Cardiac involvement in patients with acute neurologic disease: confirmation with cardiac troponin I
1Mayo Clinic, 200 First St SW, Mayo Clinic Building, 16th Floor, Rochester, MN 55905, USA.
Insights
Cardiac troponin I (cTnI) elevations indicate myocardial injury in patients with acute neurologic illness. This cardiac injury is common and associated with increased early mortality, impacting patient prognosis.
Area of Science:
- Cardiology
- Neurology
- Clinical Biochemistry
Background:
- Acute neurologic illness frequently presents with signs of cardiac injury.
- The interpretation and prognostic significance of cardiac injury in these patients remain unclear.
- This study investigates the incidence and impact of cardiac injury in acute neurologic illness.
Purpose of the Study:
- To assess the incidence of cardiac injury, defined by cardiac troponin I (cTnI) elevation, in patients with acute neurologic illness.
- To determine the short- and long-term prognostic effect of this cardiac injury.
Main Methods:
- Blinded evaluation of patients presenting within 24 hours of a neurologic event.
- Serial measurement of cTnI levels via immunoassay.
- Comprehensive clinical, electrocardiographic, and echocardiographic assessments with daily follow-up.
Main Results:
- Elevated cTnI levels (> or =0.4 microg/L) were observed in 19% of patients.
- Most patients with elevated cTnI showed clinical or diagnostic evidence of cardiac injury.
- Elevated cTnI was significantly associated with higher early mortality (within 30 days).
Conclusions:
- Myocardial injury is prevalent in patients with acute neurologic conditions.
- Cardiac injury appears to adversely affect prognosis in this patient population, particularly in the short term.
Background:
Patients with acute neurologic illness often manifest findings suggestive of cardiac injury. Their proper interpretation is unclear. Accordingly, we conducted a blinded evaluation to assess the incidence of cardiac injury determined by elevations of cardiac troponin I (cTnI) in patients presenting within 24 hours of a neurologic event and to determine their short- and long-term prognostic effect.
Methods:
Blood samples for measurement of cTnI levels were obtained on hospital admission and daily for 3 days and were run by immunoassay. Extensive clinical evaluations including electrocardiograms and echocardiograms were obtained from all patients; daily follow-up evaluations were performed. The clinical electrocardiographic, echocardiographic, and biochemical data were analyzed independently by blinded observers.
Results:
Peak levels of cTnI were elevated (> or =0.4 microg/L) in 17 patients (19%) (mean + SD, 2.5 + 2.7 microg/L). All patients with elevated cTnI levels had clinical, electrocardiographic, or echocardiographic evidence of cardiac injury except those (n = 5) with minor elevations. One-year mortality was 29% (23/80). Early death (< or =30 days) accounted for 44% of total mortality (n = 10) and was significantly higher in patients with elevated cTnI levels (Wilcoxon P =.01; odds ratio, 6. 4). This difference was less marked by 1 year (Wilcoxon P =.07).
Conclusions:
There is a substantial prevalence of myocardial injury in patients with acute neurologic illness. Cardiac injury in this population, as in others, seems to adversely affect prognosis.
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