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Multicenter Study
. 2010;14(3):R99.
doi: 10.1186/cc9034. Epub 2010 May 27.

Elevation of cardiac troponin I during non-exertional heat-related illnesses in the context of a heatwave

Affiliations
Multicenter Study

Elevation of cardiac troponin I during non-exertional heat-related illnesses in the context of a heatwave

Pierre Hausfater et al. Crit Care. 2010.

Abstract

Introduction: The prognostic value of cardiac troponin I (cTnI) in patients having a heat-related illness during a heat wave has been poorly documented.

Methods: In a post hoc analysis, we evaluated 514 patients admitted to emergency departments during the August 2003 heat wave in Paris, having a core temperature >38.5 degrees C and who had analysis of cTnI levels. cTnI was considered as normal, moderately elevated (abnormality threshold to 1.5 ngxmL-1), or severely elevated (>1.5 ngxmL-1). Patients were classified according to our previously described risk score (high, intermediate, and low-risk of death).

Results: Mean age was 84 +/- 12 years, mean body temperature 40.3 +/- 1.2 degrees C. cTnI was moderately elevated in 165 (32%) and severely elevated in 97 (19%) patients. One-year survival was significantly decreased in patients with moderate or severe increase in cTnI (24 and 46% vs 58%, all P < 0.05). Using logistic regression, four independent variables were associated with an elevated cTnI: previous coronary artery disease, Glasgow coma scale <12, serum creatinine >120 micromolxL-1, and heart rate >110 bpm. Using Cox regression, only severely elevated cTnI was an independent prognostic factor (hazard ratio 1.93, 95% confidence interval 1.35 to 2.77) when risk score was taken into account. One-year survival was decreased in patients with elevated cTnI only in high risk patients (17 vs 31%, P = 0.04).

Conclusions: cTnI is frequently elevated in patients with non-exertional heat-related illnesses during a heat wave and is an independent risk factor only in high risk patients where severe increase (>1.5 ngxmL-1) indicates severe myocardial damage.

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Figures

Figure 1
Figure 1
Receiver-operating curve showing the relationship between cardiac troponin I elevation and death (n = 514). The best threshold (0.30 ng.mL-1) was associated with a sensitivity of 0.66 and a specificity of 0.66 (arrow). The threshold retained to define severe myocardial damage (1.50 ng.mL-1; see Methods) was associated with a sensitivity of 0.33 and a specificity of 0.89 (arrow). The area under the ROC curve was 0.68 (95% confidence interval 0.63 to 0.73) and was significantly different (P < 0.001) from the no discrimination curve (dotted line).
Figure 2
Figure 2
Kaplan-Meier Survival Curves in patients, according to troponin elevation ranges. Without elevation of cardiac troponin I (cTnI) (n = 252), moderate increase (abnormality threshold to 1.5 ng.mL-1, n = 165) and severe increase in cTnI (>1.5 ng.mL-1, n = 97). All differences were significant (P < 0.05).
Figure 3
Figure 3
Kaplan-Meier Survival Curves in patients with or without elevation of cardiac troponin I according to the risk score categories (low-, intermediate-, and high-risk sub-groups, n = 90, 229 and 147 respectively), as previously defined [11]. P-values refer to difference between groups with or without elevation of cTnI. NS, non significant.
Figure 4
Figure 4
Kaplan-Meier Survival Curves in the subgroup of patients with a core temperature >40°C (n = 281), according to troponin elevation ranges. Without elevation of cardiac troponin I (cTnI, n = 105), with moderate increase (abnormality threshold to 1.5 ng.mL-1, n = 102) and severe increase in cTnI (>1.5 ng.mL-1, n = 74). All differences were significant (P < 0.05).

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