BACKGROUND: 

Increased high-sensitive cardiac troponin I (hs-cTnI) is a common finding in patients with acute ischemic stroke, occurring in more than 50% of the patients. However, only the minority of patients with elevated troponin demonstrates culprit lesions on coronary angiography with the need of immediate intervention. Therefore, other unknown mechanisms of myocardial damage causing elevated troponin levels must be present. Myocardial tissue damage of non-ischemic causes, e.g. inflammation, might be an alternative reason. Cardiac magnetic resonance (CMR) is the preferred method for non-invasive myocardial tissue characterization, with its technique of Late Gadolinium Enhancement (LGE) allowing distinct differentiation between ischemic and non-ischemic myocardial damage, and with the addition of recent mapping techniques (T1, T2, extracellular volume (ECV)) allowing even the detection of diffuse myocardial processes.

In this study, we sought to evaluate in troponin-positive stroke patients the prevalence of 1) culprit lesions by coronary angiography, and 2) myocardial tissue abnormalities by the use of a comprehensive CMR protocol including LGE-CMR and recent mapping techniques.

METHODS: 

Patients with: 1) acute ischemic stroke, 2) no history of coronary artery disease, demonstrating increased troponin levels were prospectively enrolled. Beside coronary angiography, LGE-CMR was performed within the first days of the acute event. Ischemic LGE was defined as subendocardial or transmural enhancement; non-ischemic LGE was defined as intramural or subepicardial enhancement. Mapping values (T1, T2, ECV) were compared to the values of a healthy control group.   

RESULTS: 

Twenty-five stroke patients (mean age 62 years; 44% females) with increased hs-cTnI [peak median 882 ng/L] had evaluable datasets with both coronary angiography and CMR exam. Only 2 patients (8%) with elevated troponin demonstrated culprit lesions in coronary angiography and underwent percutaneous coronary intervention (PCI). Overall, 13 patients (52%) showed evidence of LGE: (i) n=4 ischemic LGE, (ii) n=4 non-ischemic LGE, (iii) n=5 a combination of ischemic AND non-ischemic LGE pattern. The 2 patients who underwent PCI had both ischemic (transmural) scars. However, the majority of LGE-positive patients (n=9) showed exclusively non-ischemic LGE, or at least a combination of non-ischemic and ischemic myocardial lesions as demonstrated by LGE-CMR. In the 12 LGE-negative (but troponin-positive) patients, CMR mapping techniques revealed myocardial damage by the presence of at least one increased mapping parameter (T1, T2, ECV) in n=9 (75%) patients.

CONCLUSIONS: 

Our data confirm a low prevalence (8%) of culprit lesions in troponin-positive stroke patients. However, 52% of our patients demonstrated myocardial damage detected by LGE-CMR, with the majority of patients showing non-ischemic lesions or at least a combination of non-ischemic and ischemic lesions. The addition of CMR mapping techniques additionally detected 75% of the LGE negative patients with myocardial tissue abnormalities, underlining the important role of mapping techniques in the detection of even subtle and diffuse myocardial changes compared to LGE-CMR alone. Therefore, a comprehensive CMR protocol including both LGE and mapping techniques seems to add important value to the challenging clinical work-up of troponin-positive stroke patients.