Association of Serum Troponin Obtained During Stroke Codes with Cardioembolic Strokes
1Montefiore Medical Center, The Bronx, NY.
Insights
Elevated troponin levels during acute stroke codes are significantly associated with cardioembolic strokes. This finding suggests troponin may help identify stroke patients needing further investigation for cardiac sources.
Area of Science:
- Cardiology
- Neurology
- Biomarkers
Background:
- Troponin is a key indicator of cardiac ischemia.
- Elevated troponin is observed in approximately 30% of stroke patients.
- The association between troponin elevation during acute stroke and cardioembolic sources requires further investigation.
Purpose of the Study:
- To investigate the association between elevated troponin levels during acute stroke codes and the presence of a cardioembolic source.
- To determine if troponin levels can aid in differentiating cardioembolic from noncardioembolic strokes.
Main Methods:
- Retrospective chart review of patients evaluated for acute strokes between July 2014 and March 2018.
- Inclusion criteria: intravenous alteplase, troponin drawn during stroke code, confirmed new stroke on neuroimaging.
- Exclusion criteria: dialysis or glomerular filtration rate ≤ 40 ml/min.
- Stroke etiology classified as cardioembolic (CE) or noncardioembolic (NCE) using Trial of Org 10172 in Acute Stroke Treatment criteria.
- Troponin cutoff: ≥ 0.05 ng/mL.
Main Results:
- 144 patients met inclusion criteria.
- 40.74% of CE patients had troponin ≥ 0.05 ng/mL vs. 12.22% of NCE patients.
- Troponin ≥ 0.05 ng/mL during stroke code significantly differed between CE and NCE strokes (OR, 4.94; P < .001).
- High specificity (87.78%) and low sensitivity (40.74%) for excluding noncardioembolic stroke.
Conclusions:
- Troponin elevation (≥ 0.05 ng/mL) during acute stroke codes is significantly associated with cardioembolic strokes.
- This finding has clinical implications for stroke workup.
- Patients with elevated troponin may require further investigation for cardioembolic sources, especially if not initially identified.
Background:
Troponin is a marker of cardiac ischemia and is elevated in about 30% of stroke patients. We investigated if the elevation of troponin during an acute stroke code is associated with a cardioembolic source.
Methods:
We performed a retrospective chart review of patients evaluated for acute strokes from July 2014 to March 2018. Patients included in the study were all given intravenous alteplase, had blood drawn for troponins during the acute stroke code and had confirmation of a new stroke on neuroimaging during hospitalization. Patients who were on dialysis or had a glomerular filtration rate of less than or equal to 40 ml/minutes on initial laboratory evaluation were excluded. Stroke etiology was classified into noncardioembolic (NCE) and cardioembolic (CE), according to Trial of Org 10172 in Acute Stroke Treatment criteria. The NCE group was compared with the CE group with respect to troponin levels. Troponin was considered as a dichotomous categorical variable, with a cut-off point at greater than or equal to.05 ng/ml.
Results:
144 patients met the inclusion criteria. In our cohort, 40.74% of patients in the CE group had troponin levels of greater than or equal to .05 ng/mL compared to 12.22% in NCE group. A troponin level of greater than or equal to.05 ng/ml obtained during a stroke code showed a significant difference between cardioembolic and noncardioembolic strokes (OR, 4.94; 95% CI, 2.15-11.35; P < .001), with high specificity (87.78%) but low sensitivity (40.74%) to exclude noncardioembolic stroke.
Conclusions:
A troponin level of greater than or equal to .05 ng/ml obtained during a stroke code showed a significant difference between CE and NCE strokes. This finding may have implications for clinical workup, and patients with admission troponin levels of greater than or equal to .05 ng/mL may need further clinical investigations to look for a cardioembolic source. A troponin level of greater than or equal to .05 ng/ml may prompt a more thorough search for a cardioembolic source in cases in which such a source is not identified on initial evaluation.
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