurance exercise may depress global left ventricular (LV) diastolic and systolic function and in the majority of cases this is associated with elevations in circulating serum markers of cardiac damage, including troponin T and I, myoglobin, creatine kinase (CK), CK-MB, and brain natriuretic peptide (BNP) [1–5]. Debate continues as to the clinical significance of changes in cardiac biomarkers and function after acute and chronic endurance exercise. Whether exercise induced cardiac biomarker release is a physiological or pathological process remains a contentious issue. It is likely that acute elevations of cardiac troponins following endurance exercise are physiological owing to the low peak levels recorded and the rapid return to baseline; troponin release may simply be related to cardiac adaptation to exercise where transient myocardial injury acts as a physiological signal for adaptation leading to enhanced structure and function . Animal studies have however demonstrated that endurance exercise can trigger the development of myocardial inflammation and fibrosis and a limited number of post mortem studies have demonstrated both replacement and interstitial fibrosis in the hearts of athletes who have died suddenly [7–9]. A possible mechanism underlying troponin release with exercise and transient cardiac dysfunction may be related to exercise induced myocardial inflammation.
Cardiovascular magnetic resonance (CMR) is the reference standard imaging modality for the assessment of ventricular volumes, function, and mass. Measurements are accurate with no geometrical assumptions about the ventricle and very reproducible [10, 11]. Using specialised imaging protocols, CMR can also image focal and global myocardial inflammation and oedema, owing to the relaxation properties of water, using T2-weighted techniques [12–14]. Imaging after intravenous gadolinium can detect regional hyperemia secondary to inflammation and focal areas of myocardial fibrosis [15–17]. The utility of CMR to detect myocardial inflammation has been validated in numerous studies and the subject of a recent white paper from the ACC .
We sought to assess the potential relationship between acute bouts of ultra endurance exercise leading to troponin release and the presence of myocardial inflammation and fibrosis using CMR.
We studied 17 recreational athletes before and after a marathon run (26.2 miles). Exclusion criteria included the presence of pre-existing cardiovascular or pulmonary diseases, hypertension, diabetes, and peripheral vascular diseases. No participant had taken part in any significant endurance event in the preceding 12 weeks. Cardiac biomarkers (cTnI, NTproBNP) were collected at an initial assessment 24 hrs prior to, immediately after completion of the marathon, and again 6 hours later. Post marathon CMR was performed 6 hours after marathon completion. This time point was chosen based on an assumption that 6 hours would allow a sufficient amount of time for inflammation to develop and be detectable, corresponding with the time when TnI is typically detectable in ischaemic models representing the liberation of these proteins and enzymes from damaged myocytes . Each participant completed a detailed questionnaire detailing their training history (hours training per week, type of training). The study was approved by the Brompton, Harefield and NHLI research ethics committee and all participants signed informed consent.
Analysis of cTnI was determined using the TnI-Ultra assay for the ADVIA Centaur (Siemens Healthcare Diagnostics, Frimley, UK). The detection limit of the instrument was 0.006 μg/L, upper limit of 50 μg/L. The claimed 10% CV was 0.03 μg/L with a 99th centile of 0.04 μg/L. The total assay imprecision was 2.7 to 5.3% in the range 0.8 to 27.2 μg/L. NTproBNP was analysed using the Elecsys 2010 system (Roche Diagnostics, Burgess Hill, UK). The assay is an electrochemiluminescent sandwich immunoassay that uses two polyclonal antibodies directed at residues 1-21 and 39-50 of the NTproBNP molecule. The %CV of the assay is 3.2-2.4% from 20.7-585.5 pmol/L (175-4962 ng/L) with an analytical range of 0.6-4138.6 pmol/L (5-35,000 ng/L).
Cardiovascular Magnetic Resonance (CMR)
CMR data was collected 24 hrs pre- and 6 hrs post-marathon. A standard volumes and LGE sequence was performed on a dedicated scanner (Siemens Avanto 1.5-T, Erlangen, Germany), with full myocardial coverage using an 8-channel phased array coil . Ventricular volumes, function and mass were quantified using customised analysis software (CMRTools, Cardiovascular Imaging Solutions, London, UK) by a blinded single experienced investigator. Papillary muscles were included in the mass and excluded from the volume. Wall motion was analyzed based on the 16 segment AHA/ACC model .
Two CMR validated methods to image myocardial inflammation were performed.
1. Myocardial Inflammation
A value of > 1.9 was considered diagnostic of global myocardial oedema/inflammation .
2. Regional Hyperaemia
This was deemed to be positive if the ratio was > 4.0
The ratio of SI increase before and after contrast for myocardium was deemed to be positive for hyperaemia if % SI myocardial increase was > 45% between pre and post contrast images using commercially available software (CMR Tools, London, UK) .
Imaging for late gadolinium enhancement (LGE) to identify fibrosis was performed 5-10 min after contrast injection in identical short-axis planes to cine images using a breath hold inversion-recovery (FLASH) gradient echo sequence . Inversion times were optimized to null normal myocardium. In all patients, LGE imaging was repeated for each short-axis image in two separate phase-encoding directions to exclude artefact. LGE images were analyzed quantitatively by 2 independent readers using customized software (MRI-MASS, Medis, Leiden, Netherlands). In brief, the endocardial and epicardial borders were traced for each short-axis slice. A region of interest (ROI) averaging 50 mm2 was defined within the normal, remote myocardium in an area with uniform myocardial suppression free of artefacts. A multi-pass region-growing algorithm was used to identify the fibrotic boundaries based on the "full width half maximum" technique and myocardial LGE was expressed as present/absent (LGE+,LGE-), as gram mass, and a percentage of total LV mass [24–26].
All data values were presented as mean ± SD. Changes from pre-marathon to post-marathon were analysed using paired t-tests. Relationships between data indices CMR measures of systolic function against serum biomarkers of cardiac damage were examined via Pearson's product-moment correlation analysis. The critical α level was set at 0.05 and all analyses were carried out on SPSS 16.0 software.
Individual marathon times, peak troponin level, and volumetric indices pre and post marathon.
LVEF Pre (%)
LVEF Post (%)
RVEF Pre (%)
RVEF Post (%)
Marathon Time (mins)
Data for indices of biological markers of cardiac damage pre-, post-, 6 hr post-marathon.
6 h Post-marathon
0.04 ± 0.008*
0.075 ± 0.024*
P = 0.002
37.4 ± 5.9
59.3 ± 10.5*
68.1 ± 11*
P = 0.007
Data indices for LV/RV function pre-, post- and 6 hr post-marathon.
CMR Volumetric Indices
6 Hrs Post-Marathon
211 ± 8.4
201 ± 7.8
P = 0.002
76 ± 4.3
66 ± 4.0
P = 0.002
135 ± 5
135 ± 5.3
P = 0.955
64 ± 1
67 ± 1.2
P = 0.014
219 ± 9.9
219 ± 9.7
P = 0.933
84 ± 5.4
82 ± 5.4
P = 0.571
135 ± 5.5
137 ± 6.0
P = 0.399
62 ± 1.3
63 ± 1.4
P = 0.512
Myocardial oedema (STIR), hyperemia assessment (rGE), and fibrosis (LHE) pre and post marathon.
Post Marathon (SD)
Myocardial:Skeletal STIR Ratio
1.3 (SD 0.3)
1.4 (SD 0.3)
Percentage SI Increase in rGE
30% (SD 8%)
31% (SD 9.6%)
rGE Myocardium:Skeletal Muscle Ratio
Relationships between blood markers and myocardial damage
No significant correlations between biomarkers of cardiac damage (cTnI and NTproBNP) at any of the time points and measures of CMR systolic function, inflammation, hyperemia, or myocardial fibrosis were found.
This study demonstrates that exercise induced cardiac biomarker release is not associated with changes in biventricular systolic function or indeed any detectable myocardial damage (inflammation, oedema, hyperemia, or fibrosis) using current gold standard imaging modalities. The release of cardiac troponins (cTnT and cTnI) following prolonged exercise has been extensively documented and the high prevalence of cTnI and NTproBNP release following endurance exercise in this cohort is consistent with previous endurance studies [3–5]. The relationship between cardiac biomarkers and cardiac function following prolonged exercise continues to be a subject that generates much debate in the literature. Many studies have reported a lack of association between troponin release and functional changes, suggesting that they are distinctly separate phenomena . Our data concur with these studies demonstrating no significant relationship between cTnI and NTproBNP and measures of cardiac function and support the hypothesis that alterations in cardiac function and the presence of cardiac biomarkers are unrelated.
The aetiology and clinical significance of post-exercise troponin release is yet to be elucidated. Shave et al. suggested that post-exercise release of troponin may represent either necrosis of cardiac myocytes leading to irreversible damage, or may be a transient and reversible change in membrane permeability of the myocyte . The mechanisms for troponin release may come from the unbound pool found in the cardiomyocyte cytoplasm and may reflect a physiologic as opposed to a pathologic process . It appears unlikely that the minor elevations in biomarkers of cardiac damage observed following prolonged endurance exercise indicate myocardial necrosis of sufficient magnitude to cause LV dysfunction. Furthermore, no single participant was found to meet criteria for myocardial inflammation or fibrosis following the marathon run. This suggests that elevated cardiac troponins represent reversible cardiomyocyte membrane damage that may reflect part of a remodelling process however further study is required to elucidate the mechanism.
A significant elevation in CMR EF was observed 6 hrs post-marathon, with no change in SV. This data contrasts with recent data that demonstrates persistent RV dysfunction post endurance exercise but is in agreement with the work of others [29–32]. In our work, the increase in EF noted after the marathon appears to be a compensatory increase to preserve stroke volume in the presence of reduced end-diastolic and end-systolic volumes. Whether this elevation in EF is a systolic rebound or over-performance issue remains to be confirmed. In the work by Mousavi et al, significant reductions in RVEF were noted in 14 participants studied following a marathon run. Important differences between this and our study should be highlighted which may account for the differences in our results and theirs. In particular we studied a male only population, whereas just over 40% of participants were female in the Mousavi study. It is also difficult to compare marathon completion times between both studies since the mean time for completion in their work of 245 minutes may reflect slower completion times for the female participants. We have provided a table to show completion times with peak biomarker release and CMR findings to avoid any confusion regarding individual differences in results.
Like many studies of this type, the numbers our cohort studied are small and the findings may not necessarily be applicable to larger populations. The spatial resolution of the CMR technique may also be insufficient to image small focal areas of myocardial inflammation or scarring caused by subclinical myocyte damage. We chose a 6 hour time point to perform the post marathon CMR and this may have influenced our findings. It is possible that changes in inflammation may not be detectable until after 6 hours but it was reassuring that 4 participants that returned within 4 days for a repeat CMR were not found to have any demonstrable structural or functional changes. The ratio used to evaluate myocardial oedema and hyperaemia was similar to that used in the Lake Louise criteria although we acknowledge that there were some differences in the protocol used with regard to the slice thickness. Work from our group suggests that this does not significantly alter the interpretation.
This study showed that cardiac biomarkers suggestive of myocyte damage are elevated after a marathon, but these elevations are not associated with any detectable myocardial damage or acute changes in left or right ventricular function. Biomarkers of myocardial cell damage following an acute bout of prolonged exercise are not associated with functional changes using CMR and do not seem to be associated with any detectable myocardial inflammation, oedema, or scarring. This investigation provides further evidence for the careful consideration in assessing and treating symptomatic athletes following arduous exercise in the presence of elevated cardiac troponins and ECG anomalies.
Cardiovascular magnetic resonance
Brain natriuretic peptide
creatine kinase-MB subunit
cardiac troponin I
N-terminal brain natriuretic peptide
turbo spin secho
field of view
late gadolinium enhancement
fast low angle shot
region of interest
short-tau inversion recovery
relative gadolinium enhancement
- George K, Oxborough D, Forster J, Whyte G, Shave R, Dawson E, Stephenson C, Dugdill L, Edwards B, Gaze D: Mitral annular myocardial velocity assessment of segmental left ventricular diastolic function after prolonged exercise in humans. J Physiol. 2005, 569: 305-313. 10.1113/jphysiol.2005.095588.PubMed CentralView ArticlePubMedGoogle Scholar
- Middleton N, George K, Whyte G, Gaze D, Collinson P, Shave R: Cardiac troponin T release is stimulated by endurance exercise in healthy humans. J Am Coll Cardiol. 2008, 52: 1813-1814. 10.1016/j.jacc.2008.03.069.View ArticlePubMedGoogle Scholar
- Shave R, George KP, Atkinson G, Hart E, Middleton N, Whyte G, Gaze D, Collinson PO: Exercise induced cardiac troponin T release: a meta-analysis. Med Sci Sports Exerc. 2007, 39: 2099-2106. 10.1249/mss.0b013e318153ff78.View ArticlePubMedGoogle Scholar
- Neilan TG, Januzzi JL, Lee-Lewandrowski E, Ton-Nu TT, Yoerger DM, Jassal DS, Lewandrowski KB, Siegel AJ, Marshall JE, Douglas PS, Lawlor D, Picard MH, Wood MJ: Myocardial injury and ventricular dysfunction related to training levels among nonelite participants in the Boston marathon. Circulation. 2006, 114: 2325-2333. 10.1161/CIRCULATIONAHA.106.647461.View ArticlePubMedGoogle Scholar
- Neilan TG, Yoerger DM, Douglas PS, Marshall JE, Halpern EF, Lawlor D, Picard MH, Wood MJ: Persistent and reversible cardiac dysfunction among amateur marathon runners. Eur Heart J. 2006, 27: 1079-1084. 10.1093/eurheartj/ehi813.View ArticlePubMedGoogle Scholar
- Whyte GP: Clinical significance of cardiac damage and changes in function after exercise. Med Sci Sports Exerc. 2008, 40: 1416-1423. 10.1249/MSS.0b013e318172cefd.View ArticlePubMedGoogle Scholar
- Rowe WJ: Extraordinary unremitting endurance exercise and permanent injury to normal heart. Lancet. 1992, 340: 712-714. 10.1016/0140-6736(92)92243-9.View ArticlePubMedGoogle Scholar
- Whyte G, Sheppard M, George K, Shave R, Wilson M, Prasad S, O'Hanlon R, Sharma S: Post mortem evidence of idiopathic left ventricular hypertrophy and idiopathic interstitial myocardial fibrosis: is exercise the cause?. Br J Sports Med. 2008, 42: 304-305. 10.1136/bjsm.2007.038158.View ArticlePubMedGoogle Scholar
- Chen Y, Serfass RC, Mackey-Bojack SM, Kelly KL, Titus JL, Apple FS: Cardiac troponin T alterations in myocardium of serum of rats after stressful prolonged intense exercise. J Appl Physiol. 2000, 88: 1749-1755.PubMedGoogle Scholar
- Bellenger NG, Pennell DJ: Ventricular function. Cardiovascular magnetic resonance. Edited by: Manning WJ, Pennell DJ. 2002, Churchill Livingstone, New York, USA, 99-111.Google Scholar
- Grothues F, Smith GC, Moon JC, Bellenger NG, Collins P, Klein HU, Pennell DJ: Comparison of interstudy reproducibility of cardiovascular magnetic resonance with two-dimensional echocardiography in normal subjects and in patients with heart failure or left ventricular hypertrophy. Am J Cardiol. 2002, 90: 29-34. 10.1016/S0002-9149(02)02381-0.View ArticlePubMedGoogle Scholar
- Simonetti OP, Finn JP, White RD, Laub G, Henry DA: "Black blood" T2-weighted inversion recovery MR imaging of the heart. Radiology. 1996, 199: 49-57.View ArticlePubMedGoogle Scholar
- Laissy JP, Messin B, Varenne O, Iung B, Karila-Cohen D, Schouman-Claeys E, Steg PG: MRI of acute myocarditis: a comprehensive approach based on various imaging sequences. Chest. 2002, 122: 1938-1648. 10.1378/chest.122.5.1638.View ArticleGoogle Scholar
- Abdel-Aty H, Boyé P, Zagrosek A, Wassmuth R, Kumar A, Messroghli D, Bock P, Dietz R, Friedrich MG, Schulz-Menger J: Diagnostic performance of cardiovascular magnetic resonance in patients with suspected acute myocarditis: comparison of different approaches. J Am Coll Cardiol. 2005, 45: 1815-1822. 10.1016/j.jacc.2004.11.069.View ArticlePubMedGoogle Scholar
- Miller DD, Holmvang G, Gill JB, Dragotakes D, Kantor HL, Okada RD, Brady TJ: MRI detection of myocardial perfusion changes by gadolinium-DTPA infusion during dipyrimadole hyperemia. Magn Reson Med. 1989, 10: 246-255. 10.1002/mrm.1910100209.View ArticlePubMedGoogle Scholar
- Friedrich MG, Strohm O, Schulz-Menger J, Marciniak H, Luft FC, Dietz R: Contrast media-enhanced magnetic resonance imaging visualizes myocardial changes in the course of viral myocarditis. Circulation. 1998, 97: 1802-1809.View ArticlePubMedGoogle Scholar
- Roditi GH, Hartnell GC, Cohen MC: MRI: changes in myocarditis-evaluation with spin echo, cine MR angiography and contrast enhanced spin echo imaging. Clin Radiol. 2000, 55: 752-758. 10.1053/crad.2000.0519.View ArticlePubMedGoogle Scholar
- Friedrich MG, Sechtem U, Schulz-Menger J, Holmvang G, Alakija P, Cooper LT, White JA, Abdel-Aty H, Gutberlet M, Prasad S, Aletras A, Laissy JP, Paterson I, Filipchuk NG, Kumar A, Pauschinger M, Liu P, International Consensus Group on Cardiovascular Magnetic Resonance in Myocarditis: Cardiovascular magnetic resonance in myocarditis: a JACC white paper. J Am Coll Cardiol. 2009, 53: 1475-1487. 10.1016/j.jacc.2009.02.007.PubMed CentralView ArticlePubMedGoogle Scholar
- Abdel-Aty H, Cocker M, Meek C, Tyberg JV, Friedrich MG: Edema as a very early marker for acute myocardial ischemia. A cardiovascular magnetic resonance study. J Am Coll Cardiol. 2009, 53: 1194-1201. 10.1016/j.jacc.2008.10.065.View ArticlePubMedGoogle Scholar
- Kramer CM, Barkhausen J, Flamm SD, Kim RJ, Nagel E: Standardised cardiovascular magnetic resonance imaging (CMR) protocols, society for cardiac magnetic resonance: board of trustees' task force on standardised protocols. J Cardiovasc Magn Reson. 2008, 10: 35-10.1186/1532-429X-10-35.PubMed CentralView ArticlePubMedGoogle Scholar
- Cerqueira MD, Weissman NJ, Dilsizian V, Jacobs AK, Kaul S, Laskey WK, Pennell DJ, Rumberger JA, Ryan T, Verani MS, American Heart Association Writing Group on Myocardial Segmentation and Registration for Cardiac Imaging: Standardized myocardial segmentation and nomenclature for tomographic imaging of the heart: a statement for healthcare professionals from the Cardiac Imaging Committee of the Council on Clinical Cardiology of the American Heart Association. Circulation. 2002, 105: 539-542. 10.1161/hc0402.102975.View ArticlePubMedGoogle Scholar
- Friedrich MG, Strohm O, Schulz-Menger J, Marciniak H, Luft FC, Dietz R: Contrast-media magnetic resonance imaging visualizes myocardial changes in the course of viral myocarditis. Circulation. 1998, 97: 1802-1809.View ArticlePubMedGoogle Scholar
- Simonetti OP, Kim RJ, Fieno DS, Hillenbrand HB, Wu E, Bundy JM, Finn JP, Judd RM: An improved MR imaging technique for the visualisation of myocardial infarction. Radiology. 2001, 218: 215-223.View ArticlePubMedGoogle Scholar
- Amado LC, Gerber BL, Gupta SN, Rettmann DW, Szarf G, Schock R, Nasir K, Kraitchman DL, Lima JA: Accurate and objective infarct sizing by contrast-enhanced magnetic resonance imaging in a canine myocardial infarction model. J Am Coll Cardiol. 2004, 44: 2383-2389. 10.1016/j.jacc.2004.09.020.View ArticlePubMedGoogle Scholar
- Schmidt A, Azevedo CF, Cheng A, Gupta SN, Bluemke DA, Foo TK, Gerstenblith G, Weiss RG, Marbán E, Tomaselli GF, Lima JA, Wu KC: Infarct tissue heterogeneity by magnetic resonance imaging identifies enhanced cardiac arrhythmia susceptibility in patients with left ventricular dysfunction. Circulation. 2007, 115: 2006-2014. 10.1161/CIRCULATIONAHA.106.653568.PubMed CentralView ArticlePubMedGoogle Scholar
- Spiewak M, Malek LA, Misko J, Chojnowska L, Milosz B, Klopotowski M, Petryka J, Dabrowski M, Kepka C, Ruzyllo W: Comparison of different quantification methods of late gadolinium enhancement in patients with hypertrophic cardiomyopathy. Eur J Radiol. 2009,Google Scholar
- Whyte G, George K, Shave R, Dawson E, Stephenson C, Edwards B, Gaze D, Oxborough D, Forster J, Simspon R: Impact of marathon running on cardiac structure and function in recreational runners. Clin Sci (Lond). 2005, 108: 73-80. 10.1042/CS20040186.View ArticleGoogle Scholar
- Dawson EA, Whyte GP, Black MA, Jones H, Hopkins N, Oxborough D, Gaze D, Shave RE, Wilson M, George KP, Green DJ: Changes in vascular and cardiac function after prolonged strenuous exercise in humans. J Appl Physiol. 2008, 105: 1562-1569. 10.1152/japplphysiol.90837.2008.View ArticlePubMedGoogle Scholar
- Mousavi N, Czarnecki A, Kumar K, Fallah-Rad N, Lytwyn M, Han SY, Francis A, Walker JR, Kirkpatrick ID, Neilan TG, Sharma S, Jassal DS: Relation of biomarkers and cardiac magnetic resonance imaging after marathon running. Am J Cardiol. 2009, 103: 1467-1472. 10.1016/j.amjcard.2009.01.294.View ArticlePubMedGoogle Scholar
- Neilan TG, Ton-Nu TT, Jassal DS, Popovic ZB, Douglas PS, Halpern EF, Marshall JE, Thomas JD, Picard MH, Yoerger DM, Wood MJ: Myocardial adaptation to short-term high-intensity exercise in highly trained athletes. J Am Soc Echocardiogr. 2006, 19: 1280-1285. 10.1016/j.echo.2006.05.001.View ArticlePubMedGoogle Scholar
- Middleton N, Shave R, George K, Whyte G, Hart E, Atkinson G: Left ventricular dysfunction immediately following prolonged exercise: a meta-analysis. Med Sci Sports Exerc. 2006, 38: 681-687. 10.1249/01.mss.0000210203.10200.12.View ArticlePubMedGoogle Scholar
- Knebel F, Schimke I, Schroeckh S, Peters H, Eddicks S, Schattke S, Brechtel L, Lock J, Wernecke KD, Dreger H, Grubitz S, Schmidt J, Baumann G, Borges AC: Myocardial function in older male amateur marathon runners: assessment by tissue doppler echocardiography, speckle tracking, and cardiac biomarkers. J Am Soc Echocardiogr. 2009, 22: 803-809. 10.1016/j.echo.2009.04.009.View ArticlePubMedGoogle Scholar
This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.