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Elevated serum cardiac troponin and mortality in acute pulmonary embolism: Systematic review and meta-analysis
Ayman El-Menyar1, Brijesh Sathian2, Hassan Al-Thani3
1Department of Surgery, Clinical Research, Trauma & Vascular Surgery, Hamad Medical Corporation (HMC), Doha, Qatar; Clinical Medicine, Weill Cornell Medical College, Doha, Qatar.
Insights
Elevated cardiac troponin levels significantly increase mortality risk in patients with acute pulmonary embolism (PE). This finding holds true across various troponin assays, highlighting its importance in risk stratification.
Area of Science:
- Cardiology
- Pulmonary Medicine
- Biomarkers
Background:
- Acute pulmonary embolism (PE) is a significant cause of mortality.
- Cardiac troponins are biomarkers of myocardial injury.
- The prognostic value of elevated troponin in acute PE requires comprehensive evaluation.
Purpose of the Study:
- To systematically review and meta-analyze the association between elevated cardiac troponin levels and mortality in patients with acute PE.
- To determine the pooled effect of troponin elevation on all-cause mortality in PE patients.
Main Methods:
- Systematic review and meta-analysis of studies published between 2000-2018.
- Inclusion of retrospective, prospective, and randomized controlled trials assessing troponin levels and PE outcomes.
- Statistical analysis using fixed effect models and heterogeneity testing (Cochrane Q).
Main Results:
- Analysis of 46 studies involving 10,842 PE patients.
- Pooled odds ratio (OR) for elevated troponin and mortality was 4.33.
- Significant associations observed across different troponin assays (HsTnT, HsTnI, cTnT, cTnI) and risk groups.
Conclusions:
- Elevated cardiac troponin is a significant predictor of increased mortality in patients with acute PE.
- This association is consistent regardless of the specific troponin assay used.
- Troponin levels are crucial for risk stratification and management of acute 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.
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