Magnetic resonance imaging of myocardial injury and ventricular torsion after marathon running.
Recent reports provide indirect evidence of myocardial injury and ventricular dysfunction after prolonged exercise. However, existing data is conflicting and lacks direct verification of functional myocardial alterations by CMR [cardiac MR (magnetic resonance)]. The present study sought to examine structural myocardial damage and modification of LV (left ventricular) wall motion by CMR imaging directly after a marathon. Analysis of cTnT (cardiac troponin T) and NT-proBNP (N-terminal pro-brain natriuretic peptide) serum levels, echocardiography [pulsed-wave and TD (tissue Doppler)] and CMR were performed before and after amateur marathon races in 28 healthy males aged 41 ± 5 years. CMR included LGE (late gadolinium enhancement) and myocardial tagging to assess myocardial injury and ventricular motion patterns. Echocardiography indicated alterations of diastolic filling [decrease in E/A (early transmitral diastolic filling velocity/late transmitral diastolic filling velocity) ratio and E' (tissue Doppler early transmitral diastolic filling velocity)] postmarathon. All participants had a significant increase in NT-proBNP and/or cTnT levels. However, we found no evidence of LV LGE. MR tagging demonstrated unaltered radial shortening, circumferential and longitudinal strain. Myocardial rotation analysis, however, revealed an increase of maximal torsion by 18.3% (13.1 ± 3.8 to 15.5 ± 3.6 °; P=0.002) and maximal torsion velocity by 35% (6.8 ± 1.6 to 9.2 ± 2.5 °·s-1; P<0.001). Apical rotation velocity during diastolic filling was increased by 1.23 ± 0.33 °·s-1 after marathon (P<0.001) in a multivariate analysis adjusted for heart rate, whereas peak untwist rate showed no relevant changes. Although marathon running leads to a transient increase of cardiac biomarkers, no detectable myocardial necrosis was observed as evidenced by LGE MRI (MR imaging). Endurance exercise induces an augmented systolic wringing motion of the myocardium and increased diastolic filling velocities. The stress of marathon running seems to be better described as a burden of myocardial overstimulation rather than cardiac injury.
Hanssen
Henner
H
Department of Prevention and Sports Medicine, Klinikum Rechts der Isar, Technische Universität München, Munich, Germany. hennerhanssen@hotmail.com
Keithahn
Alexandra
A
Hertel
Gernot
G
Drexel
Verena
V
Stern
Heiko
H
Schuster
Tibor
T
Lorang
Dan
D
Beer
Ambros J
AJ
Schmidt-Trucksäss
Arno
A
Nickel
Thomas
T
Weis
Michael
M
Botnar
Rene
R
Schwaiger
Markus
M
Halle
Martin
M
D000328:Adult; D015415:Biomarkers / Q000097:blood; D009202:Cardiomyopathies / Q000175:diagnosis / Q000209:etiology*; D006801:Humans; D008279:Magnetic Resonance Imaging; D008297:Male; D008875:Middle Aged; D020097:Natriuretic Peptide, Brain / Q000097:blood; D010446:Peptide Fragments / Q000097:blood; D012420:Running / Q000293:injuries* / Q000502:physiology; D014102:Torsion Abnormality / Q000175:diagnosis / Q000209:etiology*; D020107:Troponin T / Q000097:blood; D018487:Ventricular Dysfunction, Left / Q000175:diagnosis / Q000209:etiology
D015415:Biomarkers; D010446:Peptide Fragments; D020107:Troponin T; C109794:pro-brain natriuretic peptide (1-76); D020097:Natriuretic Peptide, Brain