scholarly journals Antithrombotic effects of losartan in patients with hypertension complicated by atrial fibrillation: 4A (Angiotensin II Antagonist of platelet Aggregation in patients with Atrial fibrillation), a pilot study

2014 ◽  
Vol 37 (6) ◽  
pp. 513-518 ◽  
Author(s):  
Tomohiro Sakamoto ◽  
Takashi Kudoh ◽  
Kenji Sakamoto ◽  
Kunihiko Matsui ◽  
Hisao Ogawa
Keyword(s):  
Atrial Fibrillation ◽  
Platelet Aggregation ◽  
Angiotensin Ii ◽  
Pilot Study ◽  
Angiotensin Ii Antagonist ◽  
Antithrombotic Effects

scholarly journals Data mining experiments on the Angiotensin II-Antagonist in Paroxysmal Atrial Fibrillation (ANTIPAF-AFNET 2) trial: ‘exposing the invisible’

EP Europace ◽  
2016 ◽  
pp. euw084 ◽  
Author(s):  
Sercan Okutucu ◽  
Deniz Katircioglu-Öztürk ◽  
Emre Oto ◽  
H. Altay Güvenir ◽  
Ergun Karaagaoglu ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Data Mining ◽  
Angiotensin Ii ◽  
Paroxysmal Atrial Fibrillation ◽  
Angiotensin Ii Antagonist ◽  
The Invisible

scholarly journals Effect of Frailty and Age on Platelet Aggregation and Response to Aspirin in Older Patients with Atrial Fibrillation: A Pilot Study

2016 ◽  
Vol 5 (1) ◽  
pp. 51-62 ◽  
Author(s):  
Tu N. Nguyen ◽  
Dominic Pepperell ◽  
Marie-Christine Morel-Kopp ◽  
Robert G. Cumming ◽  
Christopher Ward ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Platelet Aggregation ◽  
Pilot Study ◽  
Older Patients

Angiotensin II Antagonist in Paroxysmal Atrial Fibrillation (ANTIPAF) Trial

2007 ◽  
Vol 27 (10) ◽  
pp. 697-705 ◽  
Author(s):  
Andreas Goette ◽  
G??nter Breithardt ◽  
Thomas Fetsch ◽  
Peter Hanrath ◽  
Helmut U Klein ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Angiotensin Ii ◽  
Paroxysmal Atrial Fibrillation ◽  
Angiotensin Ii Antagonist

scholarly journals Angiotensin II-Antagonist in Paroxysmal Atrial Fibrillation (ANTIPAF) Trial

2012 ◽  
Vol 5 (1) ◽  
pp. 43-51 ◽  
Author(s):  
Andreas Goette ◽  
Norbert Schön ◽  
Paulus Kirchhof ◽  
Günter Breithardt ◽  
Thomas Fetsch ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Angiotensin Ii ◽  
Paroxysmal Atrial Fibrillation ◽  
Angiotensin Ii Antagonist

scholarly journals Angiotensin II Antagonist Prevents Electrical Remodeling in Atrial Fibrillation

Circulation ◽  
2000 ◽  
Vol 101 (22) ◽  
pp. 2612-2617 ◽  
Author(s):  
Hideko Nakashima ◽  
Koichiro Kumagai ◽  
Hidenori Urata ◽  
Naoki Gondo ◽  
Munehito Ideishi ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Angiotensin Ii ◽  
Electrical Remodeling ◽  
Angiotensin Ii Antagonist

Antiarrhythmische Pharmakotherapie

2012 ◽  
Vol 31 (11) ◽  
pp. 826-829
Author(s):  
A. Goette ◽  
P. Kirchhof ◽  
A. Treszl ◽  
K. Wegscheider ◽  
T. Meinertz
Keyword(s):  
Atrial Fibrillation ◽  
Drug Therapy ◽  
Angiotensin Ii ◽  
Catheter Ablation ◽  
Early Treatment ◽  
Stroke Prevention ◽  
Conventional Treatment ◽  
Ventricular Dysfunction ◽  
Left Ventricular ◽  
Atrial Fibrillation Trial

ZusammenfassungEs werden die Ergebnisse von Studien sowie die Protokolle laufender „Megastudien“ mit Bezug zum Vorhofflimmer-Netzwerk dargestellt. Bei den abgeschlossenen Studien handelt es sich um die Flecainide Short-Long trial (Flec-SL) und die Angiotensin-II-Rezeptorblocker in Paroxysmal Atrial FibrillationStudie (ANTIPAF). Bei den „Megastudien“ um Studien mit den Kürzeln EAST (Early Treatment of Atrial Fibrillation for Stroke Prevention Trial), CABANA (Catheter Ablation Versus Anti-arrhythmic Drug Therapy for Atrial Fibrillation Trial) und CASTLE-AF (Catheter Ablation versus Standard conventional Treatment in patients with LEft ventricular dysfunction and Atrial Fibrillation). Die Ergebnisse der Studien: Eine präventive Kurzzeittherapie nach Kardio-version ist sinnvoller als der Verzicht auf jegliche Antiarrhythmika-Nachbehandlung. Noch effektiver scheint eine antiarrhythmische Langzeit-Nachbehandlung über sechs Monate zu sein. In der ANTIPAF-Studie zeigte sich, dass bei Patienten mit paroxysmalem Vorhofflimmern (VHF) ohne strukturelle Herzkrankheit der Angiotensinrezeptorblocker Olmesartan nicht in der Lage ist, die Häufigkeit der Anfälle zu reduzieren. Wichtigstes therapeutisches Ziel ist die Verhinderung der Progression von VHF. In der EAST-Studie wird geprüft, ob eine frühzeitig eingeleitete, „aggressive“ Therapie zur Kontrolle des Herzrhythmus eher in der Lage ist, Morbidität und Mortalität von VHF zu senken als die Standardtherapie.

Antithrombotic Effects and Bleeding Time Prolongation with Synthetic Platelet GPIIb/llla Inhibitors in Animal Models of Platelet-Mediated Thrombosis

1994 ◽  
Vol 71 (01) ◽  
pp. 095-102 ◽  
Author(s):  
Désiré Collen ◽  
Hua Rong Lu ◽  
Jean-Marie Stassen ◽  
Ingrid Vreys ◽  
Tsunehiro Yasuda ◽  
...  
Keyword(s):  
Platelet Aggregation ◽  
Bleeding Time ◽  
Bolus Injection ◽  
Cell Injury ◽  
Ex Vivo ◽  
Thrombus Formation ◽  
Femoral Vein ◽  
Thrombotic Occlusion ◽  
Antithrombotic Effects

SummaryCyclic Arg-Gly-Asp (RGD) containing synthetic peptides such as L-cysteine, N-(mercaptoacetyl)-D-tyrosyl-L-arginylglycyl-L-a-aspartyl-cyclic (1→5)-sulfide, 5-oxide (G4120) and acetyl-L-cysteinyl-L-asparaginyl-L-prolyl-L-arginyl-glycyl-L-α-aspartyl-[0-methyltyrosyl]-L-arginyl-L-cysteinamide, cyclic 1→9-sulfide (TP9201) bind with high affinity to the platelet GPIIb/IIIa receptor.The relationship between antithrombotic effect, ex vivo platelet aggregation and bleeding time prolongation with both agents was studied in hamsters with a standardized femoral vein endothelial cell injury predisposing to platelet-rich mural thrombosis, and in dogs with a carotid arterial eversion graft inserted in the femoral artery. Intravenous administration of G4120 in hamsters inhibited in vivo thrombus formation with a 50% inhibitory bolus dose (ID50) of approximately 20 μg/kg, ex vivo ADP-induccd platelet aggregation with ID50 of 10 μg/kg, and bolus injection of 1 mg/kg prolonged the bleeding time from 38 ± 9 to 1,100 ± 330 s. Administration of TP9201 in hamsters inhibited in vivo thrombus formation with ID50 of 30 μg/kg, ex vivo platelet aggregation with an ID50 of 50 μg/kg and bolus injection of 1 mg/kg did not prolong the template bleeding time. In the dog eversion graft model, infusion of 100 μg/kg of G4120 over 60 min did not fully inhibit platelet-mediated thrombotic occlusion but was associated with inhibition of ADP-induccd ex vivo platelet aggregation and with prolongation of the template bleeding time from 1.3 ± 0.4 to 12 ± 2 min. Infusion of 300 μg/kg of TP9201 over 60 min completely prevented thrombotic occlusion, inhibited ex vivo platelet aggregation, but was not associated with prolongation of the template bleeding time.TP9201, unlike G4120, inhibits in vivo platelet-mediated thrombus formation without associated prolongation of the template bleeding time.

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