Cardiac Troponin Measurement in the Critically Ill

Abstract

BackgroundElevated cardiac troponin (cTn) in the absence of acute coronary syndromes (ACS) is associated with increased mortality in critically ill patients. There are no evidence-based interventions that reduce mortality in this group.ObjectivesWe performed a retrospective investigation of the Veterans Administration Inpatient Evaluation Center database to determine whether drugs used in ACS (β-blockers, aspirin, and statins) are associated with reduced mortality in critically ill patients.MethodsThirty-day mortality was determined for non-ACS patients admitted to any Veterans Administration Intensive Care Unit between October 1, 2007, and September 30, 2008, adjusted for severity of illness. Troponin assay values were normalized across institutions.ResultsMultivariate analyses for 30-day mortality showed an odds ratio (OR) of 1.82 for patients with high cTn (P < 0.0001, cTn > 10% coefficient of variation) and 1.18 for intermediate cTn (P = 0.0021, cTn between lowest limit detectable and 10% coefficient of variation) compared with patients with no elevation, adjusting for severity of illness (n = 19,979). Logistic regression models showed that patients with no or intermediate elevations of cTn taking statins within 24 hours of cTn measurement had a lower mortality than patients not taking statins (OR, 0.66; 95% confidence interval [95% CI], 0.53–0.82; P = 0.0003), whereas patients with high cTn had a lower mortality if they were taking β-blockers or aspirin within 24 hours of cTn measurement compared to patients not taking β-blockers or aspirin (β-blockers: OR, 0.80; 95% CI, 0.68–0.94; P = 0.0077; aspirin: OR, 0.81;95% CI, 0.69–0.96; P = 0.0134).ConclusionsThis retrospective study confirms an association between elevated troponin and outcomes in critically ill patients without ACS and identifies statins, β-blockers, and aspirin as potential outcome modifiers in a cTn-dependent manner.

Association between troponin-I levels and outcome in critically ill patients admitted to non-cardiac intensive care unit with high prevalence of cardiovascular risk factors

“…Additionally, data on medications that may be cardioprotective were also not available. This latter effect was recently studied by Poe et al who found that statins, β-blockers and aspirin have the potential to modify the mortality in patients with elevated cardiac troponin-I [ 27 ]. Notably, they showed that patients with no or intermediate elevation in cardiac troponin-I taking statins within 24 h of measurement had a lower mortality than those not taking statins.…”

“…Unlike patients with STEMI, who myocardial infarction due to an atherosclerotic plaque, [ 28 ] troponin-I elevation in general ICU patients is seldom related to obstructive coronary disease [ 1 ]. They usually experience Type II MI secondary to a variety of factors that increase mismatch between myocardial oxygen supply and demand; these include tachycardia, shock, vasopressors, inotropes, hypoxemia, anemia, and hypertension [ 27 ]. The mechanism of myocardium injury is important because most of data on MI treatment come from studies on Type I MI, and there are little data regarding the treatment of Type II MI.…”

“…Our study is consistent with the VISION (Vascular Events in Noncardiac Surgery Patients Cohort Evaluation) study that included 15,000 patients, which showed that peak troponin-I measurement added incremental prognostic value to discriminate those likely to die within 30 days of non-cardiac surgery [ 29 ]. Although statins, β-blockers, and aspirin are often prescribed for ICU patients with troponin-I elevation, there are limited data regarding the effectiveness [ 27 ].…”

Optimal VAsopressor TitraTION in patients 65 years and older (OVATION-65): protocol and statistical analysis plan for a randomised clinical trial

“…Cardiac troponins are consistently associated with worse outcomes in critical illness, [33][34][35][36][37] and cardiac biomarkers may be modifiable by administration of albumin 34 and medications. 35 Given that coronary blood flow is maintained over a broad range of coronary perfusion pressures under most circumstances, 38 we hypothesise that increasing vasopressors to achieve a higher MAP will have little effect on coronary perfusion but may increase the severity of demandrelated myocardial ischaemia via increased heart rate (ie, reduced coronary perfusion time) and transmural pressure (ie, afterload). If OVATION-65 shows that permissive hypotension prevents or limits hsTnT elevation, then patients at increased risk of secondary myocardial ischaemia, possibly identified by baseline hsTnT, may benefit the most from this strategy.…”

Evaluation of cardiac troponin I as a predictor of death in critically ill cats

“…Myocardial injury is common in critically ill people 1 , 2 and dogs. 3 , 4 , 5 Confirmation of cellular injury requires biomarkers reflective of content leakage from the cell.…”