Key result
Peak 24-hour body temperature after ST elevation AMI was significantly correlated with infarct size markers including creatine kinase (r=0.42, p=0.01) and wall motion index (r=0.41, p=0.01).
Observational (n=40)
p-value: p=0.01
Peak 24-hour body temperature after STEMI treated with primary PCI correlates with markers of infarct size rather than nonspecific inflammation.
May signal larger infarcts post-STEMI; hypothesis-generating and should not yet change practice.
We measured body temperature in 40 consecutive patients treated for a first ST elevation acute myocardial infarction (AMI) with primary percutaneous coronary interventions. Left ventricular function was assessed by echocardiography, and blood samples were drawn for highly sensitive C-reactive protein (hs-CRP), white blood cell (WBC) count, fibrinogen, creatine kinase (CK), and cardiac troponin I levels (cTnI). The median (25th, 75th quartiles) peak 24-hour temperature was 37.4 degrees C (36.9 degrees C, 37.6 degrees C). Variables significantly associated with peak 24-hour temperature were CK (p = 0.01, r = 0.42), wall motion index (p = 0.01, r = 0.41), hs-CRP (p = 0.01, r = 0.41), and cTnI (p = 0.03, r = 0.35). There was no significant correlation between peak 24-hour temperature and WBC count (p = 0.39, r = 0.14) and fibrinogen (p = 0.12, r = 0.21). Thus, peak 24-hour body temperature after ST elevation AMI probably reflects infarct size rather than a nonspecific inflammatory response.
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Ben‐Dor et al. (2005) conducted an observational in ST elevation acute myocardial infarction (AMI) (n=40). Peak 24-hour body temperature was evaluated on Correlation of peak 24-hour body temperature with markers of infarct size and inflammation (p=0.01). Peak 24-hour body temperature after ST elevation AMI was significantly correlated with infarct size markers including creatine kinase (r=0.42, p=0.01) and wall motion index (r=0.41, p=0.01).
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