Body Temperature – A Marker of Infarct Size in the Era of Early Reperfusion

Abstract

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°C (36.9°C, 37.6°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.

The Systemic Inflammatory Response Syndrome in Patients With ST-Segment Elevation Myocardial Infarction*

“…Elevated heart rate, respiratory rate, and leukocytosis are all reported independent risk factors for mortality (25)(26)(27)(28)(29). Elevated heart rate, respiratory rate, and leukocytosis are all reported independent risk factors for mortality (25)(26)(27)(28)(29).…”

“…Elevated heart rate, respiratory rate, and leukocytosis are all reported independent risk factors for mortality (25)(26)(27)(28)(29). A small series of 40 patients reported a positive correlation with infarct size, whereas a previous CARDINAL analysis has reported statistically nonsignificant negative association between body temperature and infarct size (28,29). The relationship between body temperature and infarct size remains unclear.…”

Serious Infection After Acute Myocardial Infarction

“…However, it can often be a clinical challenge to determine whether the fever is due to the MI, to a complicating infection, or to other causes of systemic inflammation. Regardless of the etiology, because fever has a strong influence on oxygen consumption, it is important to recognize preventable or treatable underlying causes of fever that might predispose a patient to infarct extension and greater infarct size (19,20). …”

“…They concluded that inappropriate vasodilation in patients with systemic inflammatory response syndrome may play an important role in the pathogenesis and persistence of shock, with or without infection (22). While Ben-Dor and colleagues found that fever was frequent after reperfusion, they concluded that it was due to infarct size and not to a nonspecific systemic inflammatory response (19). In their study, fever was correlated with high-sensitivity C-reactive protein but not with fibrinogen levels or white blood cell count.…”

The diagnostic role of Procalcitonin and other biomarkers in discriminating infectious from non-infectious fever

“…A relationship between the extent of necrosis and the rise in temperature has been shown. 60,61 Animal studies indicate that elevated corporal temperature might be harmful prior to and directly after an acute coronary syndrome or myocardial infarction. 62 Fever after myocardial tissue loss occurs due to ischemic cell death, resulting in the production of cytokines.…”