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Published on: June 11, 2019
TRoponin of Unknown origin in STroke evaluated by multi-component cardiac Magnetic resonance Imaging - The TRUST-MI
Annerose Mengel1, Lilyana Nenova2, Karin A L Müller2
1Department of Neurology and Stroke, Hertie Institute for Clinical Brain Research, University of Tübingen, Tübingen, Germany.
Insights
Elevated cardiac troponin in stroke patients is common, but coronary artery disease is rare. Cardiac MRI reveals myocardial damage in over half of patients, often due to inflammation, not just blockages.
Area of Science:
- Cardiology and Neurology
- Cardiovascular Imaging
- Biomarker Research
Background:
- Elevated high-sensitive cardiac troponin I (hs-cTnI) is frequent in acute ischemic stroke.
- Culprit coronary artery lesions are found in a minority, suggesting non-ischemic causes like inflammation.
- Cardiac magnetic resonance (CMR) with mapping techniques can detect focal and diffuse myocardial abnormalities.
Purpose of the Study:
- To investigate the prevalence of coronary culprit lesions in troponin-positive stroke patients.
- To assess myocardial tissue abnormalities using a comprehensive CMR protocol (LGE, T1/T2 mapping, ECV).
- To explore the etiology of myocardial damage in acute ischemic stroke patients with elevated troponin.
Main Methods:
- Prospective enrollment of troponin-positive acute ischemic stroke patients without prior coronary artery disease.
- Performance of coronary angiography and CMR (LGE, T1/T2 mapping, ECV) within days of stroke onset.
- Analysis of 25 patients (mean age 62, 44% female) for culprit lesions and myocardial abnormalities.
Main Results:
- Only 2 patients (8%) had coronary culprit lesions requiring intervention.
- Late Gadolinium Enhancement (LGE) detected myocardial scars in 13 patients (52%), both ischemic and non-ischemic.
- In LGE-negative patients, mapping revealed diffuse myocardial damage (mostly inflammatory) in 9 additional patients (75%).
Conclusions:
- A low prevalence of obstructive coronary artery disease exists in troponin-positive stroke patients.
- Cardiac MRI, including LGE and mapping, identifies myocardial abnormalities in over 50% of these patients.
- Comprehensive CMR provides crucial etiological insights for managing troponin elevation in stroke.
Aims:
Increased high-sensitive cardiac troponin I (hs-cTnI) levels are common in patients with acute ischemic stroke. However, only a minority demonstrates culprit lesions on coronary angiography, suggesting other mechanisms, e.g., inflammation, as underlying cause of myocardial damage. Late Gadolinium Enhancement (LGE)-cardiac magnetic resonance (CMR) with mapping techniques [T1, T2, extracellular volume (ECV)] allow the detection of both focal and diffuse myocardial abnormalities. We investigated the prevalence of culprit lesions by coronary angiography and myocardial tissue abnormalities by a comprehensive CMR protocol in troponin-positive stroke patients.
Methods And Results:
Patients with troponin-positive acute ischemic stroke and no history of coronary artery disease were prospectively enrolled. Coronary angiography and CMR (LGE, T1 + T2 mapping, ECV) were performed within the first days of the acute stroke. Twenty-five troponin-positive patients (mean age 62 years, 44% females) were included. 2 patients (8%) had culprit lesions on coronary angiography and underwent percutaneous coronary intervention. 13 patients (52%) demonstrated LGE: (i) n = 4 ischemic, (ii) n = 4 non-ischemic, and (iii) n = 5 ischemic AND non-ischemic. In the 12 LGE-negative patients, mapping revealed diffuse myocardial damage in additional 9 (75%) patients, with a high prevalence of increased T2 values.
Conclusions:
Our data show a low prevalence of culprit lesions in troponin-positive stroke patients. However, > 50% of the patients demonstrated myocardial scars (ischemic + non-ischemic) by LGE-CMR. Mapping revealed additional myocardial abnormalities (mostly inflammatory) in the majority of LGE-negative patients. Therefore, a comprehensive CMR protocol gives important insights in the etiology of troponin which might have implications for the further work-up of troponin-positive stroke patients.
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