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. 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). 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.

Until recently, it has been generally held that stable angina pectoris (SAP) primarily reflects the presence of epicardial coronary artery stenoses due to atheromatous plaque(s), while acute myocardial infarction (AMI) results from thrombus formation on ruptured plaques. This concept is now challenged, especially by results of the ORBITA and ISCHEMIA trials, which showed that angioplasty/stenting does not substantially relieve SAP symptoms or prevent AMI or death in such patients. These disappointing outcomes serve to redirect attention towards anomalies of small coronary physiology. Recent studies suggest that coronary microvasculature is often both structurally and physiologically abnormal irrespective of the presence or absence of large coronary artery stenoses. Structural remodelling of the coronary microvasculature appears to be induced primarily by inflammation initiated by mast cell, platelet, and neutrophil activation, leading to erosion of the endothelial glycocalyx. This leads to the disruption of laminar flow and the facilitation of endothelial platelet interaction. Glycocalyx shedding has been implicated in the pathophysiology of coronary artery spasm, cardiovascular ageing, AMI, and viral vasculitis. Physiological dysfunction is closely linked to structural remodelling and occurs in most patients with myocardial ischemia, irrespective of the presence or absence of large-vessel stenoses. Dysfunction includes the impairment of platelet and vascular responsiveness to autocidal coronary vasodilators, such as nitric oxide, prostacyclin, and hydrogen sulphide, and predisposes both to coronary vasoconstriction and to a propensity for microthrombus formation. These findings emphasise the need for new directions in medical therapeutics for patients with SAP, as well as a wide range of other cardiovascular disorders.