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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

Representative images of CMR acquisitions to detect myocardial oedema/inflammation (STIR) (A), hyperaemia (rGE) (B), and myocardial fibrosis (LGE) (C).
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Figure 4: Representative images of CMR acquisitions to detect myocardial oedema/inflammation (STIR) (A), hyperaemia (rGE) (B), and myocardial fibrosis (LGE) (C).

Mentions: The LV end-diastolic and end-systolic volumes were reduced post marathon but the stroke volume was preserved (135.4 ± 5.0 vs. 135.5 ± 5.3 ml, P = NS) and a corresponding small increase in LV EF 6 hrs post-marathon reached significance (64.4% ± 1.0% vs 67.4% ± 1.2%; p = 0.014), Table 3, Figure 3a. No significant difference in the RV volumes, RV stroke volume or RV ejection fraction was seen post-marathon, Figure 3b. No patient demonstrated detectable focal or global myocardial oedema on pre and post marathon STIR imaging, Figure 4. Myocardial rGE pre and post contrast ratio was less than 45% in all, and none reached the rGE threshold of myocardium/skeletal muscle ratio of > 4.0, Table 4. Finally, no LGE was seen pre or post marathon in any participant. Four participants returned within 4 days to undergo a repeat CMR to look for any late changes in function or detectable tissue changes. None however demonstrated any LV or RV changes from baseline and none had detectable myocardial inflammation or fibrosis.


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)

Representative images of CMR acquisitions to detect myocardial oedema/inflammation (STIR) (A), hyperaemia (rGE) (B), and myocardial fibrosis (LGE) (C).
© Copyright Policy - open-access
Related In: Results  -  Collection

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

Figure 4: Representative images of CMR acquisitions to detect myocardial oedema/inflammation (STIR) (A), hyperaemia (rGE) (B), and myocardial fibrosis (LGE) (C).
Mentions: The LV end-diastolic and end-systolic volumes were reduced post marathon but the stroke volume was preserved (135.4 ± 5.0 vs. 135.5 ± 5.3 ml, P = NS) and a corresponding small increase in LV EF 6 hrs post-marathon reached significance (64.4% ± 1.0% vs 67.4% ± 1.2%; p = 0.014), Table 3, Figure 3a. No significant difference in the RV volumes, RV stroke volume or RV ejection fraction was seen post-marathon, Figure 3b. No patient demonstrated detectable focal or global myocardial oedema on pre and post marathon STIR imaging, Figure 4. Myocardial rGE pre and post contrast ratio was less than 45% in all, and none reached the rGE threshold of myocardium/skeletal muscle ratio of > 4.0, Table 4. Finally, no LGE was seen pre or post marathon in any participant. Four participants returned within 4 days to undergo a repeat CMR to look for any late changes in function or detectable tissue changes. None however demonstrated any LV or RV changes from baseline and none had detectable myocardial inflammation or fibrosis.

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