Abciximab Facilitates the Rate and Extent of Thrombolysis

Antman, Elliott M.; Giugliano, Robert P.; Gibson, C. Michael; McCabe, Carolyn H.; Coussement, Patrick; Kleiman, Neal S.; Vahanian, Alec; Adgey, A. A. J.; Menown, Ian; Rupprecht, Hans J.; Wieken, Ron van der; Ducas, John; Scherer, John R.; Anderson, Keaven M.; Werf, Frans Van de; Braunwald, Eugene

doi:10.1161/01.cir.99.21.2720

Cited by 593 publications

(120 citation statements)

References 45 publications

(30 reference statements)

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“…Overall recanalization rates of total occlusions could be expected to increase from Ϸ50% to 80% with such therapy, an improvement that is in keeping with results of the TIMI 14A trial. 90 In the 20% of patients whose occlusive coronary thrombi consist predominantly of platelets, glycoprotein IIb/IIIa inhibition may be particularly useful. It appears quite possible, however, that brisk reflow can be achieved in these patients only with the use of mechanical interventions.…”

Section: Discussionmentioning

confidence: 99%

Thrombi in Acute Coronary Syndromes

2000

Circulation

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O ver the past 35 years, the view has evolved that the acute coronary syndromes, ie, unstable angina pectoris, myocardial infarction, and sudden death, are caused by plaque rupture and formation of a platelet thrombus. There is at least a transient total or subtotal coronary occlusion in all cases of acute myocardial infarction. Q-wave infarcts are thought to differ from non-Q-wave infarcts by more stable platelet thrombi causing more prolonged and/or severe ischemia, leading to more extensive infarction. The greater platelet stability in transmural infarction is attributed to more severe or extensive plaque rupture. 1-3 Unstable angina and non-Qwave infarction, in the present view, are due to less extensive, less stable platelet thrombi that cause less severe, less extensive ischemia and/or infarction.However, autopsy data and more recent clinical findings require significant refinement of this viewpoint on the basis of the following observations. The occlusive thrombi causing Q-wave myocardial infarction contain more fibrin than the thrombi found in the other acute coronary syndromes that are characterized by more platelets and less fibrin. The higher fibrin content of thrombi causing Q-wave infarction explains their greater stability. Furthermore, this higher fibrin content suggests that the coagulation cascade is activated to a greater degree during Q-wave infarction than during non-Q-wave infarction in which platelets play a more dominant role. This review analyzes our evolving concepts focusing on the growing divergence of the different mechanisms underlying the different acute coronary syndromes and their clinical and therapeutic implications. Morphological Basis for the Current Concept of Acute Coronary SyndromesBy the mid-1930s, acute myocardial infarction was shown to be caused by coronary thrombosis resulting from intimal fissuring, which is often associated with dissecting hemorrhage into the underlying plaque. 4 -7 In the late 1930s, however, intimal fissuring was questioned and subendothelial hemorrhages were ascribed to rupture of capillaries within the plaque. 8,9 The causative role of coronary thrombosis became controversial in 1956 when pathologists first reported a low prevalence of thrombi in fatal infarction. 10 -16 The pendulum began to swing back in the mid-1960s because of improved autopsy techniques. Coronary thrombi were found in Ͼ90% of fatal infarcts, most being occlusive.Plaque hemorrhages, which were usually traceable to an intimal tear within the thrombosed segment, were found in most cases. [17][18][19][20][21] These observations reaffirmed that intimal rupture was the essential mechanism causing both subendothelial hemorrhage and intraluminal thrombosis. 22 Having found that three quarters of occlusive coronary thrombi were composed of layers of different ages, Sinapius 17,21 concluded that these thrombi developed in a protracted, recurring course. The oldest portion of thrombus usually sealed the intimal fissure and was rich in platelets. The finding that mural thrombus forma...

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Section: Discussionmentioning

confidence: 99%

Thrombi in Acute Coronary Syndromes

2000

Circulation

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“…4 Whereas conjunctive therapy with intravenous glycoprotein IIb/IIIa (IV GP IIb/IIIa) inhibitors enhances epicardial flow and myocardial perfusion and reduces reinfarction, these advantages have not resulted in the expected improvement in survival. 5,6 Indeed, the increase in systemic bleeding and apparent excess of intracranial hemorrhage among STEMI patients over 75 years has led to reassessment of the suitability of combination reperfusion with IV GP IIb/IIIa inhibitors and reduced dose fibrinolysis. 7,8 Currently, the combination of full dose fibrinolysis and low molecular weight heparin or a direct antithrombin appears to be an attractive strategy because of reduced reinfarction and recurrent ischemia.…”

Section: Evolution Of Pharmacological Reperfusion Regimensmentioning

confidence: 99%

Fibrinolysis for Acute Myocardial Infarction

2003

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“…Glycoprotein IIb ⁄ IIIa inhibitors are believed to facilitate the rate and extent of clot dissolution and produce early increases in coronary blood flow when they are combined with fibrinolytic therapy. 25 The early use of glycoprotein IIb ⁄ IIIa inhibitors can induce reperfusion before primary PCI for acute STEMI. 26 The combination of a glycoprotein IIb ⁄ IIIa inhibitor plus heparin significantly reduces the intracoronary thrombus burden of the culprit lesions, improves the perfusion grade, and decreases the severity of the obstruction in patients with unstable angina or non-Q-wave MI.…”

Section: Discussionmentioning

confidence: 99%

Impact of an Audit Program and Other Factors on Door‐to‐balloon Times in Acute ST‐elevation Myocardial Infarction Patients Destined for Primary Coronary Intervention

Lai

Fan

Liao

et al. 2009

Academic Emergency Medicine

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Objectives: This before-after study investigated the association between an audit program and door-toballoon times in patients with acute ST-elevation myocardial infarction (STEMI) and explored other factors associated with the door-to-balloon time.Methods: An audit program that collected time data for essential time intervals in acute STEMI was developed with data feedback to both the Department of Emergency Medicine and the Department of Cardiology. The door-to-balloon times for 76 consecutive acute STEMI patients were collected from February 16, 2007, through October 31, 2007, after the implementation of the audit program, as the intervention group. The control group was defined by 104 consecutive acute STEMI patients presenting from April 1, 2006, through February 15, 2007, before the audit was applied. A multivariate linear regression model was used for analysis of factors associated with the door-to-balloon time.Results: The geometric mean 95% CI of the door-to-balloon time decreased from 164.9 (150.3, 180.9) minutes to 141.9 (127.4, 158.2) minutes (p = 0.039) in the intervention phase. The median door-to-balloon time was 147.5 minutes in the control group and 136.0 minutes in the intervention group (p = 0.09). In the multivariate regression model, the audit program was associated with a shortening of the door-toballoon time by 35.5 minutes (160.4 minutes vs. 195.9 minutes, p = 0.004); female gender was associated with a mean delay of 58.4 minutes (208.9 minutes vs. 150.5 minutes; p = 0.001); posterolateral wall infarction was associated with a mean delay of 70.5 minutes compared to anterior wall infarction (215.4 minutes vs. 144.9 minutes; p = 0.037) and a mean delay of 69.5 minutes compared to inferior wall infarction (215.4 minutes vs. 145.9 minutes; p = 0.044). The use of a glycoprotein IIb ⁄ IIIa inhibitor was associated with a 46.1 minutes mean shortening of door-to-balloon time (155.7 minutes vs. 201.8 minutes; p < 0.001). Conclusions:The implementation of an audit program was associated with a significant reduction in door-to-balloon times among patients with acute STEMI. In addition, female patients, posterolateral wall infarction territory, and nonuse of glycoprotein IIb ⁄ IIIa inhibitor were associated with longer door-toballoon times.ACADEMIC EMERGENCY MEDICINE 2009; 16:333-342 ª

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Abciximab Facilitates the Rate and Extent of Thrombolysis

Cited by 593 publications

References 45 publications

Thrombi in Acute Coronary Syndromes

Thrombi in Acute Coronary Syndromes

Fibrinolysis for Acute Myocardial Infarction

Impact of an Audit Program and Other Factors on Door‐to‐balloon Times in Acute ST‐elevation Myocardial Infarction Patients Destined for Primary Coronary Intervention

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