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Drug Combinations
Published in Josef Hladovec, Antithrombotic Drugs in Thrombosis Models, 2020
The problem of interaction of ASA with oral anticoagulants is an old one. It is generally considered unfavorable and explained as displacement of anticoagulants from protein binding and a direct effect on liver metabolism. On the other hand, little attention is paid to the possibility of a well-controlled combination which could be more effective. Thus ASA with warfarin in rabbit jugular autografts was superior to the effect of either drug alone in preserving graft patency.44 Some authors reported no effect of combined clinical administration of ASA 1500 mg together with phenprocoumon on Quick’s time, bleeding tests, and the occurrence of complications.45
Fibrinolytic Enzymes for Thrombolytic Therapy
Published in Peter Grunwald, Pharmaceutical Biocatalysis, 2019
Swaroop S. Kumar, Sabu Abdulhameed
Anticoagulants like coumarin derivatives were discovered in 1939 by the identification of dicumarol from spoiled sweet clover hay which is a vitamin K antagonist by Link and Campbell (Stahmann et al., 1941). Further studies on coumarin derivatives led to the discovery of warfarin which was initially used as rodenticide and later approved for clinical use as anticoagulant. It was the first oral thrombin inhibitor and found useful in preventing embolic strokes (Aguilar and Hart, 2005). Limitations of these vitamin K antagonists were bleeding complications, interaction with food, necrosis, and hair loss (Dantas et al., 2004; Ansell et al., 2008; Pirmohamed, 2006). Even though other coumarin derivatives such as phenprocoumon and acenocoumarol also were used as anticoagulants, warfarine is the most common vitamin K antagonist in practice and remains as affordable in cardiovascular disease management.
Briefing Therapeutic Approaches in Anticoagulant, Thrombolytic, and Antiplatelet Therapy
Published in Debarshi Kar Mahapatra, Sanjay Kumar Bharti, Medicinal Chemistry with Pharmaceutical Product Development, 2019
Many of the drug-drug interactions are associated with enhanced or inhibited metabolism of warfarin via CYP2C9 induction or inhibition. As warfarin is highly protein bound drug, any other substances that displace bound drug from protein binding sites increases the levels of free drug and, as a result, can cause warfarin toxicity, which usually is manifested by hemorrhage. The activity of warfarin is affected by diet and by genetic make-up: polymorphisms in the gene that encodes vitamin K epoxide reductase and in the cytochrome P450 gene CYP2C9 account for up to 50% of the inter-individual variability of warfarin dosing. Dicumarol, phenprocoumon, and acenocoumarol have also been investigated as anticoagulants in humans, although no significant advantages were found [45–47].
Drug-drug interactions with direct oral anticoagulants for the prevention of ischemic stroke and embolism in atrial fibrillation: a narrative review of adverse events
Published in Expert Review of Clinical Pharmacology, 2023
Claudia Stöllberger, Birke Schneider, Josef Finsterer
So far, DOAC were only compared with warfarin in randomized trials [1–4]. Phenprocoumon, a further VKA, is a long-acting substance and associated with a more stable anticoagulant effect compared with warfarin [5,6]. It would be of great value to conduct an industry-independent large randomized prospective trial comparing DOAC with different VKA, sponsored by social insurance companies, academic institutions and ministries of health. Reasons for such a trial are controversial findings regarding the superiority of DOAC versus VKA [5–9]. A further argument for such a trial is the financial burden which entails DOAC-therapy for health care systems compared with VKA, especially in middle- or low-income countries [81–83]. Results of these studies and trials will hopefully result in practical recommendations and guidelines for an individualized anticoagulant therapy.
Real-time echocardiography-fluoroscopy fusion imaging for left atrial appendage closure: prime time for fusion imaging?
Published in Acta Cardiologica, 2021
Shazia Afzal, Kerstin Piayda, Katharina Hellhammer, Verena Veulemans, Georg Wolff, Houtan Heidari, Dominique Stüwe, Dominika Kanschik, Amin Polzin, Malte Kelm, Tobias Zeus
Patients were seen for follow-up in our outpatient clinic after 3, 6, and 12 months. Ten + FI patients (8%) and one − FI patient (3%) were lost to follow-up. In three patients mild PDL and in two patients moderate PDL was detected after three months and not demonstrated in the follow up TEE. No severe PDL was observed (mild PDL + FI/−FI: n = 4 (3.6%) vs. n = 0; moderate PDL + FI/−FI: n = 1 (0.9%) vs. n = 0; severe PDL + FI/−FI: n = 0 vs. n = 0). During this period no cerebrovascular events occurred. Furthermore, the TEE examination of two patients in the + FI group revealed a nonmobile laminar device-related thrombus without causing any thromboembolic events. In both patients, an intermittent oral anticoagulation with phenprocoumon was administered. A TEE examination was performed 8 weeks later, and the oral anticoagulation was discontinued because the thrombi material resolved. No further cardiovascular complications occurred.
Clinical pharmacology of antiplatelet drugs
Published in Expert Review of Clinical Pharmacology, 2022
Georg Gelbenegger, Bernd Jilma
Several other drugs that are CYP3A4 inhibitors or are metabolized by CYP3A4 have been shown to decrease the antiplatelet effect of clopidogrel. Ketoconazole and itraconazole, both potent inhibitors of CYP3A4, significantly decrease the ability of clopidogrel to inhibit platelet function [93,94]. Nifedipine and amlodipine, both dihydropyridine calcium channel blockers, inhibit CYP3A4 and decrease clopidogrel responsiveness [95,96]. The vitamin K antagonist phenprocoumon, metabolized by CYP3A4 and CYP2C9, significantly attenuates the antiplatelet effect of clopidogrel [97].