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Troponin release following endurance exercise: is inflammation the cause? a cardiovascular magnetic resonance study.

O'Hanlon R, Wilson M, Wage R, Smith G, Alpendurada FD, Wong J, Dahl A, Oxborough D, Godfrey R, Sharma S, Roughton M, George K, Pennell DJ, Whyte G, Prasad SK - J Cardiovasc Magn Reson (2010)

Bottom Line: 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).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.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Cardiovascular Magnetic Resonance, Royal Brompton and Harefield NHS Foundation Trust, London, UK. r.ohanlon9@btinternet.com

ABSTRACT

Background: 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.

Methods: 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.

Results: 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.

Conclusion: Exercise induced cardiac biomarker release is not associated with any functional changes by CMR or any detectable myocardial inflammation or fibrosis.

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Related in: MedlinePlus

Cardiac troponin I (cTnI) release pre-, immediately post- and 6 hrs post-completion of a marathon. Values are mean (± SEM).
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Figure 1: Cardiac troponin I (cTnI) release pre-, immediately post- and 6 hrs post-completion of a marathon. Values are mean (± SEM).

Mentions: No participant had elevations of TnI or NTproBNP at baseline. Eight participants were found to have cTnI elevations immediately post-marathon above the cut off level for acute myocardial infarction (AMI; ≥ 0.03 μg/L. cTnI was further elevated at 6 h post-marathon in 11 of the 17 runners in this study, p = 0.007, Tables 1 and 2, Figure 1. NTproBNP levels rose significantly from baseline at both time points post marathon, p = 0.002, Table 2, Figure 2.


Troponin release following endurance exercise: is inflammation the cause? a cardiovascular magnetic resonance study.

O'Hanlon R, Wilson M, Wage R, Smith G, Alpendurada FD, Wong J, Dahl A, Oxborough D, Godfrey R, Sharma S, Roughton M, George K, Pennell DJ, Whyte G, Prasad SK - J Cardiovasc Magn Reson (2010)

Cardiac troponin I (cTnI) release pre-, immediately post- and 6 hrs post-completion of a marathon. Values are mean (± SEM).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC2908607&req=5

Figure 1: Cardiac troponin I (cTnI) release pre-, immediately post- and 6 hrs post-completion of a marathon. Values are mean (± SEM).
Mentions: No participant had elevations of TnI or NTproBNP at baseline. Eight participants were found to have cTnI elevations immediately post-marathon above the cut off level for acute myocardial infarction (AMI; ≥ 0.03 μg/L. cTnI was further elevated at 6 h post-marathon in 11 of the 17 runners in this study, p = 0.007, Tables 1 and 2, Figure 1. NTproBNP levels rose significantly from baseline at both time points post marathon, p = 0.002, Table 2, Figure 2.

Bottom Line: 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).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.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Cardiovascular Magnetic Resonance, Royal Brompton and Harefield NHS Foundation Trust, London, UK. r.ohanlon9@btinternet.com

ABSTRACT

Background: 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.

Methods: 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.

Results: 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.

Conclusion: Exercise induced cardiac biomarker release is not associated with any functional changes by CMR or any detectable myocardial inflammation or fibrosis.

Show MeSH
Related in: MedlinePlus