Comparison of rheolytic thrombectomy before direct infarct artery stenting versus direct stenting alone in patients undergoing percutaneous coronary intervention for acute myocardial infarction
Abstract:This randomized trial compared rheolytic thrombectomy before direct infarct artery stenting with direct infarct artery stenting alone in 100 patients with a first acute myocardial infarction (AMI). The primary end point of the study was early ST-segment elevation resolution, and the secondary end points were corrected Thrombolysis In Myocardial Infarction (TIMI) frame count, infarct size, and 1-month clinical outcome. The primary end point rates were 90% in the thrombectomy group and 72% in the placebo group (… Show more
“…208 Also, no reduction of microvascular obstruction and infarct size was found with MRI. [209][210][211] Hyperoxemia, 212,213 aspiration or mechanical thrombectomy, [214][215][216][217][218][219][220][221] and intra-aortic balloon counterpulsation 222 did not reduce infarct size or improve coronary blood flow. More recently, also the cardioprotection by cyclosporine A which had been shown in a small-scale proof-of-concept trial 223 was not confirmed in another smaller study with prethrombolytic cyclosporine A 224 and, importantly, not in 2 larger-scale phase III trials, Does Cyclosporine Improve Clinical Outcome in ST Elevation Myocardial Infarction Patients (CIRCUS) and CyclosporinE A in Reperfused Myocardial Infarct (CYCLE).…”
Abstract:The atherosclerotic coronary vasculature is not only the culprit but also a victim of myocardial ischemia/ reperfusion injury. Manifestations of such injury are increased vascular permeability and edema, endothelial dysfunction and impaired vasomotion, microembolization of atherothrombotic debris, stasis with intravascular cell aggregates, and finally, in its most severe form, capillary destruction with hemorrhage. In animal experiments, local and remote ischemic pre-and postconditioning not only reduce infarct size but also these manifestations of coronary vascular injury, as do drugs which recruit signal transduction steps of conditioning. Clinically, no-reflow is frequently seen after interventional reperfusion, and it carries an adverse prognosis. The translation of cardioprotective interventions to clinical practice has been difficult to date. Only 4 drugs (brain natriuretic peptide, exenatide, metoprolol, and esmolol) stand unchallenged to date in reducing infarct size in patients with reperfused acute myocardial infarction; unfortunately, for these drugs, no information on their impact on the ischemic/reperfused coronary circulation is available. (Circ Res.
“…208 Also, no reduction of microvascular obstruction and infarct size was found with MRI. [209][210][211] Hyperoxemia, 212,213 aspiration or mechanical thrombectomy, [214][215][216][217][218][219][220][221] and intra-aortic balloon counterpulsation 222 did not reduce infarct size or improve coronary blood flow. More recently, also the cardioprotection by cyclosporine A which had been shown in a small-scale proof-of-concept trial 223 was not confirmed in another smaller study with prethrombolytic cyclosporine A 224 and, importantly, not in 2 larger-scale phase III trials, Does Cyclosporine Improve Clinical Outcome in ST Elevation Myocardial Infarction Patients (CIRCUS) and CyclosporinE A in Reperfused Myocardial Infarct (CYCLE).…”
Abstract:The atherosclerotic coronary vasculature is not only the culprit but also a victim of myocardial ischemia/ reperfusion injury. Manifestations of such injury are increased vascular permeability and edema, endothelial dysfunction and impaired vasomotion, microembolization of atherothrombotic debris, stasis with intravascular cell aggregates, and finally, in its most severe form, capillary destruction with hemorrhage. In animal experiments, local and remote ischemic pre-and postconditioning not only reduce infarct size but also these manifestations of coronary vascular injury, as do drugs which recruit signal transduction steps of conditioning. Clinically, no-reflow is frequently seen after interventional reperfusion, and it carries an adverse prognosis. The translation of cardioprotective interventions to clinical practice has been difficult to date. Only 4 drugs (brain natriuretic peptide, exenatide, metoprolol, and esmolol) stand unchallenged to date in reducing infarct size in patients with reperfused acute myocardial infarction; unfortunately, for these drugs, no information on their impact on the ischemic/reperfused coronary circulation is available. (Circ Res.
“…In this regard, the use of a mechanical device for thrombus removal or trapping to improve clinical outcomes after p-PCI is attractive, and the efficacy of these devices has been tested in many clinical trials. Although some data, especially those regarding the use of distal protection devices, have failed to show clinical benefits due in part to patient and device selection [48][49][50][51][52][53] , many recent large-scale randomized trials have demonstrated significant improvements in myocardial perfusion 45,[54][55][56][57][58][59][60][61][62][63][64][65][66][67] and the left ventricular function 64,65) in addition to reduced mortality 68) ( 69) . In addition, Burzotta et 70) .…”
Section: Thrombus Aspiration/distal Protection Therapy and Its Efficacymentioning
Inflammation and oxidative stress play key roles in atherosclerotic plaque instability, and plaque rupture/erosion and subsequent thrombus formation constitute the principal mechanisms of total vessel occlusion and acute ST-elevation myocardial infarction (STEMI). Plaque disruption triggers the formation of initial platelet aggregates that grow in association with an increase in fibrin formation, leading to persistent coronary flow obstruction and blood coagulation. The fibrin network may trap large numbers of erythrocytes and inflammatory cells to form an erythrocyte-rich thrombus. In fact, previous clinical studies have shown that not only platelet-rich white thrombi, but also erythrocyte-rich red thrombi can be visualized using angioscopy in patients with acute coronary syndrome. Recently, the development of thrombus aspiration and distal protection devices has significantly improved the clinical outcomes of percutaneous intervention in STEMI patients and has enabled the evaluation of antemortem coronary artery thrombi. This is important because previous autopsy studies were unable to differentiate coronary thrombi responsible for myocardial ischemia from postmortem clots. Using frozen samples of aspirated thrombi and specific monoclonal antibodies, we investigated the cellular components of thrombi (platelets, erythrocytes, fibrin and inflammatory cells, such as myeloperoxidase-positive cells) and pathologically evaluated the relationships between erythrocyterich thrombi and inflammation, oxidative stress and clinical outcomes in STEMI patients. Therefore, this review article focuses on the efficacy of thrombus aspiration therapy and the components of aspirated intracoronary thrombi in STEMI patients and presents the results of recent studies regarding the relationship between the composition of aspirated intracoronary thrombi and clinical outcomes.
“…16 Angiographically visible thrombus was required in 5 trials. 13,24,32,33,35 Patients in shock or those requiring intra-aortic balloon counterpulsation or mechanical ventilation were excluded from 11 trials, 13,15,16,18,20,24,26,29,31,34,35 and patients with previous coronary artery bypass were excluded from 9 trials. 12,14,16,18,20,24,28,34,35 Only 2 RCTs specifically excluded patients with a left ventricular ejection fraction Ͻ30%.…”
Section: Differences In Inclusion and Exclusion Criteria In Selected mentioning
Background-In available trials and meta-analyses, adjunctive thrombectomy in acute myocardial infarction (MI) improves markers of myocardial reperfusion but has limited effects on clinical outcomes.
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