title: Treatment strategies for microvascular dysfunction following acute myocardial infarction.
abstract: Successful reperfusion following acute myocardial infarction is considered to be restoration of epicardial infarct vessel patency, but recent studies suggest that disrupted microvascular function and inadequate myocardial tissue perfusion are often present despite epicardial patency. New angiographic techniques, including the corrected Thrombolysis in Myocardial Infarction (TIMI) frame count and myocardial blush grade, have been used to demonstrate that restoration of downstream coronary flow and tissue perfusion may be the key links to improved clinical outcomes. Additionally, other diagnostic techniques, including infarct size measurement with cardiac marker release patterns, or (99m) Tc-sestamibi single photon emission computed tomography imaging, and analysis of ST-segment resolution have also been used to assess microvascular function and tissue perfusion. Promising adjunctive therapies that target microvascular dysfunction, including platelet glycoprotein IIb/IIIa inhibitors, anti-inflammatory agents, vasodilators, glucose-insulin-potassium, and embolization protection devices, may ameliorate microvascular dysfunction following epicardial reperfusion. However, these therapies have not yet been shown to improve clinical outcomes and are thus currently being studied together with fibrinolytics and primary angioplasty in clinical trials. Therefore, shifting the focus of reperfusion therapy to the microcirculation offers the potential to further improve myocardial salvage and clinical outcomes following acute myocardial infarction.
authors.affiliation: Duke Clinical Research Institute, PO Box 17969, Durham, NC 27715, USA. Roe00001@mc.duke.edu
authors.forename: M T
authors.initials: MT
authors.lastname: Roe
mesh_terms: D017023:Coronary Angiography; D006801:Humans; D008833:Microcirculation; D009203:Myocardial Infarction / Q000188:drug therapy* / Q000503:physiopathology*; D015425:Myocardial Reperfusion; D009206:Myocardium / Q000378:metabolism; D010975:Platelet Aggregation Inhibitors / Q000627:therapeutic use; D014654:Vascular Patency / Q000187:drug effects; D014665:Vasodilator Agents / Q000627:therapeutic use
chemical_list: D010975:Platelet Aggregation Inhibitors; D014665:Vasodilator Agents