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Association Between Troponin Levels and Visceral Infarction in Patients with Acute Ischemic Stroke
Shobana Ramasamy1, Praneil Patel2, Ajay Gupta2
1Clinical and Translational Neuroscience Unit, Feil Family Brain and Mind Research Institute and Department of Neurology.
Insights
Elevated troponin levels in acute ischemic stroke patients were linked to visceral infarction. This finding suggests that troponin elevation may signal underlying embolic sources, aiding in stroke diagnosis.
Area of Science:
- Cardiology
- Neurology
- Radiology
Background:
- Visceral infarctions are noted in embolic stroke subtypes.
- The link between visceral infarction and troponin elevation is unclear.
Purpose of the Study:
- To investigate the association between elevated troponin and visceral infarction in acute ischemic stroke patients.
Main Methods:
- Utilized data from the Cornell AcutE Stroke Academic Registry (CAESAR) (2011-2016).
- Included patients with troponin assays and abdominal CT scans.
- Defined troponin elevation and visceral infarction (renal or splenic).
- Employed multivariable logistic regression to assess the association.
Main Results:
- 153 patients met inclusion criteria; 33% had elevated troponin, 22% had visceral infarction.
- Visceral infarction prevalence was higher in patients with elevated troponin (30%) versus those without (10%).
- Elevated troponin showed a significant association with visceral infarction (OR, 3.9; 95% CI, 1.5-10.4) after adjustments.
Conclusions:
- Elevated troponin in acute ischemic stroke patients is associated with visceral infarction.
- Poststroke troponin elevation may indicate occult embolic sources.
Background:
Visceral infarctions appear to be more common in patients with embolic stroke subtypes, but their relation to troponin elevation remains uncertain.
Methods:
Among patients with acute ischemic stroke enrolled in the Cornell AcutE Stroke Academic Registry (CAESAR) from 2011 to 2016, we included those with troponin measured within 24 hours from stroke onset and a contrast-enhanced abdominal computed tomographic scan within 1 year of admission. A troponin elevation was defined as a value exceeding our laboratory's upper limit of normal (.04 ng/ mL) in the absence of a clinically recognized acute ST-segment elevation myocardial infarction. Visceral infarction was defined as a renal or splenic infarction as ascertained by a single radiologist blinded to patients' other characteristics. Multivariable logistic regression was used to evaluate the association between elevated troponin and visceral infarction.
Results:
Among 2116 patients registered in CAESAR from 2011 to 2016, 153 patients had both a troponin assay and a contrast-enhanced abdominal computed tomographic scan, of whom 33 (21%) had an elevated troponin and 22 (14%) had a visceral infarction. The prevalence of visceral infarction was higher among patients with an elevated troponin (30%; 95% confidence interval [CI], 16%-49%) than among patients without an elevated troponin (10%; 95% CI, 5%-17%) (P = .003). After adjustment for demographics and comorbidities, we found a significant association between elevated troponin and visceral infarction (odds ratio, 3.9; 95% CI, 1.5-10.4).
Conclusions:
Among patients with acute ischemic stroke, elevated troponin was associated with visceral infarction. Our results demonstrate that poststroke troponin elevation may indicate the presence of underlying embolic sources.
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