title: Diabetes and acute coronary syndrome.
abstract: Contrary to the decline in the prevalence of several risk factors such as hypertension, hypercholesterolemia and smoking, diabetes is an expanding health burden in the Western world. Because of the proatherosclerotic, proinflammatory, and prothrombotic states associated with diabetes, diabetic patients with acute coronary syndromes (ACS) are at high risk of subsequent cardiovascular events. However, they derive at the same time greater benefit from evidence-based therapy than the non-diabetic individuals. The two mainstays of acute ACS therapy for diabetic patients are an aggressive platelet inhibition and an early invasive strategy. Aspirin should be administered in all patients and prasugrel is to be considered superior to clopidogrel in this setting. While the use of glycoprotein IIb/IIIa receptor inhibitors in the diabetic ACS population has been associated with a mortality reduction, the role of these agents in the prasugrel era remains to be elucidated. Importantly, the aggressiveness of anti-thrombotic therapy should be balanced in each individual patient with the risk of bleeding. The benefit of early coronary angiography and, if needed, revascularization, in the setting of non-ST-segment elevation ACS is more pronounced in diabetic than in non-diabetic individuals. All patients, diabetics and non-diabetics, qualify for primary percutaneous coronary intervention (PCI) as the therapy of choice for ST-segment elevation myocardial infarction. In order to reduce hemorrhagic complications related to vascular access for PCI, the radial approach should be favored. Additional important secondary preventive measures include high-dose statin therapy, ACE-Inhibition/angiotensin II receptor blockade, and adequate glucose metabolism control. Despite the documented efficacy, diabetic patients with ACS receive evidence-based treatments less frequently than non-diabetic individuals.
authors.affiliation: Division of Cardiology, Geneva University Hospital, Geneva, Switzerland. pierre-frederic.keller@hcuge.ch
authors.forename: P F
authors.initials: PF
authors.lastname: Keller
authors.forename: D
authors.initials: D
authors.lastname: Carballo
authors.forename: M
authors.initials: M
authors.lastname: Roffi
mesh_terms: D054058:Acute Coronary Syndrome / Q000503:physiopathology / Q000628:therapy*; D015906:Angioplasty, Balloon, Coronary; D000925:Anticoagulants / Q000627:therapeutic use; D003925:Diabetic Angiopathies / Q000503:physiopathology / Q000628:therapy*; D004730:Endothelium, Vascular / Q000503:physiopathology; D006470:Hemorrhage / Q000139:chemically induced / Q000517:prevention & control; D006801:Humans; D007004:Hypoglycemic Agents / Q000627:therapeutic use; D009203:Myocardial Infarction / Q000628:therapy*; D010879:Piperazines / Q000627:therapeutic use; D010975:Platelet Aggregation Inhibitors / Q000009:adverse effects / Q000627:therapeutic use*; D000068799:Prasugrel Hydrochloride; D013876:Thiophenes / Q000627:therapeutic use
chemical_list: D000925:Anticoagulants; D007004:Hypoglycemic Agents; D010879:Piperazines; D010975:Platelet Aggregation Inhibitors; D013876:Thiophenes; D000068799:Prasugrel Hydrochloride