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.
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.
Authors: Francesco Ruggieri; Marco Gemma; Maria Rosa Calvi; Elisa Nicelli; Andrea Agarossi; Luigi Beretta Journal: Neurocrit Care Date: 2012-12 Impact factor: 3.210
Authors: E Di Angelantonio; M Fiorelli; D Toni; M L Sacchetti; S Lorenzano; A Falcou; M V Ciarla; M Suppa; L Bonanni; G Bertazzoni; F Aguglia; C Argentino Journal: J Neurol Neurosurg Psychiatry Date: 2005-01 Impact factor: 10.154