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Minerva Cardioangiologica 2008 October;56(5):445-52


language: English

Admission glycemia and markers of inflammation are independent outcome predictors in primary PCI in non-diabetic patients

Corrada E. 1, Cappelleri A. 1, Belli G. 1, Genovese S. 2, Barbaro C. 1, Gasparini G. 1, Pagnotta P. 1, Rossi M. 1, Zavalloni D. 1, Presbitero P. 1

1 Unit of Hemodynamics, Invasive Cardiology and Coronary Care Humanitas Clinical Institute, Milan, Italy 2 Unit of Endocrinology and Diabetology Humanitas Clinical Institute Milan, Italy


Aim. To assess the prognostic value of admission plasma glucose (APG) respect to clinical variables and inflammatory markers in a selected population of non-diabetic patients with ST elevation myocardial infarction (STEMI) treated with primary angioplasty (primary coronary intervention, PCI).
Methods. A total of 188 consecutive non-diabetic STEMI patients undergoing primary PCI were divided into four quartiles based on APG (<117, 117-140, 141-170, >170 mg/dL). Combin-ed end-point of major adverse cardiac events (MACE) was defined as death, acute heart failure, re-infarction, unstable angina or inducible ischemia.
Results. Event-free survival from MACE was significantly (P<0.001) correlated with APG quartiles and decrease from the lowest to the highest: 6 months event-free survival was 89.3%, 77.4%, 59.1%, 42.5%. Patients with higher APG were characterized by a significantly higher Killip class (P<0.001), higher serum creatinine (P<0.05) on admission, and a lower rate of thrombolysis in myocardial infarction (TIMI) 3 flow after PCI (P<0.05). Multivariate analysis showed APG>170 mg/dL (hazard ratio [HR] 2.39, 95% confidence interval [CI] 1.24 to 4.65, P<0.01), admission high-sensitivity C-reactive protein level (HR 1.19, 95% CI 1.07 to 1.31, P<0.001), white blood cells count (HR 1.07, 95% CI 1.00 to 1.14, P<0.04) and heart rate (HR 1.02, 95% CI 1.00 to 1.04, P<0.02) to be independent predictors of MACE.
Conclusion. Admission glycemia and inflammatory markers are independent predictors of MACE in the mid-term follow-up in non-diabetic STEMI treated with primary PCI. Further investigations are needed to study the pathogenesis of stress hyperglycaemia, interactions with mechanisms of inflammation and whether early and aggressive treatment with insulin may influence outcome of primary PCI.

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