Troponin as a risk factor for mortality in critically ill patients without acute coronary syndromes

Ammann, Peter; Maggiorini, Marco; Bertel, Osmund; Haenseler, Edgar; Joller‐Jemelka, H. I.; Oechslin, Erwin; Minder, Elisabeth I.; Rickli, Hans; Fehr, Thomas

doi:10.1016/s0735-1097(03)00421-2

Cited by 334 publications

(129 citation statements)

References 26 publications

Supporting

Mentioning

116

Contrasting

Unclassified

Order By: Relevance

“…This study has generated the hypothesis that cardiac cell damage in acute stroke may be enhanced by the stress response as well as the cytokine response, like in sepsis or acute MI [9]. The finding that critically ill troponin-positive patients have higher plasma-levels of proinflammatory cytokines and higher mortality [22]supports this view. Further understanding of the mechanisms of secondary damage in stroke may lead to better detection and possible treatment of these complications.…”

Section: Discussionmentioning

confidence: 97%

Serum Cardiac Troponin I in Acute Stroke Is Related to Serum Cortisol and TNF-α

et al. 2004

View full text Add to dashboard Cite

Background: Serum cardiac troponin I (cTnI) is a specific marker of myocardial injury related to in-patient fatality and cardiac injury in acute stroke. We investigated whether cTnI in acute stroke is related to serum cortisol, acute inflammatory response, and insular damage. We also investigated whether cTnI predicted outcome at 3 months. Patients and Methods: The study was based on 155 patients with CT-confirmed acute cerebral infarction and study inclusion within 24 h (50% within 12 h) of stroke onset. Blood samples were obtained on inclusion. Stroke severity was assessed by the Scandinavian Stroke Scale (SSS) and outcome was assessed by the modified Rankin Scale (mRS), death or dependency was defined as mRS ≧3 three months after stroke. Results: 35% of all patients and 63% of patients who died within 3 months were troponin positive. Tumor necrosis factor-α (TNF-α) and cortisol were independently related to detection of cTnI: TNF-α_{+100 pg/ml} OR 1.5 (CI 95% 1.1–2.2), cortisol_{+100 nmol/l} OR 1.1 (CI 95% 1.01–1.2). SSS and age were also included in this model and did not reach significance. cTnI positivity was, together with age, stroke severity and prestroke mRS, but not s-cortisol, an independent explanatory variable of outcome at 3 months (death or dependency) with OR 4.1 (CI 95% 1.1–14.5). cTnI did not relate to insular involvement. Conclusion: In this study, cortisol and TNF-α were independently related to cTnI, which was predictive of 3-month prognosis.

show abstract

Section: Discussionmentioning

confidence: 97%

Serum Cardiac Troponin I in Acute Stroke Is Related to Serum Cortisol and TNF-α

et al. 2004

View full text Add to dashboard Cite

show abstract

“…The timing of troponin measurement, troponin assay used (ie, TnT versus TnI), and hemodynamic stability at the time of troponin measurement differ substantially in prior studies 2, 7, 8. The majority of prior studies have examined short‐term mortality, while this study included assessment of 1‐year death rate.…”

Section: Discussionmentioning

confidence: 99%

“…Electrocardiography and echocardiography in these patients rarely demonstrate ischemic changes, and few patients have inducible ischemia on stress testing or occlusive coronary thrombus on autopsy 8, 26, 30. Postulated causes for troponin elevations in septic patients include ischemic mechanisms (eg, supply–demand imbalance or microvascular spasm or thrombosis) and nonischemic mechanisms (eg, reversible myocardial membrane leakage of cytosolic TnT pool or direct cellular toxicity from inflammatory mediators, microbial toxins, or excessive catecholamine levels) 7, 31, 32. While relative hypovolemia, inadequate resuscitation, and prolonged hypotension may contribute to myocardial injury in patients with septic shock, fluid resuscitation does not appear to influence the subsequent values of hs‐TnT on serial testing 12…”

Section: Discussionmentioning

confidence: 99%

“…Increased sensitivity of the contemporary TnT assay has resulted in more frequent clinical detection of myocardial injury from noncoronary causes, including critical illness 5, 6. Elevations in TnT levels are present in up to 60% of all intensive care unit (ICU) patients and identify patients with increased risk of short‐term and long‐term mortality 6, 7…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Role of Admission Troponin‐T and Serial Troponin‐T Testing in Predicting Outcomes in Severe Sepsis and Septic Shock

Vallabhajosyula

Sakhuja

Geske

et al. 2017

JAHA

View full text Add to dashboard Cite

BackgroundTroponin‐T elevation is seen commonly in sepsis and septic shock patients admitted to the intensive care unit. We sought to evaluate the role of admission and serial troponin‐T testing in the prognostication of these patients.Methods and ResultsThis was a retrospective cohort study from 2007 to 2014 on patients admitted to the intensive care units at the Mayo Clinic with severe sepsis and septic shock. Elevated admission troponin‐T and significant delta troponin‐T were defined as ≥0.01 ng/mL and ≥0.03 ng/mL in 3 hours, respectively. The primary outcome was in‐hospital mortality. Secondary outcomes included 1‐year mortality and lengths of stay. During this 8‐year period, 944 patients met the inclusion criteria with 845 (90%) having an admission troponin‐T ≥0.01 ng/mL. Serial troponin‐T values were available in 732 (78%) patients. Elevated admission troponin‐T was associated with older age, higher baseline comorbidity, and severity of illness, whereas significant delta troponin‐T was associated with higher severity of illness. Admission log10 troponin‐T was associated with unadjusted in‐hospital (odds ratio 1.6; P=0.003) and 1‐year mortality (odds ratio 1.3; P=0.04), but did not correlate with length of stay. Elevated delta troponin‐T and log10 delta troponin‐T were not significantly associated with any of the primary or secondary outcomes. Admission log10 troponin‐T remained an independent predictor of in‐hospital mortality (odds ratio 1.4; P=0.04) and 1‐year survival (hazard ratio 1.3; P=0.008).ConclusionsIn patients with sepsis and septic shock, elevated admission troponin‐T was associated with higher short‐ and long‐term mortality. Routine serial troponin‐T testing did not add incremental prognostic value in these patients.

show abstract

“…Interestingly, our patients, none of whom had acute coronary syndrome, had elevated troponin T levels but normal troponin I levels, suggesting that troponin T level could be affected by reversible myocardial ischemia associated with cardiac hypertrophy and decreased heart function, rather than by irreversible myocardial damage [17]. On the basis of our observations, we hypothesize the possibility that chronic myocardial damage reflected in increased levels of troponin T and fibrinogen, may be associated with cardiac hypertrophy and dysfunction, and high CRP may arise from a pathological response of the heart to chronic inflammation.…”

Section: Discussionmentioning

confidence: 99%

Persistent Elevation of C-Reactive Protein May Predict Cardiac Hypertrophy and Dysfunction in Patients Maintained on Hemodialysis

et al. 2005

View full text Add to dashboard Cite

Background: C-reactive protein (CRP), which reflects chronic inflammation, is a strong predictor of cardiovascular mortality in hemodialysis patients. We investigated whether persistent elevation of CRP is associatedwith cardiac function and morphology in patients maintained on hemodialysis. Methods: Predialysis high-sensitivity CRP (hs-CRP) was measured twice at an interval of 3 weeks in 52 stable hemodialysis patients, and echocardiographic studies were performed. Results: 25 patients showed persistent elevation of predialysis hs-CRP (>3 mg/l, high CRP group). Patients in the high CRP group had a lower dialysis dose (p < 0.01), higher troponin T (p < 0.01), and higher fibrinogen (p < 0.01). Echocardiographic studies showed that left atrial diameter (LA, p < 0.05), interventricular septal thickness (IVST, p < 0.05), left ventricular end-diastolic volume (LVEDV, p < 0.05), and left ventricular mass index (LVMI, p < 0.05) were higher in the high CRP group. However the ejection fraction (EF) was lower in the high CRP group (p < 0.05), which also contained more patients with low EF (<40%) (p < 0.01). There was no difference in diabetes mellitus, acute infection and type of vascular access between the groups. hs-CRP level was positively correlated with troponin T (r = 0.416, p < 0.01) and fibrinogen (r = 0.560, p < 0.001), and IVST with hs-CRP level (r = 0.291, p < 0.05), whereas the EF was negatively correlated with hs-CRP(r = –0.301, p < 0.05). In addition, the high CRP group correlated positively with IVST (r = 0.281, p < 0.05), LVEDV (r = 0.322, p < 0.05), and LVMI (r = 0.312, p < 0.05) and negatively with EF (r = –0.311, p < 0.05). On multivariate analysis, the high CRP group (β = –0.312, β = 0.238, and β = 0.318, respectively) was a significant predictor of EF (R = 0.62, p = 0.025), LVMI (R = 0.928, p = 0.02) and IVST (R = 0.64, p = 0.01). Conclusions: Persistent elevation of CRP, which is an independent risk factor for EF, LVMI and IVST, may predict cardiac hypertrophy and dysfunction in patients maintained on hemodialysis.

show abstract

Troponin as a risk factor for mortality in critically ill patients without acute coronary syndromes

Abstract: Elevated troponin is a mortality risk factor for medical intensive care patients admitted for reasons other than ACS. It is associated with decreased left ventricular function and higher levels of TNF-alpha and IL-6.

Cited by 334 publications

References 26 publications

Serum Cardiac Troponin I in Acute Stroke Is Related to Serum Cortisol and TNF-α

Serum Cardiac Troponin I in Acute Stroke Is Related to Serum Cortisol and TNF-α

Role of Admission Troponin‐T and Serial Troponin‐T Testing in Predicting Outcomes in Severe Sepsis and Septic Shock

Persistent Elevation of C-Reactive Protein May Predict Cardiac Hypertrophy and Dysfunction in Patients Maintained on Hemodialysis

Contact Info

Product

Resources

About