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Oxford University Press (OUP), European Heart Journal - Cardiovascular Pharmacotherapy, 4(1), p. 220-228

DOI: 10.1093/ehjcvp/pvv023

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Meta-analysis of admission hyperglycaemia in acute myocardial infarction patients treated with primary angioplasty: a cause or a marker of mortality?

This paper was not found in any repository, but could be made available legally by the author.
This paper was not found in any repository, but could be made available legally by the author.

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Abstract

sec> Aims Admission hyperglycaemia (AH) has been associated with worse outcomes in acute myocardial infarction (AMI). In the current review, we evaluated the impact of primary angioplasty (pPCI) on mortality in AMI patients with AH. Our second aim was to evaluate if AH is a marker of baseline risk or an independent predictor of mortality. Methods and results A comprehensive search of four major databases was performed. We included original research studies reporting data on mortality in AMI patients with AH (mean plasma glucose >156 mg/dL/8.7 mmol) and euglycaemia who were treated with pPCI. Of 481 citations, 12 studies were included in the analysis. Admission hyperglycaemia was associated with a higher 30-day [risk ratio (RR) 4.30, P < 0.0001] and 1- to 3-year mortality (RR 2.26, P < 0.0001). As well, AH was more prevalent in women and in patients with an increasing number of cardiac risk factors or angiographic predictors of mortality, such as previous AMI (RR 0.89, P = 0.01), multivessel coronary disease (RR 0.72, P = 0.0001), and involvement of left anterior descending artery (RR 0.92, P < 0.0001). Moreover, patients with AH had larger infarcts (higher creatine kinase-MB; P = 0.004) and more frequent ventricular arrhythmias ( P = 0.002). Conclusion Despite rapid revascularization and treatment of hyperglycaemia, patients with AH continue to have a higher mortality. Admission hyperglycaemia occurs more commonly in patients who have traditional predictors of worse outcomes—specifically prior infarction, anterior wall infarctions, and multivessel disease. Likely, AH is a predictor of rather than a bona fide therapeutic target in AMI. </sec