Yeon Joo Lee1, Hongyeul Lee2, Ji Soo Park3, Se Joong Kim4, Young-Jae Cho5, Ho Il Yoon6, Jae Ho Lee7, Choon-Taek Lee8, Jong Sun Park9. 1. Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, Seoul National University Bundang Hospital, Seongnam-si, Gyeonggi-do, Republic of Korea. Electronic address: yjlee1117@snubh.org. 2. Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, Seoul National University Bundang Hospital, Seongnam-si, Gyeonggi-do, Republic of Korea. Electronic address: yeurry@naver.com. 3. Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, Seoul National University Bundang Hospital, Seongnam-si, Gyeonggi-do, Republic of Korea. Electronic address: ji-soo@snubh.org. 4. Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, Seoul National University Bundang Hospital, Seongnam-si, Gyeonggi-do, Republic of Korea. Electronic address: ksj1146@snubh.org. 5. Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, Seoul National University Bundang Hospital, Seongnam-si, Gyeonggi-do, Republic of Korea. Electronic address: lungdrcho@gmail.com. 6. Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, Seoul National University Bundang Hospital, Seongnam-si, Gyeonggi-do, Republic of Korea. Electronic address: dextro70@gmail.com. 7. Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, Seoul National University Bundang Hospital, Seongnam-si, Gyeonggi-do, Republic of Korea. Electronic address: jhlee7@snubh.org. 8. Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, Seoul National University Bundang Hospital, Seongnam-si, Gyeonggi-do, Republic of Korea. Electronic address: ctlee@snubh.org. 9. Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, Seoul National University Bundang Hospital, Seongnam-si, Gyeonggi-do, Republic of Korea. Electronic address: jspark.im@gmail.com.
Abstract
PURPOSE: Elevated cardiac troponin (cTn) has been associated with worse outcomes in critically ill patients, but few studies have focused on whether these markers are related to outcomes in patients with severe pneumonia. We investigated the levels of cTnI in critically ill patients hospitalized for severe pneumonia and whether elevated levels of cTnI correlated with the clinical outcome of this patient group. MATERIALS AND METHODS: We conducted a retrospective study of patients admitted to the medical intensive care unit (ICU) with severe pneumonia with levels of cTnI obtained within 24 hours of admittance. Patients with evidence of acute coronary syndrome were excluded. A cTnI level greater than 0.034 ng/mL was considered positive. P value < .05 was considered significant. RESULTS: A total of 152 patients (community-acquired pneumonia [39.5%], health care-associated pneumonia [40.8%], and hospital-acquired pneumonia [19.7%]) were included in the study. Eighty-eight (58%) patients had detectable cTnI levels (median, 0.049 ng/mL). Patients with increased cTnI levels showed higher in-ICU mortality (38.6% vs 21.9%, P = .028). The association between elevated cTnI levels and mortality remained significant after adjustment using a multivariate model (adjusted hazard ratio = 1.398; 95% confidence interval, 1.005-1.945; P = .047). CONCLUSIONS: Increased levels of cTnI are an independent predictor of ICU mortality in patients hospitalized with severe pneumonia without evidence of acute coronary syndrome.
PURPOSE: Elevated cardiac troponin (cTn) has been associated with worse outcomes in critically illpatients, but few studies have focused on whether these markers are related to outcomes in patients with severe pneumonia. We investigated the levels of cTnI in critically illpatients hospitalized for severe pneumonia and whether elevated levels of cTnI correlated with the clinical outcome of this patient group. MATERIALS AND METHODS: We conducted a retrospective study of patients admitted to the medical intensive care unit (ICU) with severe pneumonia with levels of cTnI obtained within 24 hours of admittance. Patients with evidence of acute coronary syndrome were excluded. A cTnI level greater than 0.034 ng/mL was considered positive. P value < .05 was considered significant. RESULTS: A total of 152 patients (community-acquired pneumonia [39.5%], health care-associated pneumonia [40.8%], and hospital-acquired pneumonia [19.7%]) were included in the study. Eighty-eight (58%) patients had detectable cTnI levels (median, 0.049 ng/mL). Patients with increased cTnI levels showed higher in-ICU mortality (38.6% vs 21.9%, P = .028). The association between elevated cTnI levels and mortality remained significant after adjustment using a multivariate model (adjusted hazard ratio = 1.398; 95% confidence interval, 1.005-1.945; P = .047). CONCLUSIONS: Increased levels of cTnI are an independent predictor of ICU mortality in patients hospitalized with severe pneumonia without evidence of acute coronary syndrome.
Authors: F Moccia; A Gerbino; V Lionetti; M Miragoli; L M Munaron; P Pagliaro; T Pasqua; C Penna; C Rocca; M Samaja; T Angelone Journal: Geroscience Date: 2020-05-20 Impact factor: 7.713
Authors: Nina Rosa Neuendorff; Kah Poh Loh; Alice S Mims; Konstantinos Christofyllakis; Wee-Kheng Soo; Bediha Bölükbasi; Carlos Oñoro-Algar; William G Hundley; Heidi D Klepin Journal: Blood Adv Date: 2020-02-25