Mortality at 1 Year With Combination Platelet Glycoprotein IIb/IIIa Inhibition and Reduced-Dose Fibrinolytic Therapy vs Conventional Fibrinolytic Therapy for Acute Myocardial Infarction

Lincoff, A. Michael; Califf, Robert M.; Werf, Frans Van de; Willerson, James T.; White, Harvey D.; Armstrong, Paul W.; Guetta, Victor; Gibler, W. Brian; Hochman, Judith S.; Bode, Christoph; Vahanian, Alec; Steg, Philippe Gabriel; Ardissino, Diego; Savonitto, Stefano; Bär, Frits W.; Sadowski, Zygmunt; Betriu, Amadeo; Booth, John V.; Wolski, Kathy; Waller, Michael; Topol, Eric J.; Investigators, for the GUSTO V

doi:10.1001/jama.288.17.2130

Cited by 117 publications

(4 citation statements)

References 19 publications

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“…Clinical trials suggest the mortality benefit of antiplatelet agents, such as aspirin and α IIb β 3 integrin antagonists, may result from effects more complex than simple thrombus inhibition. [9][10][11] In animal studies, several platelet-activating factor antagonists [12][13][14] reduced ischemia-induced VF incidence. Moreover, aspirin pretreatment reduced ischemia-induced VF in various animal models.…”

Section: Clinical Perspective On P 1001mentioning

confidence: 99%

Trapped Platelets Activated in Ischemia Initiate Ventricular Fibrillation

Dhanjal

Medina

Leem

et al. 2013

Circ: Arrhythmia and Electrophysiology

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Background-We tested the hypothesis that ischemia-induced ventricular fibrillation (VF) is facilitated by platelets, trapped regionally in the ischemic zone and activated to release arrhythmogenic secretome. Methods and Results-In a randomized study in blood-free, buffer-perfused isolated rat hearts, ischemic zone territory (34±1% of left ventricle) was selected so that ischemia evoked VF in only 42% of controls. VF incidence was increased to 91% (P<0.05) by coronary ligation-induced trapping of freshly prepared autologous platelets (infused before and during coronary ligation, with trapping confirmed by 111 In-labeled platelet autoradiographic imaging). Trapping of platelet secretome prepared ex vivo, or platelet-sized fluorospheres, did not increase ischemia-induced VF incidence. Secretome alone did, however, evoke VF in 2 sham coronary-ligated hearts. Perfusion did not activate infused platelets in sham coronary-ligated hearts, whereas ligation activated trapped platelets (assessed by thromboxane release). In a separate study, trapping whole-heparinized blood mimicked the ability of trapped platelets to increase VF incidence. This effect was not prevented by >5 days oral pretreatment in vivo with clopidogrel (10 mg/kg per day) or indomethacin (2.4 mg/kg per day). Conclusions-Platelets facilitate VF during acute ischemia independently of their ability to participate in occlusive thrombosis.Moreover, the effect is unresponsive to antiplatelet drugs commonly used. Labile secretome constituents appear to be responsible. This opens a novel avenue for antiarrhythmic drug research. (Circ Arrhythm Electrophysiol. 2013;6:995-1001.)

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Section: Clinical Perspective On P 1001mentioning

confidence: 99%

Trapped Platelets Activated in Ischemia Initiate Ventricular Fibrillation

Dhanjal

Medina

Leem

et al. 2013

Circ: Arrhythmia and Electrophysiology

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“…Hinsichtlichd er Ein-Jahres-Überlebensrate konnte jedochkeinVorteil einerkombinier-tenTherapie gegenübereineralleinigen Fibrinolyseg ezeigt werden. Das Risiko schwerer Blutungskomplikationen lag zudemv or allemb ei älterenP atienten( >75 Jahre) deutlichü berd em Niveau derS tandard-Fibrinolysetherapie (3,18,36,50,53 Literatur…”

Section: Glykoprotein-iib/iiia-rezeptorblockerunclassified

Antikoagulanzien und Thrombolytika beim akuten Koronarsyndrom

Saurbier

Bode²

2005

Hamostaseologie

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The term acute coronary syndrome (ACS) pertains to the instable and life-threatening forms of a clinically manifest coronary artery disease with biochemical and/or electrocardiographic evidence od myocyte cell death. In detail, it includes the unstable angina pectoris, the non-ST segment elevation myocardial infarction (NSTEMI) the ST segment elevation myocardial infarction (STEMI) and as well the sudden cardiac death. As early reperfusion of ischaemic myocardium is the most effective way for limiting infarct size by restoring the balance between myocardial oxygen supply and demand, it is the most important therapeutic goal to achieve early and complete antegrade flow in the occluded or restricted vessel, related with a reduction of short and longtime complications as heart failure and severe arrhythmias. It is generally accepted, that the primary percutaneous coronary intervention (PCI) is the method of choice in acute myocardial infarction (STEMI) to restore TIMI-3 blood flow in occluded coronary arteries, if this can be performed within two hours of symptom onset and by a highly specialized team. Since this requirements are only met in 20% of hospitals caring for patients with STEMI in Germany, the therapy with thrombolytic and anticoagulant agents plays still an important role. Apart from a rapid and effective prehospital primary care, it depends furthermore on a differentiated anticoagulatory and antithrombotic therapy during coronary intervention to get optimal results.

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“…Recently, 1-year data from GUSTO V were published, demonstrating no difference in all-cause mortality between the treatment groups. 53 The smaller ASSENT-3 investigation found slightly different results when abciximab was administered with tenecteplase (half dose) for the management of STEMI. 52 In addition to evaluating abciximab plus tenecteplase (half dose), the investigators compared enoxaparin plus tenecteplase (full dose) with standard of care.…”

Section: Medical Managementmentioning

confidence: 99%