Ayman El-Menyar1, Brijesh Sathian2, Hassan Al-Thani3. 1. Department of Surgery, Clinical Research, Trauma & Vascular Surgery, Hamad Medical Corporation (HMC), Doha, Qatar; Clinical Medicine, Weill Cornell Medical College, Doha, Qatar. Electronic address: aelmenyar@hamad.qa. 2. Department of Surgery, Clinical Research, Trauma & Vascular Surgery, Hamad Medical Corporation (HMC), Doha, Qatar. 3. Department of Surgery, Trauma & Vascular Surgery, HMC, Doha, Qatar.
Abstract
OBJECTIVES: To evaluate whether elevated levels of cardiac troponin increases the risk of mortality in patients with acute PE. METHODS: We conducted a systematic review and meta-analysis with rigorous statistical evaluation using publications (2000-2018) from Cochrane Library, MEDLINE, PubMed, Scopus, Cochrane Central Register of Controlled Trials (CENTRAL), WHO International Clinical Trials Registry Platform, and Google Scholar databases. We searched for retrospective, prospective, and randomized controlled trials (RCT) or quasi-RCT studies that assessed the effect of elevated troponin versus normal levels on the outcomes of PE. The main outcome of interest was all-cause mortality. Extracted data included authors, the origin of studies, source population, study settings and duration, inclusion/exclusion criteria, data sources and measurement, sample size, and mortality. Data heterogeneity was assessed using the Cochrane Q homogeneity test with a significance set at p < 0.10. If the studies were statistically homogeneous, a fixed effect model was selected. RESULTS: Out of 1825 references, 46 analytical studies were included with a total of 10842 patients with PE. The effect of elevated troponin on mortality had a pooled odd ratio (OR) of 4.33 for all studies, 3.7for HsTnT, 14.81 for HsTnI, 7.85 for cTnT, 2.81 for cTnI, 9.02 for low-risk PE and 4.80 for 90-day mortality. The pooled negative likelihood ratios for all-cause mortality using HsTnI, cTnI and cTnT assay were 0.21, 0.33 and 0.65, respectively. CONCLUSION: Regardless of the troponin assay, pooled analysis indicates that elevated troponin is significantly associated with higher mortality in patients with PE.
OBJECTIVES: To evaluate whether elevated levels of cardiac troponin increases the risk of mortality in patients with acute PE. METHODS: We conducted a systematic review and meta-analysis with rigorous statistical evaluation using publications (2000-2018) from Cochrane Library, MEDLINE, PubMed, Scopus, Cochrane Central Register of Controlled Trials (CENTRAL), WHO International Clinical Trials Registry Platform, and Google Scholar databases. We searched for retrospective, prospective, and randomized controlled trials (RCT) or quasi-RCT studies that assessed the effect of elevated troponin versus normal levels on the outcomes of PE. The main outcome of interest was all-cause mortality. Extracted data included authors, the origin of studies, source population, study settings and duration, inclusion/exclusion criteria, data sources and measurement, sample size, and mortality. Data heterogeneity was assessed using the Cochrane Q homogeneity test with a significance set at p < 0.10. If the studies were statistically homogeneous, a fixed effect model was selected. RESULTS: Out of 1825 references, 46 analytical studies were included with a total of 10842 patients with PE. The effect of elevated troponin on mortality had a pooled odd ratio (OR) of 4.33 for all studies, 3.7for HsTnT, 14.81 for HsTnI, 7.85 for cTnT, 2.81 for cTnI, 9.02 for low-risk PE and 4.80 for 90-day mortality. The pooled negative likelihood ratios for all-cause mortality using HsTnI, cTnI and cTnT assay were 0.21, 0.33 and 0.65, respectively. CONCLUSION: Regardless of the troponin assay, pooled analysis indicates that elevated troponin is significantly associated with higher mortality in patients with PE.
Authors: Christopher Kabrhel; David R Vinson; Alice Marina Mitchell; Rachel P Rosovsky; Anna Marie Chang; Jackeline Hernandez-Nino; Stephen J Wolf Journal: J Am Coll Emerg Physicians Open Date: 2021-12-15