ORIGINAL ARTICLE Influence of Bedside Blood Insulin Measurement on Acute Coronary Syndrome Pathways Jose ´ Panza-Nduli, MD,* Very Coulic, MD,* Dominique Willems, MD,† Jacques Devriendt, MD,* Philippe Gottignies, MD,* Michel Staroukine, MD,* and David De Bels, MD* Background: The aim of the study was to evaluate the influence of blood insulin measurements on acute coronary syndrome (ACS) pathways. Methods: All patients admitted to the emergency department within 12 months for acute, retrosternal, constrictive chest pain lasting for more than 30 minutes; cardiogenic pulmonary edema; electrocardiogram ST changes; and echographic alterations were included. The study parameters were clinical (age, sex, blood pressure, presence of pulmonary rales and gallop), including classic laboratory tests associated with troponin T, blood insulin levels, and hemoglobin A 1C , and echographic values. These were taken on admission and throughout hospital stay. All patients underwent a coronary angiography for ACS diagnosis confirmation as well as treatment intention. Results: Sixty patients were included in the study. Abnormal blood insulin levels were present on admission in 47% of the population. Blood insulin level was significantly correlated to thrombolysis in myocardial infarction coronary perfusion score (Spearman Rank, 0.55, P  0.0001). Abnormal insulinemia was normalized with reperfusion. Insulin was administered essentially to the 16 patients with hypoinsulinemia. Patients with hypoinsu- linemia seem to have the most severe coronary lesions and highest Killip score. Conclusions: In ACS, insulin levels are altered in half of the patients. After the investigators noted its tight correlation with the thrombolysis in myocar- dial infarction coronary flow score, its determination could be important in ACS for triggering emergency coronary angiography for percutaneous cor- onary intervention. This could modify the critical pathways of ACS patients in the emergency department. Key Words: coronary artery disease, insulin, diabetes, critical pathways, percutaneous coronary intervention, acute coronary syndrome (Crit Pathways in Cardiol 2011;10: 185–188) R ecent studies have shown that, in acute coronary syndromes (ACSs), as in situations of shock, glycemia is often very high, even in nondiabetic patient, 1,2 and that this has a negative progno- sis. 3 Although mechanisms are not clearly understood, hyperglyce- mia in acute situations was attributed to hyperglycemic stress or to undiagnosed diabetes with insulin resistance. 4 On one hand, a relationship between insulin resistance and severe coronary atheromatosis has been suggested, and this resis- tance to insulin could be an independent cardiovascular risk factor. 5 On the other hand, it is not excluded that the pancreas’ incapacity to secrete insulin might play a role in the hyperglycemia associated with acute situations. However, blood insulin values during an ACS do not seem to have been extensively studied in the literature, although this hormone plays an important role in the body’s use of glucose; furthermore, its injection is recommended for the tight control of glycemia in the treatment of patients during acute ill- ness, 2,6,7 even though this has been recently debated. 8 The aim of this prospective study is to estimate the influence of blood insulin measurement on the critical pathways of patients with an ACS in emergency department (ED). METHODS After obtaining institutional ethical committee approval and written informed consent, all patients admitted during 12 months to the ED of the Brugmann University Hospital within the setting of an ACS and hospitalized in an ICU or CCU after coronary angiography were prospectively included in the study. Inclusion criteria for a suspected ACS were defined as at least one of the following: • Acute, retrosternal, constrictive chest pain lasting for more than 30 minutes. • Cardiogenic pulmonary edema. • Electrocardiogram ST (ECG ST) changes. • Elevated troponin T blood levels. Patients were excluded if one of the following criteria was met: • A normal coronary angiography. • Insulin-dependant diabetes mellitus. • Cardiac arrest. • Patients under hemodialysis or peritoneal dialysis. Clinical parameters were recorded on admission, after percuta- neous coronary intervention (PCI), and on each day until day 5. These included age, sex, systolic arterial pressure, presence of lung rales, presence of a S3 gallop, and evidence of peripheral vasoconstriction (oliguria, cyanosis, sweating). The Killip classification was used to estimate the severity and the prognosis of patients admitted to ED. Patient history of non-insulin-dependent diabetes mellitus was recorded. For each patient, blood sampling was taken on admission, after PCI, and each day until day 5. Creatine kinase, troponin T, blood glucose and insulin, creatinine, and blood urea nitrogen were measured at each time. Hemoglobin A 1C was recorded only on admission (recent results of this test were also taken into account). Insulin was measured by chemiluminescence (ADVIA Centaur, Siemens Healthcare Diagnostics Inc., Deerfield, IL). Normal values for blood insulin range from 5 to 20 UI/mL. Troponin T and creatine kinase–myocardial band were measured by immunochemi- luminescence (E 170 modular analytics, Roche Diagnostics). Nor- mal troponin T values are 0.1 ng/dL. The dosages of HbA 1C were performed by high-performance liquid chromatography (HA-8160, Menarini). Normal HbA 1C values are 6%. The insulinogenic index was calculated (blood insulin to glucose ratio) and expressed in %. Insulin therapy as well as final diagnosis was also recorded. Percutaneous coronary angiography was realized as quickly as possible to ensure optimal diagnosis and best treatment for the patient. TIMI (thrombolysis in myocardial infarction) coronary blood flow scores are according to literature: TIMI 0, no perfusion; From the Departments of *Critical Care, and †Clinical Biology, Brugmann University Hospital, Brussels, Belgium. Reprints: David De Bels, MD, Intensive Care Unit, Salle 92, Brugmann Univer- sity Hospital, Place A. Van Gehuchten, 4, B 1020 Brussels, Belgium. E-mail: david.debels@chu-brugmann.be. Copyright © 2011 by Lippincott Williams & Wilkins ISSN: 1535-282X/11/1004-0185 DOI: 10.1097/HPC.0b013e318238c5ca Critical Pathways in Cardiology • Volume 10, Number 4, December 2011 www.critpathcardio.com | 185