A prospective study of the impact of serial troponin measurements on the diagnosis of myocardial infarction and hospital and six-month mortality in patients admitted to ICU with non-cardiac diagnoses

Abstract

IntroductionTroponin T (cTnT) elevation is common in patients in the Intensive Care Unit (ICU) and associated with morbidity and mortality. Our aim was to determine the epidemiology of raised cTnT levels and contemporaneous electrocardiogram (ECG) changes suggesting myocardial infarction (MI) in ICU patients admitted for non-cardiac reasons.MethodscTnT and ECGs were recorded daily during week 1 and on alternate days during week 2 until discharge from ICU or death. ECGs were interpreted independently for the presence of ischaemic changes. Patients were classified into four groups: (i) definite MI (cTnT ≥15 ng/L and contemporaneous changes of MI on ECG), (ii) possible MI (cTnT ≥15 ng/L and contemporaneous ischaemic changes on ECG), (iii) troponin rise alone (cTnT ≥15 ng/L), or (iv) normal. Medical notes were screened independently by two ICU clinicians for evidence that the clinical teams had considered a cardiac event.ResultsData from 144 patients were analysed (42% female; mean age 61.9 (SD 16.9)). A total of 121 patients (84%) had at least one cTnT level ≥15 ng/L. A total of 20 patients (14%) had a definite MI, 27% had a possible MI, 43% had a cTNT rise without contemporaneous ECG changes, and 16% had no cTNT rise. ICU, hospital and 180-day mortality was significantly higher in patients with a definite or possible MI.Only 20% of definite MIs were recognised by the clinical team. There was no significant difference in mortality between recognised and non-recognised events.At the time of cTNT rise, 100 patients (70%) were septic and 58% were on vasopressors. Patients who were septic when cTNT was elevated had an ICU mortality of 28% compared to 9% in patients without sepsis. ICU mortality of patients who were on vasopressors at the time of cTnT elevation was 37% compared to 1.7% in patients not on vasopressors.ConclusionsThe majority of critically ill patients (84%) had a cTnT rise and 41% met criteria for a possible or definite MI of whom only 20% were recognised clinically. Mortality up to 180 days was higher in patients with a cTnT rise.

Study of troponin-t elevation in critically ill patients-incidence and outcome

“…It can be concluded that troponin levels were higher among patients who died compared to live group. 17 Even though it was found that troponin T levels were significantly high among the mortality group, it was not statistically significant: p=0.56, 0.84 and 0.67 on day 1, 3 and 5 respectively. It's proved here that in the outcome of patients in relation to high and normal troponin T levels, among patients with high troponin T levels, 82.4% it accounted to mortality.…”

Should blood transfusion be individualised? We are not sure

“…Coronary oxygen supplydemand imbalance may result in ''type II'' myocardial infarction or injury. Troponin release is prevalent in the critically ill and is associated with higher mortality [4,5].…”

Anemia and Blood Transfusion in the Critically Ill Patient with Cardiovascular Disease

“…Evidence is also limited by the under-representation of patients with CVD in trials. Observational studies suggest the prevalence of CVD in ICU patients is around 30% [1,3]; however patients with CVD accounted for only 20% of patients recruited to the Transfusion Requirements in Critical Care (TRICC) trial compared with 29% of patients excluded [9], and only 14% of patients recruited to the Transfusion Requirements in Septic Shock (TRISS) trial [11]. A trial undertaken in patients presenting with acute gastrointestinal bleeding trial excluded all patients with significant CVD [12].…”

“…EKGs are not performed routinely and there is significant interobserver variability [35]. Troponin release is prevalent in the critically ill [1,36] and there are multiple causes. Potential cardiac mechanisms include increased thrombogenicity leading to coronary plaque rupture and thrombosis (type I myocardial infarction) or underlying critical coronary artery disease leading to an oxygen supply/demand imbalance (type II myocardial infarction) [34].…”