The correct answer is: C. Rest MRI

Cardiac MRI would be the single best test. It can accurately assess myocardial perfusion, left and right ventricular function, and valvular structure and function simultaneously. Given the patient’s symptoms and signs, it is highly unlikely that she has had an acute MI. Although highly unlikely, the patient potentially could have an underlying cardiac myopathy; this can be determined using cardiac MRI, as it can accurately distinguish between myocardial necrosis related to an acute MI or myocarditis. The distinction between the two is important, particularly in patients with normal coronary angiography after acute MI. If increased Tn values are related to acute plaque rupture, more aggressive secondary treatment would be warranted. In contrast, if the Tn elevations are from myocarditis or another cardiac myopathy, treatment could be more appropriately directed.

Current recommendations for marker assessment recognize the limitations in very low risk patients; however, as often is the case in the emergency department, patients are “shot gunned” with numerous labs that if abnormal, need to be addressed.

Except for coronary angiography, other tests would be reasonable if cardiac MRI was not available, although all have limitations. Cardiac angiography would not be indicated given the atypical symptoms, normal ECG, and lack of risk factors. Echocardiography allows assessment of valvular function and systolic function, but cannot assess perfusion, and cannot distinguish between different etiologies of LV dysfunction. Stress myocardial perfusion imaging would be somewhat “over kill” given a normal resting ECG. Also, rest MPI has a lower sensitivity compared to MRI for identifying MI. Given the troponin-T of only 0.1 ng/ml, it is unlikely that this would result in an infarction that would be detectable by MPI.

Given a lack of symptoms, stress testing likely would not be indicated in this case. However, if there was concern about participating in an exercise program, routine treadmill without imaging would be the most appropriate test given the normal ECG.

Discussion
Troponin elevation after exercise are relatively common¹. The frequency of elevations will vary based on the troponin assay type, sensitivity, and diagnostic value used to define abnormal, as well as the type and duration of exercise, the fitness levels of participants, the type and the timing of post-exercise sampling,. A recent meta-analysis² found that post-exercise cTn concentrations were measurable in about 50% of participants. Interestingly, cTn detection was increasingly common as duration shortened. This might be because shorter races are usually performed at higher exercise intensities.

Most studies have included participants in events required to maintain an elevated cardiac output, heart rate, and systolic blood pressure for several hours. This sustained increase in cardiac work stresses the myocardium, which in conjunction with the physiologic milieu of prolonged exercise (e.g., elevations in reactive oxygen species, altered pH, and increased core temperature) could potentially damage cardiomyocytes.

Data from serum cTn during controlled laboratory-based exercise testing demonstrated that release of cTn begins as early as 30 min into sustained endurance exercise³, and in a study of marathoners, TnT peaked very early⁴, a pattern distinctly different from acute MI. In one study, cTnT was measured and echocardiography performed 20 min after the race in non-elite participants completing the Boston Marathon (5). Detectable cTnT was found in a majority of participants (cTnT >0.01 ng/ml), 45% had a serum cTnT 0.03 ng/ml, and 13% had cTnT levels >0.10 ng/ml. Increases in cTnT were associated with reductions in right ventricular contractility. Elevations were inversely proportional to training prior to the event, suggesting vital exhaustion as a potential etiology. Others have also found an association between exercise, RV dysfunction and troponin elevations⁵. Elevations have also been associated with increased brain naturietic peptide, indicating increased myocardial stretch as a potential cause⁵. Elevations due not appear pathologic as cardiac MRI 1 week after marathon completion did not show any evidence of persistent myocardial dysfunction or myocardial fibrosis⁶.

cTn increases post exercise have been hypothesized to result from increased membrane permeability, with release from the cytosolic pool, rather than direct myocardial injury. cTn release resulting from myocardial cell necrosis appears to unlikely, given the relatively small elevations in cTn that have been observed after exercise and the difference in release kinetics. Given the increased use of more sensitive cTn assays, and increased participation in exercise events, this is likely to be a problem seen more frequently.

References

1. Shave R, Baggish A, George K, Wood M, Scharhag J, Whyte G, Gaze D, Thompson PD. Exercise-induced cardiac troponin elevation: evidence, mechanisms, and implications. J Am Coll Cardiol 2010 Jul 13;56(3):169-76.
2. Shave R, George KP, Atkinson G, et al. Exercise-induced cardiac troponin T release: a meta-analysis Med Sci Sports Exerc 2007;39:2099-2106.
3. 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.
4. Herrmann M, Scharhag J, Miclea M, Urhausen A, Herrmann W, Kindermann W. Post-race kinetics of cardiac troponin T and I and N-terminal pro-brain natriuretic peptide in marathon runners. Clin Chem. 2003;49:831-4.
5. Neilan TG, Januzzi JL, Lee-Lewandrowski E, et al. Myocardial injury and ventricular dysfunction related to training levels among nonelite participants in the Boston marathon Circulation 2006;114:2325-2333.
6. Mousavi N, Czarnecki A, Kumar K, et al. Relation of biomarkers and cardiac magnetic resonance imaging after marathon running Am J Cardiol 2009;103:1467-1472.