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Type 2 diabetes mellitus (T2DM) and diminished myocardial perfusion increase the risk of heart failure (HF) and/or all-cause mortality during 6-year follow up following primary percutaneous coronary intervention (pPCI) for ST elevation myocardial infarction (STEMI). The aim of the present study was to evaluate the impact of myocardial perfusion on infarct size and left ventricular ejection fraction (LVEF) in patients with T2DM and STEMI treated with pPCI. This is an ancillary analysis of an observational cohort study of T2DM patients with STEMI. We enrolled 406 patients with STEMI, including 104 with T2DM. Myocardial perfusion was assessed with the Quantitative Myocardial Blush Evaluator (QUBE) and infarct size with the creatine kinase myocardial band (CK-MB) maximal activity and troponin area under the curve. LVEF was measured with biplane echocardiography using Simpson’s method at admission and hospital discharge. Analysis of covariance was used for modeling the association between myocardial perfusion, infarct size and left ventricular systolic function. Patients with T2DM and diminished perfusion (QUBE below median) had the highest CK-MB maximal activity (252.7 ± 307.2 IU/L, P < 0.01) along with the lowest LVEF (40.6 ± 10.0, P < 0.001). Older age (p = 0.001), QuBE below median (p = 0.026), and maximal CK-MB activity (p < 0.001) were independent predictors of LVEF. Diminished myocardial perfusion assessed by QuBE predicts significantly larger enzymatic infarct size and lower LVEF among patients with STEMI treated with pPCI, regardless of diabetes status.

Patients with type 2 diabetes mellitus (T2DM) who undergo primary percutaneous coronary intervention (pPCI) for ST-elevation myocardial infarction (STEMI) have worse myocardial perfusion than normoglycemic patients. It is not known whether these factors combined influence prognosis in term of heart failure (HF) and/or all-cause mortality. We aimed to evaluate the impact of T2DM and myocardial perfusion on long-term risk of HF and/or all-cause mortality following interventional treatment of STEMI. 4STEMI patients (104 with T2DM) treated with pPCI were enrolled into the study. Myocardial perfusion was reassessed with: myocardial blush grade (MBG), Quantitative myocardial Blush Evaluator (QuBE), resolution of ST-segment elevation (STR). Follow-up data was collected during 6 years. 23.1% patients with T2DM developed HF vs. 16.9% without T2DM (P=NS). 34.6% of patients with T2DM have died vs. 14.9% patients without T2DM (P=0.000). Patients with T2DM and HF have had the highest mortality rate of 75%. Survival of patients with T2DM in relation to QuBe score is presented in the Figure. There was no difference in myocardial perfusion assessed by STR. T2DM and diminished myocardial perfusion increase the risk of HF and/or all cause death in 6 years follow-up. Disclosure A. Tomasik: None. K. Nabrdalik: None. H. Kwiendacz: None. T. Sawczyn: None. M. Kukla: None. E. Radzik: None. K. Pigon: None. T. Młyńczak: None. J. Gumprecht: Speaker's Bureau; Self; AstraZeneca. Consultant; Self; Bayer AG. Speaker's Bureau; Self; Bioton, Berlin-Chemie AG, Eli Lilly and Company, Merck Sharp & Dohme Corp., Boehringer Ingelheim GmbH, Novo Nordisk A/S, Polfa Tarchomin S.A., Polpharma. W. Grzeszczak: Speaker's Bureau; Self; Boehringer Ingelheim GmbH, Bioton, Merck & Co., Inc., Novo Nordisk A/S. Stock/Shareholder; Self; Eli Lilly and Company. Speaker's Bureau; Self; Bayer AG. E. Nowalany-Kozielska: None.

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