Rapid Fire Abstracts
Edyta Blaszczyk, MD
Cardiologist
Charité - Universitätsmedizin Berlin, Germany
Edyta Blaszczyk, MD
Cardiologist
Charité - Universitätsmedizin Berlin, Germany
Jan Gröschel, MD
MD
Charite, Germany
Leonhard Grassow
Medical student
Charité – Universitätsmedizin Berlin, Germany
Johanna Kuhnt
Medical student
Charité – Universitätsmedizin Berlin, Germany
Darian Steven Viezzer, MSc
Researcher
Charite, Germany
Halil Noyan
medical student
Charité – Universitätsmedizin Berlin, Germany
Richard Hickstein, MD
Physician and Researcher
Charité – Universitätsmedizin Berlin, Germany
Josephine Kermer, MD
MD
DRK Kliniken Berlin Köpenick, Germany
Karl P. Kunze, PhD
Senior Cardiac MR Scientist
Siemens Healthineers, United Kingdom
Michaela Schmidt
Applications Developer
Siemens Healthineers, Germany
Allan S. Jaffe, MD
Professor Cardiologist
Mayo Clinic
Jeanette Schulz-Menger, MD
Head Working Group Cardiac MRI
Charité/ University Medicine Berlin and Helios, Germany
Cardiac troponins T (cTnT) and I (cTnI) are the sensitive biomarkers for detection of myocardial injury. Elevated cTn levels indicate cardiac injury, but do not define the cause. This influences the interpretation of increased cTn in different conditions such as stroke, pulmonary embolism, septic shock, acute myocarditis or heart failure(1-3).
Muscular dystrophies (MD) are diseases of the skeletal muscles potentially affecting other organs including the heart. The interpretation of elevated ccTn in patients with MD is challenging as there is often no evidence of acute cardiac injury based on routine clinical work-up(4).
This study assessed the relation between elevated troponins and cardiac Magnetic Resonancee (CMR) findings in MD patients, hypothesizing that increased troponin values would likely correlate with the extent of myocardial tissue injury and arrhythmias.
Methods:
N=61MD - patients underwent comprehensive cardiac evaluation, including ECG, 24-hour-holter, serum hscTnT and hscTnI analysis as well as CMR (1.5T). CMR-parameters assessed were biventricular and biatrial function, strain, native parametric T2-mapping for inflammation and T1-mapping for quantifying diffuse fibrosis. After Administration of 0.2 mmol/kg Gadoteridol a free-breating high-resolution isotropic GRE 3D-late-gadolinium-enhancement(LGE) research sequence with Dixon fat-water seperation was used to differentiate between fat deposits and focal fibrosis. All image-analyses were performed by using CVI42. Mapping values were matched with N=20 healthy volunteers (HV).
Results:
The cohort consisted of 33 males (54%) and 28 females(46%). ECG and 24-hour-holter revealed abnormalities in 15/61(24.6%) and 13/61(21.3%) cases, respectively. HscTnT was increased in 37/61(60.7%) but hscTnI in only 4/59(6.8%) patients. All patients with increased hscTnI had concomitantly elevated hscTnT values.
Left ventricular (LV) fat infiltration was present in 9/61(14.7%) and focal fibrosis in 22/61(36.1%) participants.
Patients with elevated hscTnT had lower systolic LV function(p=0.048), and higher prevalence of focal fibrosis(p=0.048) than patients with no hscTnT elevation. No significant differences were found for T2-times(p=0.512) and fat infiltration(p=0.770). Table 1. All patients with elevation in both troponins (N=4) manifested focal fibrosis as well as increased T2-times(p=0.040) compared to HV. Figure 1.
HscTnT was increased in 19 patients without CMR abnormalities.
Conclusion:
Troponin elevations, most notably hscTnT were frequent in this MD cohort but were not always associated with CMR abnormalities. HscTnI elevations were rare but indicated acute changes as shown by higher T2 times and ECG abnormalities.
Patients with increased hscTnT and hscTnI exhibited diffuse and focal fibrosis as well as fat infiltration.
In summary, hscTnT elevations are often but not always indicative of myocardial changes in MD. When hscTnI is also increased, imaging suggests an acute event.
