Blood glucose and HbA1c levels were measured in all patients at hospital admission. A diagnosis of DM was made if this disease and/or antidiabetic treatment, including oral agents or insulin, were recorded in the admission history. A diagnosis of unknown DM was made when patients had ≥6.5% (48 mmol/mol) HbA1c despite no previous history of the disease.13 Acute hyperglycemia was defined as a blood glucose level at admission >198 mg/dL (>11 mmol/L), according to the definition used in previous studies focusing on AMI patients.11, 14, 15, 16 Average chronic glucose levels were estimated by HbA1c, expressed as percentage value, according to the following validated formula12, 13, 17:
In all patients, we measured blood glucose at admission (acute glycemia) and estimated chronic glucose levels to calculate (1) the acute/chronic (A/C) glycemic ratio and (2) the absolute difference between acute and chronic glycemia (ΔA−C).
Serum creatinine was measured at hospital admission and each day during intensive cardiac care unit stay. Glomerular filtration rate was estimated using the abbreviated MDRD (Modification of Diet in Renal Disease) equation.18 AKI was defined applying the Acute Kidney Injury Network classification, according to the maximum serum creatinine increase recorded between baseline (hospital admission) and the first 72 hours.19
Study patients received standard medical treatment and coronary revascularization (primary or early PCI), according to the current standards of care recommended by published guidelines.20, 21 In all patients with DM, antidiabetic medications were withheld at hospital admission. In patients with acute hyperglycemia (>198 mg/dL), insulin was administered with a glucose‐level target range of 140 to 180 mg/dL.22 Nonionic, low‐osmolality contrast agents were used in all patients. In non‐STEMI patients, isotonic (0.9%) saline was given intravenously at a rate of 1 mL/kg per hour for 12 hours before and after contrast exposure; in STEMI patients, hydration was given for 12 hours after PCI. In patients with left ventricular ejection fraction <40% or overt heart failure, the hydration rate was reduced to 0.5 mL/kg per hour.
Demographic, clinical, biochemical, and echocardiographic data were obtained. Left ventricular ejection fraction was measured with echocardiography in all patients within 24 hours of hospital admission.
The primary end point of the study was the incidence of AKI. Major in‐hospital adverse clinical events, including death, were evaluated as secondary end points of the study.
Do you have any questions about this protocol?
Post your question to gather feedback from the community. We will also invite the authors of this article to respond.