Prevalence and Prognostic Association of Circulating Troponin in the Acute Respiratory Distress Syndrome

Abstract

Objective Circulating cardiac troponin has been associated with adverse prognosis in the acute respiratory distress syndrome (ARDS) in small and single center studies, however comprehensive studies of myocardial injury in ARDS using modern high-sensitivity troponin (hsTn) assays, which can detect troponin at much lower circulating concentrations, have not been performed. Design We performed a prospective cohort study. Setting We included patients enrolled in previously completed trials of ARDS. Patients 1,057 ARDS patients were included. Interventions To determine the association of circulating hsTnI (Abbott ARCHITECT), with ARDS outcomes, we measured hsTnI within 24 h of intubation. The primary outcome was 60-day mortality. Measurements and Main Results Detectable hsTnI was present in 94% of patients; 38% of patients had detectable levels below the 99th percentile of a healthy reference population (26 ng/L), while 56% of patients had levels above the 99th percentile cut point. After multivariable adjustment, age, cause of ARDS, temperature, heart rate, vasopressor use, SOFA score, creatinine, and pCO2 were associated with higher hsTnI concentration. After adjustment for age, sex, and randomized trial assignment, the hazard ratio for 60-day mortality comparing the 5th to the 1st quintiles of hsTnI was 1.61 (95% CI 1.11 – 2.32; P-trend = 0.003). Adjusting for SOFA score suggested that this association was not independent of disease severity (hazard ratio 0.95 (95% CI 0.64 – 1.39; P = 0.93). Conclusions Circulating troponin is detectable in over 90% of patients with ARDS and is associated with degree of critical illness. The magnitude of myocardial injury correlated with mortality.

Prognostic Value of Cardiovascular Biomarkers in COVID-19: A Review

“…It is worth noting that raised serum cTnI levels are similarly associated with a higher risk of mortality in other diseases such as pneumonia (odds ratio = 9.5), sepsis (odds ratio = 1.92), chronic obstructive pulmonary disease (hazard ratio = 4.5), and acute respiratory distress syndrome (hazard ratio = 1.6) [29][30][31][32]. Hence, one may logically also predict a correlation between elevated serum cTnI levels and a higher risk of mortality in COVID-19 patients.…”

Pulmonary and systemic hemodynamics are associated with myocardial injury in the acute respiratory distress syndrome

“…Myocardial injury is common in ARDS and associated with adverse outcome. 17 , 18 Whether right and left heart hemodynamics are associated with myocardial injury is not known; optimizing hemodynamics could represent a treatable manifestation of critical illness to reduce myocardial injury and possibly improve ARDS outcome. To address these knowledge gaps including the unknown relationships between myocardial injury, hemodynamics, and outcome in ARDS, we performed a multi-center retrospective cohort study of patients with ARDS with pulmonary artery catheters in place to determine the association of right and left heart hemodynamics with myocardial injury assessed with high sensitivity troponin-I (hsTnI), the association of trend in hemodynamics with progressive myocardial injury and whether adjusting for hemodynamics attenuates the association of myocardial injury with outcome.…”

Acute Cardiac Injury in COVID-19: A Systematic Review and Meta-analysis

“…15,27,28 Increased pulmonary vascular resistance (PVR) resulting from acute respiratory distress syndrome leading to extra strain on the right ventricle is proposed as another etiology of elevated troponin. 27,29,30 Moreover, this biomarker could be raised by the administration of mechanical ventilation, which most patients require in ICU settings. 29 Also, sepsis could be categorized as another possible etiology in this regard due to systemic inflammatory response syndrome and its specific manifestations due to oxygen supply-demand imbalance resulting from fever, increased body metabolism, and respiratory failure.…”

“…27,29,30 Moreover, this biomarker could be raised by the administration of mechanical ventilation, which most patients require in ICU settings. 29 Also, sepsis could be categorized as another possible etiology in this regard due to systemic inflammatory response syndrome and its specific manifestations due to oxygen supply-demand imbalance resulting from fever, increased body metabolism, and respiratory failure. 27,31,32 Even tachycardia, either alone or in the context of sepsis, might be able to raise troponin levels.…”