TY - JOUR
T1 - Optimized treatment of ST-elevation myocardial infarction the unmet need to target coronary microvascular obstruction as primary treatment goal to further improve prognosis
AU - Niccoli, Giampaolo
AU - Montone, Rocco Antonio
AU - Ibanez, Borja
AU - Thiele, Holger
AU - Crea, Filippo
AU - Heusch, Gerd
AU - Bulluck, Heerajnarain
AU - Hausenloy, Derek J.
AU - Berry, Colin
AU - Stiermaier, Thomas
AU - Camici, Paolo G.
AU - Eitel, Ingo
PY - 2019
Y1 - 2019
N2 - Primary percutaneous coronary intervention is nowadays the preferred reperfusion strategy for patients with acute ST-segment–elevation myocardial infarction, aiming at restoring epicardial infarct-related artery patency and achieving microvascular reperfusion as early as possible, thus limiting the extent of irreversibly injured myocardium. Yet, in a sizeable proportion of patients, primary percutaneous coronary intervention does not achieve effective myocardial reperfusion due to the occurrence of coronary microvascular obstruction (MVO). The amount of infarcted myocardium, the so-called infarct size, has long been known to be an independent predictor for major adverse cardiovascular events and adverse left ventricular remodeling after myocardial infarction. Previous cardioprotection studies were mainly aimed at protecting cardiomyocytes and reducing infarct size. However, several clinical and preclinical studies have reported that the presence and extent of MVO represent another important independent predictor of adverse left ventricular remodeling, and recent evidences support the notion that MVO may be more predictive of major adverse cardiovascular events than infarct size itself. Although timely and complete reperfusion is the most effective way of limiting myocardial injury and subsequent ventricular remodeling, the translation of effective therapeutic strategies into improved clinical outcomes has been largely disappointing. Of importance, despite the presence of a large number of studies focused on infarct size, only few cardioprotection studies addressed MVO as a therapeutic target. In this review, we provide a detailed summary of MVO including underlying causes, diagnostic techniques, and current therapeutic approaches. Furthermore, we discuss the hypothesis that simultaneously addressing infarct size and MVO may help to translate cardioprotective strategies into improved clinical outcome following ST-segment–elevation myocardial infarction.
AB - Primary percutaneous coronary intervention is nowadays the preferred reperfusion strategy for patients with acute ST-segment–elevation myocardial infarction, aiming at restoring epicardial infarct-related artery patency and achieving microvascular reperfusion as early as possible, thus limiting the extent of irreversibly injured myocardium. Yet, in a sizeable proportion of patients, primary percutaneous coronary intervention does not achieve effective myocardial reperfusion due to the occurrence of coronary microvascular obstruction (MVO). The amount of infarcted myocardium, the so-called infarct size, has long been known to be an independent predictor for major adverse cardiovascular events and adverse left ventricular remodeling after myocardial infarction. Previous cardioprotection studies were mainly aimed at protecting cardiomyocytes and reducing infarct size. However, several clinical and preclinical studies have reported that the presence and extent of MVO represent another important independent predictor of adverse left ventricular remodeling, and recent evidences support the notion that MVO may be more predictive of major adverse cardiovascular events than infarct size itself. Although timely and complete reperfusion is the most effective way of limiting myocardial injury and subsequent ventricular remodeling, the translation of effective therapeutic strategies into improved clinical outcomes has been largely disappointing. Of importance, despite the presence of a large number of studies focused on infarct size, only few cardioprotection studies addressed MVO as a therapeutic target. In this review, we provide a detailed summary of MVO including underlying causes, diagnostic techniques, and current therapeutic approaches. Furthermore, we discuss the hypothesis that simultaneously addressing infarct size and MVO may help to translate cardioprotective strategies into improved clinical outcome following ST-segment–elevation myocardial infarction.
KW - Adrenergic beta-Antagonists
KW - Animals
KW - Coronary Circulation
KW - Fibrinolytic Agents
KW - Humans
KW - Hydroxymethylglutaryl-CoA Reductase Inhibitors
KW - Microcirculation
KW - Myocardial infarction
KW - Myocardial reperfusion
KW - Myocardium
KW - Percutaneous coronary intervention
KW - ST Elevation Myocardial Infarction
KW - Ventricular remodeling
KW - Adrenergic beta-Antagonists
KW - Animals
KW - Coronary Circulation
KW - Fibrinolytic Agents
KW - Humans
KW - Hydroxymethylglutaryl-CoA Reductase Inhibitors
KW - Microcirculation
KW - Myocardial infarction
KW - Myocardial reperfusion
KW - Myocardium
KW - Percutaneous coronary intervention
KW - ST Elevation Myocardial Infarction
KW - Ventricular remodeling
UR - http://hdl.handle.net/10807/154399
U2 - 10.1161/CIRCRESAHA.119.315344
DO - 10.1161/CIRCRESAHA.119.315344
M3 - Article
SN - 0009-7330
VL - 125
SP - 245
EP - 258
JO - Circulation Research
JF - Circulation Research
ER -