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ELEVATION OF CARDIAC TROPONIN T IN PATIENTS WITH AMYOTROPHIC LATERAL SCLEROSIS

L. Mach, T. Konečný, K. Helánová, A. Jaffe, E. Sorenson, V. Somers, G. Reeder (London, United Kingdom, Los Angeles, CA, United States, Brno, Rochester, MN, United States)
Topic: Varia
Type: Poster - doctors, 24th CSC Annual Congress

Background: Limited evidence suggests that specificity of cardiac troponin T (cTnT), a highly sensitive biomarker of myocardial injury, is reduced in patients with skeletal myopathies. Whether amyotrophic lateral sclerosis (ALS) - the most common motor neuron disease - could be also associated with abnormal plasma or serum cTnT levels remains unclear. Our objective was to assess cTnT levels in patients with ALS without known cTnT elevating conditions.

Methods: Among ALS patients seen at our institution until 2012 we identified those who had their cTnT measured. Patients who suffered from conditions known to elevate cTnT were excluded. A case-control analysis comparing cTnT levels of these ALS patients to matched non-ALS controls fulfilling the same inclusion criteria was performed (Figure 1).

Results: We included 40 ALS patients of whom 27 (68%) patients had a positive cTnT. In the control group (n=40), 2 (5%) tested as cTnT positive (p<0.001) (Figure 2). Among the ALS patients who underwent cTnT evaluation on more occasions (n=7; median follow-up=1.08 years), 2 (29%) patients tested positive during the initial measurement while 6 (86%) of them had positive cTnT at the subsequent evaluations. Long term progression of cTnT levels in ALS patients (n=7) is shown in Figure 3. ALS patients with increased cTnT had been diagnosed with ALS significantly earlier than those without the elevation.

Conclusion: Our findings raise the possibility that ALS may cause cTnT elevations and that these elevations may correlate with temporal progression of ALS. Further studies are needed to confirm these findings, clarify the pathophysiological mechanism, and establish the significance of cTnT elevations in patients with ALS.