What is the clinical evidence from this study?

Study design: Cohort. Population: Acute cerebral infarction (n=145). Intervention: Elevated cardiac troponin I (cTnI > 0.030 μg/L) vs. Normal cardiac troponin I (cTnI < 0.030 μg/L). Primary outcome: 5-year all-cause mortality (HR 1.80, 95% CI 1.22-2.65, p=0.003).

May 17, 2022Open Access

Elevated troponin I levels on admission predict long-term mortality in patients with acute cerebral infarction following thrombolysis

Q: What are the key findings of this study?

Elevated cardiac troponin I levels on admission in patients with acute cerebral infarction treated with thrombolysis were associated with a 1.80-fold increased risk of 5-year mortality.

Key Result

Elevated cardiac troponin I levels on admission in patients with acute cerebral infarction treated with thrombolysis were associated with a 1.80-fold increased risk of 5-year mortality.

Study Design

Type

Cohort (n=145)

Multicenter

Structured PICO

Does elevated cardiac troponin I on admission predict long-term mortality in patients with acute cerebral infarction following thrombolysis?

Population

145 adults with acute cerebral infarction treated with intravenous thrombolysis, followed for a median of 5.7 years to assess the prognostic value of elevated cardiac troponin I levels.

Exposure

Elevated cardiac troponin I (cTnI) concentration on admission (> 0.030 μg/L)

Comparator

Normal cardiac troponin I (cTnI) concentration on admission (< 0.030 μg/L)

Outcome

5-year all-cause mortalityhard clinical

Elevated cardiac troponin I on admission is an independent predictor of 5-year mortality in patients with acute cerebral infarction treated with intravenous thrombolysis.

Main Result

Hazard Ratio: 1.8 (95% CI 1.22–2.65)

p-value: p=0.003

Limitations

Small sample size due to missing cTnI values on admission or loss of follow-up data
Unique population restricted to patients receiving intravenous rt-PA thrombolytic therapy
Heart disease was not confirmed by coronary CTA or coronary angiography
cTnI concentrations were not measured continuously in all patients
Insufficient data to demonstrate differences in acute cerebral infarction subtypes
Used conventional method to test cTnI instead of hypersensitive assays
Only detected a single biomarker (cTnI)

Abstract

BACKGROUND/OBJECTIVE: Cardiac diseases are frequently accompanied by elevated levels of biomarkers, among which, troponin is commonly investigated. The levels of plasma cardiac troponin I (cTnI), which has been shown to predict short-term mortality, are elevated in patients with acute cerebral infarction (ACI). However, few studies have assessed the association between cTnI concentration and long-term mortality in patients with ACI following thrombolysis. METHODS: Patients with ACI admitted between January 1, 2014, and December 31, 2016, were registered. Data on demographics and outcomes with elevated cTnI levels were also collected. RESULTS: A total of 145 patients with ACI were recruited; 97 (66%), 30 (20%), and 18 (12%) patients had cTnI concentrations 0.10 μg/L (group 3), respectively. cTnI elevation was associated with older age, atrial fibrillation, congestive heart failure, renal insufficiency, coronary artery disease, stroke severity (National Institutes of Health Stroke Scale score), and prior smoking history at admission. After adjusting for comorbidities and severity at 3 months after ACI, cTnI elevation on admission was significantly associated with ascending 5-year mortality (hazard ratio, 1.80; 95% confidence interval, 1.22-2.65). CONCLUSIONS: Even after adjusting for several possible confounders, cTnI elevation in patients with ACI treated with rt-PA was associated with a 1.80-fold increased risk of 5-year mortality.

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