natgillin/translations-raw huggingface dataset:
Because of the potential for increased risk of bleeding, chronic NSAIDs (including COX-2 inhibitors) and Efient should be co-administered with caution (see section 4.4).
Zaradi možnega povečanega tveganja za krvavitev, je pri sočasni uporabi NSAIDs (vključno z zaviralci COX- 2) in zdravila Efient (glejte poglavje 4. 4) potrebna previdnost.
Although not studied in specific interaction studies, Efient has been co-administered in the phase 3 clinical trial with low molecular weight heparin, bivalirudin, and GP IIb/ IIIa inhibitors (no information available regarding the type of GP IIb/ IIIa inhibitor used) without evidence of clinically significant adverse interactions.
Čeprav ga niso preučevali v posebnih študijah medsebojnega delovanja, so v kliničnem preskušanju faze 3 zdravilo Efient sočasno dajali z nizko molekularnim heparinom, bivalirudinom in zaviralci GP IIb/ IIIa (na voljo ni podatkov o uporabljenih zaviralcih GP IIb/ IIIa), brez dokazov o klinično pomembnem neželenem medsebojnem delovanju.
Effects of other medicinal products on Efient:
Učinki drugih zdravil na zdravilo Efient:
Although a pharmacodynamic interaction with ASA leading to an increased risk of bleeding is possible, the demonstration of the efficacy and safety of prasugrel comes from patients concomitantly treated with ASA.
Čeprav je
4 Heparin:
4 možna farmakodinamična interakcija z ASK, ki vodi v povečano tveganje za krvavitev, so dokazi o učinkovitosti in varnosti prasugrela pridobljeni pri bolnikih, ki so bili sočasno zdravljeni z ASK.
A single intravenous bolus dose of unfractionated heparin (100 U/ kg) did not significantly alter the prasugrel-mediated inhibition of platelet aggregation.
Enkratni intravenski bolusni odmerek nefrakcioniranega heparina (100 enot/ kg) ni značilno spremenil zaviranja agregacije trombocitov, povzročenega s prasugrelom.
Medicinal products that elevate gastric pH:
Zdravila, ki višajo želodčni pH:
Daily co-administration of ranitidine (an H2 blocker) or lansoprazole (a proton pump inhibitor) did not change the prasugrel active metabolite’ s AUC and Tmax, but decreased the Cmax by 14% and 29%, respectively.
Dnevno sočasno dajanje ranitidina (blokator H2) ali lanzoprazola (zaviralec protonske črpalke) ni spremenilo AUC in tmax aktivnega presnovka prasugrela, ampak je zmanjšalo Cmax za 14% oziroma 29%.
Ketoconazole (400 mg daily), a selective and potent inhibitor of CYP3A4 and CYP3A5, did not affect prasugrel-mediated inhibition of platelet aggregation or the prasugrel active metabolite’ s AUC and Tmax, but decreased the Cmax by 34% to 46%.
Ketokonazol (400 mg na dan), selektiven in močan zaviralec CYP3A4 in CYP3A5, ni vplival na zaviranje agregacije trombocitov, povzročeno s prasugrelom ali AUC in tmax aktivnega presnovka prasugrela, je pa zmanjšal Cmax za 34% do 46%.
Effects of Efient on other medicinal products:
Učinki zdravila Efient na druga zdravila:
Digoxin: prasugrel has no clinically significant effect on the pharmacokinetics of digoxin.
Digoksin: prasugrel nima klinično značilnega učinka na farmakokinetiko digoksina.
Medicinal products metabolised by CYP2C9: prasugrel did not inhibit CYP2C9, as it did not affect the pharmacokinetics of S-warfarin.
Zdravila, ki se presnavljajo s CYP2C9: prasugrel ne zavira CYP2C9, kot tudi ne vpliva na farmakokinetiko S- varfarina.
Because of the potential for increased risk of bleeding, warfarin and Efient should be co-administered with caution (see section 4.4).
Zaradi možnega povečanega tveganja za krvavitev, moramo previdno dajati sočasno varfarin in zdravilo Efient (glejte poglavje 4. 4).
Medicinal products metabolised by CYP2B6: prasugrel is a weak inhibitor of CYP2B6.
Zdravila, ki se presnavljajo s CYP2B6: prasugrel je šibek zaviralec CYP2B6.
In healthy subjects, prasugrel decreased exposure to hydroxybupropion, a CYP2B6-mediated metabolite of bupropion, by 23%.
Pri zdravih osebah je prasugrel za 23% zmanjšal izpostavljenost hidroksibupropionu, presnovku bupropiona, ki se presnavlja s CYP2B6.
This effect is likely to be of clinical concern only when prasugrel is co- administered with medicinal products for which CYP2B6 is the only metabolic pathway and have a narrow therapeutic window (e. g. cyclophosphamide, efavirenz).
Ta učinek je klinično pomemben samo, kadar prasugrel dajemo sočasno z zdravili, za katere je edina pot presnove CYP2B6 in imajo ozko terapevtsko širino (npr. ciklofosfamid, efavirenz).
No clinical study has been conducted in pregnant or lactating women.
Kliničnih študij pri nosečnicah in doječih ženskah niso opravili.
Animal studies do not indicate direct harmful effects with respect to pregnancy, embryonal/ foetal development, parturition or postnatal development (see section 5.3).
Študije na živalih ne kažejo neposrednih škodljivih učinkov na nosečnost, razvoj zarodka/ ploda, porod ali postnatalni razvoj (glejte poglavje 5. 3).
5 Prasugrel had no effect on fertility of male and female rats at oral doses up to an exposure 240 times the recommended daily human maintenance dose (based on mg/ m2).
5 Prasugrel nima učinka na plodnost samcev in samic podgan pri peroralnih odmerkih, ki so do 240- krat večji od izpostavljenosti, pri priporočenem dnevnem vzdrževalnem odmerku pri ljudeh (glede na mg/ m2).
No studies on the effects on ability to drive and use machines have been performed.
Študij o vplivu na sposobnost vožnje in upravljanja s stroji niso izvedli.
Safety in patients with acute coronary syndrome undergoing PCI was evaluated in one clopidogrel- controlled study (TRITON) in which 6741 patients were treated with prasugrel (60 mg loading dose and 10 mg once daily maintenance dose) for a median of 14.5 months (5802 patients were treated for over 6 months, 4136 patients were treated for more than 1 year).
Varnost pri bolnikih z akutnim koronarnim sindromom, ki so imeli PCI, so ocenjevali v eni, s klopidogrelom nadzorovani študiji (TRITON), v kateri je bilo 6741 bolnikov zdravljenih s prasugrelom (60 mg polnilni odmerek in 10 mg vzdrževalni odmerek enkrat na dan) z mediano 14, 5 mececev (5802 bolnikov je bilo zdravljenih preko 6 mesecev, 4136 bolnikov je bilo zdravljenih več kot 1 leto).
The rate of study drug discontinuation due to adverse events was 7.2% for prasugrel and 6.3% for clopidogrel.
Stopnja prekinitve jemanja preiskovanega zdravila zaradi neželenih učinkov je bila 7, 2% za prasugrel in 6, 3% za klopidogrel.
Of these, bleeding was the most common adverse reaction for both drugs leading to study drug discontinuation (2.5% for prasugrel and 1.4% for clopidogrel).
Od teh je bil za obe zdravili najpogostejši neželeni učinek krvavitev, ki je vodila v prekinitev jemanja preiskovanega zdravila (2, 5% za prasugrel in 1, 4% za klopidogrel).
Non-Coronary Artery Bypass Graft (CABG) related bleeding In TRITON, the frequency of patients experiencing a non-CABG related bleeding event is shown in Table 1.
Krvavitev, ki ni v povezavi z operacijo aortokoronarnega obvoda (non- Coronary Artery Bypass Graft, non- CABG) V študiji TRITON je pogostnost bolnikov, ki so imeli krvavitev, povezano z non- CABG, prikazana v Preglednici 1.
The incidence of Non-CABG-related TIMI major bleeding, including life-threatening and fatal, as well as TIMI minor bleeding, was statistically significantly higher in subjects treated with prasugrel compared to clopidogrel in the UA/ NSTEMI and All ACS populations.
Pogostnost večje krvavitve po TIMI, povezane z non- CABG, vključno smrtno nevarno in smrtno, kot tudi manjše krvavitve po TIMI, je bila v UA/ NSTEMI in vseh populacijah ACS statistično značilno višja pri bolnikih, zdravljenih s prasugrelom, v primerjavi s klopidogrelom.
The most common site of spontaneous bleeding was the gastrointestinal tract (1.7% rate with prasugrel and 1.3% rate with clopidogrel); the most frequent site of provoked bleeding was the arterial puncture site (1.3% rate with prasugrel and 1.2% with clopidogrel).
Najpogostejše mesto spontane krvavitve je bil prebavni trakt (1, 7% stopnja pri prasugrelu in 1, 3% stopnja pri klopidogrelu); najpogostejše mesto povzročene krvavitve je bilo mesto arterijskega vboda (1, 3% stopnja pri prasugrelu in 1, 2% stopnja pri klopidogrelu).
Incidence of Non-CABG related bleedinga (% Patients) Event
Incidenca krvavitev, povezane z non- CABGa (% bolnikov) Dogodek
Prasugrelb Clopidogrel b +ASA
prasugrelb klopidogrelb prasugrelb klopidogrelb +ASK +ASK +ASK +ASK
Prasugrelb +ASA
prasugrelb klopidogrelb +ASK +ASK
Clopidogrel b
(N=6741)
(N=1740) +ASA (N=1736)
(N=1740)
TIMI major bleedingc
(N=1736)
2.2 1.7
Večja krvavitev po TIMIc
1.6
1, 7
2.2 2.0
2, 2
1.3 0.3 0.3
1, 6
1.2 0.4 0.2
2, 2
1.0 0.1 0.2
2, 0
Requiring inotropes
1, 3 0, 3 0, 3
0.3 0.1
0, 8 0, 1 0, 3
0.3
1, 3 0, 3 0, 3
0.1
0, 8 0, 1 0, 3
0.3
1, 2 0, 4 0, 2
0.2
1, 0 0, 1 0, 2
Requiring surgical intervention
Zahteva inotrope Zahteva kirurški poseg
0.3
0, 1 0, 3
0.3
0, 3 0, 3
0.1
0, 3 0, 1
0.2
0, 2 0, 2
Patients may be counted in more than one row. e ICH=intracranial haemorrhage. f Clinically overt bleeding associated with a fall in haemoglobin of ≥ 3 g/ dL but < 5 g/ dL.
Bolniki so lahko našteti v več kot eni vrsti. e ICH=intracranial haemorrhage, intrakranialna krvavitev. f Klinično očitna krvavitev, povezana s padcem hemoglobina ≥ 3 g/ dl vendar < 5 g/ dl.
Patients ≥ 75 years old In the phase 3 clinical trial, non-CABG-related TIMI major or minor bleeding rates for patients in two age groups were as follows:
Bolniki, stari ≥ 75 let V kliničnem preskušanju faze 3 so bile stopnje večjih in manjših krvavitev po TIMI, povezane z non - CABG, za bolnike dveh starostnih skupin, naslednje:
≥ 75 years (N=1785) < 75 years (N=11672)
≥ 75 let (N=1785) < 75 let (N=11672)
9.0% (1.0% fatal) 3.8% (0.2% fatal)
9, 0% (1, 0% smrtno) 3, 8% (0, 2% smrtno)
6.9% (0.1% fatal) 2.9% (0.1% fatal)
6, 9% (0, 1% smrtno) 2, 9% (0, 1% smrtno)
In the phase 3 clinical trial, non-CABG-related TIMI major or minor bleeding rates for patients in two weight groups were as follows:
V kliničnem preskušanju faze 3 so bile stopnje večjih in manjših krvavitev po TIMI, povezane z non - CABG, za bolnike v dveh skupinah glede na telesno maso, naslednje:
10.1% (0% fatal) 4.2% (0.3% fatal)
10, 1% (0% smrtno) 4, 2% (0, 3% smrtno)
6.5% (0.3% fatal) 3.3% (0.1% fatal)
6, 5% (0, 3% smrtno) 3, 3% (0, 1% smrtno)
In patients ≥ 60 kg and age < 75 years, non-CABG-related TIMI major or minor bleeding rates were 3.6% for prasugrel and 2.8% for clopidogrel; rates for fatal bleeding were 0.2% for prasugrel and 0.1% for clopidogrel.
Pri bolnikih ≥ 60 kg in starih < 75 let, so bile stopnje večjih in manjših krvavitev po TIMI, povezane z non- CABG, 3, 6% za prasugrel in 2, 8% za klopidogrel; stopnje smrtnih krvavitev so bile 0, 2% za prasugrel in 0, 1% za klopidogrel.
CABG-related bleeding In the phase 3 clinical trial, 437 patients underwent CABG during the course of the study.
Krvavitev, povezana z aortokoronarnim obvodom (CABG) V kliničnem preskušanju faze 3, je 437 bolnikov prestalo CABG v času trajanja študije.
Of those patients, the rate of CABG-related TIMI major or minor bleeding was 14.1% for the prasugrel group and 4.5% in the clopidogrel group.
Izmed teh bolnikov, je bila stopnja večjih in manjših krvavitev po TIMI, povezanih s CABG, 14, 1% za skupino, ki je jemala prasugrel in 4, 5% za skupino, ki je jemala klopidogrel.
For patients who received their thienopyridine within 3 days prior to CABG, the frequencies of TIMI major or minor bleeding were 26.7% (12 of 45 patients) in the prasugrel group, compared with 5.0% (3 of 60 patients) in the clopidogrel group.
Za bolnike, ki prejemajo tienopiridin v 3 dneh pred CABG, sta bili pogostnosti večjih in manjših krvavitev po TIMI, povezanih s CABG, 26, 7% (12 od 45 bolnikov) v skupini, ki je jemala prasugrel, v primerjavi s 5, 0% (3 od 60 bolnikov) v skupini, ki je jemala klopidogrel.
For patients who received their last dose of thienopyridine within 4 to 7 days prior to CABG, the frequencies decreased to 11.3% (9 of 80 patients) in the prasugrel group and 3.3% (3 of 90 patients) in the clopidogrel group.
Za bolnike, ki so prejeli zadnji odmerek tienopiridina v 4 do 7 dneh pred CABG, je pogostnost padla na 11, 3% (9 od 80 bolnikov) v skupini, ki je jemala prasugrel in 3, 3% (3 od 90 bolnikov) v skupini, ki je jemala klopidogrel.
Beyond 7 days after drug discontinuation, the observed rates of CABG-related bleeding were similar between treatment groups (see section 4.4).
Po 7 dneh po prekinitvi jemanja zdravila, so bile opazovane stopnje krvavitve, povezane s CABG, podobne pri obeh skupinah zdravljenja (glejte poglavje 4. 4).
Adverse Reactions Table 2 summarises haemorrhagic and non-haemorrhagic adverse reactions in TRITON classified by frequency and system organ class.
Neželeni učinki Preglednica 2 vključuje hemoragične in ne- hemoragične neželene učinke v študiji TRITON, razvrščene po pogostnosti in organskih sistemih.
Very common (≥ 1/ 10); common (≥ 1/ 100 to < 1/ 10); uncommon (≥ 1/ 1000 to < 1/ 100); rare (≥ 1/ 10,000 to < 1/ 1,000); very rare (< 1/ 10,000); not known (cannot be estimated from the available data).
Pogostnosti so opredeljene kot: zelo pogosti (≥ 1/ 10); pogosti (≥ 1/ 100 do < 1/ 10); občasni (≥ 1/ 1. 000 do < 1/ 100); redki (≥ 1/ 10. 000 do < 1/ 1. 000); zelo redki (< 1/ 10. 000); neznana (ni mogoče oceniti iz razpoložljivih podatkov).
Haemorrhagic and Non-haemorrhagic adverse reactions System Organ Class Blood and Lymphatic System disorders
Hemoragični in ne- hemoragični neželeni učinki Organski sistem Bolezni krvi in limfatičnega sistema
Common Anaemia
Pogosti anemija
Eye disorders Vascular Disorders
Očesne bolezni Žilne bolezni
Retroperitoneal haemorrhage Rectal haemorrhage Haematochezia
retroperitonealna krvavitev rektalna krvavitev
Rash Ecchymosis Haematuria
izpuščaj ekhimoza
Vessel puncture site haematoma Puncture site haemorrhage
hematurija hematom na mestu žilnega vboda krvavitev na mestu vboda
Contusion
udarnina
Post-procedural haemorrhage
post- operativna krvavitev
In patients with or without a history of TIA or stroke, the incidence of stroke in the phase 3 clinical trial was as follows (see section 4.4):
Pri bolnikih, ki so bili z ali brez TIA ali kapi v anamnezi, je bila pogostnost kapi v kliničnem preskušanju faze 3 naslednja (glejte poglavje 4. 4):
History of TIA or stroke
TIA ali kap v anamnezi
* ICH=intracranial haemorrhage.
* ICH=intracranial haemorrhage, intrakranialna krvavitev.
No data are available on the reversal of the pharmacological effect of prasugrel; however, if prompt correction of prolonged bleeding time is required, platelet transfusion and/ or other blood products may be considered.
Podatkov o izničenju farmakološkega učinka prasugrela, ni; vendar, če je potreben takojšnji popravek podaljšanega časa krvavitve, lahko razmislimo o transfuziji trombocitov in/ ali drugih zdravil iz krvi.
ATC code:
Še ni dodeljena, oznaka ATC:
Not yet assigned.
Še ni dodeljena.
Pharmacodynamics Prasugrel is an inhibitor of platelet activation and aggregation through the irreversible binding of its active metabolite to the P2Y12 class of ADP receptors on platelets.
Farmakodinamika Prasugrel je zaviralec aktivacije in agregacije trombocitov preko nepovratne vezave njegovih aktivnih presnovkov na P2Y12 razred ADP receptorjev na trombocitih.
Since platelets participate in the initiation and/ or evolution of thrombotic complications of atherosclerotic disease, inhibition of platelet function can result in the reduction of the rate of cardiovascular events such as death, myocardial infarction, or stroke.
Ker trombociti sodelujejo pri začetku in/ ali razvoju trombotičnih komplikacij aterosklerotične bolezni, lahko zaviranje delovanja trombocitov vodi v zmanjšanje stopnje srčnožilnih dogodkov kot so smrt, miokardni infarkt ali kap.
The maximum inhibition by prasugrel of ADP-induced platelet aggregation is 83% with 5 µM ADP and 79% with 20 µM ADP, in both cases with 89% of healthy subjects and patients with stable atherosclerosis achieving at least 50% inhibition of platelet aggregation by 1 hour.
V obeh primerih pri 89% zdravih oseb in bolnikov s stabilno aterosklerozo doseženo najmanj 50% zaviranje agregacije trombocitov v 1 uri.
Prasugrel-mediated inhibition of platelet aggregation exhibits low between-subject (12%) and within-subject (9%) variability with both 5 µM and 20 µM ADP.
Zaviranje agregacije trombocitov, inducirano s prasugrelom, kaže majhno variabilnost med osebami (12%) in pri osebah (9%) pri obeh, 5 µM ADP in 20 µM ADP.
Mean steady-state inhibition of platelet aggregation was 74% and 69% respectively for 5 µM ADP and 20 µM ADP, and was achieved following 3 to 5 days of administration of the 10 mg prasugrel maintenance dose preceded by a 60 mg loading dose.
Srednje stanje dinamičnega ravnovesja zaviranja agregacije trombocitov je bilo 74% pri 5 µM ADP oziroma 69% pri 20 µM ADP ter je bilo doseženo po 3 do 5 dneh dajanja 10 mg vzdrževalnega odmerka prasugrela, ki je sledil 60 mg polnilnemu odmerku.
More than 98% of subjects had ≥ 20% inhibition of platelet aggregation during maintenance dosing.
Več kot 98% oseb je imelo ≥ 20% zaviranje agregacije trombocitov med vzdrževalnim odmerjanjem.
Following administration of 75 mg clopidogrel once daily for 10 days, 40 healthy subjects were switched to prasugrel 10 mg once daily with or without a loading dose of 60 mg.
8 ali močnejše zaviranje agregacije trombocitov so opazili pri prasugrelu.
Following administration of a 900 mg loading dose of clopidogrel (with ASA), 56 subjects with ACS were treated for 14 days with either prasugrel 10 mg once daily or clopidogrel 150 mg once daily, and then switched to either clopidogrel 150 mg or prasugrel 10 mg for another 14 days.
Po dajanju 900 mg polnilnega odmerka klopidogrela (z ASK), je bilo 56 preiskovancev z ACS 14 dni zdravljenih s prasugrelom 10 mg enkrat na dan ali klopidogrelom 150 mg enkrat na dan, nato pa so za nadaljnjih 14 dni zamenjali na zdravljenje s klopidogrelom 150 mg ali prasugrelom 10 mg.
Higher inhibition of platelet aggregation was observed in patients switched to prasugrel 10 mg compared with those treated with clopidogrel 150 mg.
Močnejše zaviranje agregacije trombocitov so opazili pri bolnikih, ki so jim zdravljenje zamenjali na zdravljenje s prasugrelom 10 mg v primerjavi s tistimi, ki so bili zdravljeni s klopidogrelom 150 mg.
No data are available on switching from a clopidogrel loading dose directly to a prasugrel loading dose.
Podatkov o zamenjavi s polnilnega odmerka klopidogrela neposredno na polnilni odmerek prasugrela ni.
Efficacy and Safety in Acute Coronary Syndrome (ACS) The phase 3 TRITON study compared Efient (prasugrel) with clopidogrel, both co-administered with ASA and other standard therapy.
Učinkovitost in varnost pri akutnem koronarnem sindromu (ACS) Faza 3 študije TRITON je primerjala zdravilo Efient (prasugrel) s klopidogrelom, oba s sočasnim dajanjem z ASK in drugo standardno terapijo.
TRITON was a 13,608 patient, multicentre international, randomised, double blind, parallel group study.
TRITON s 13. 608 bolniki je bila multicentrična, mednarodna, randomizirana, dvojno slepa študija s paralelno skupino.
Patients with UA/ NSTEMI within 72 hours of symptoms or STEMI between 12 hours to 14 days of symptoms were randomised after knowledge of coronary anatomy.
Bolniki z UA/ NSTEMI z 72 urami simptomov ali s STEMI med 12 urami do 14 dni simptomov so bili randomizirani po ugotovljeni srčni anatomiji.
Patients randomised to receive prasugrel (60 mg loading dose followed by 10 mg once daily) or clopidogrel (300 mg loading dose followed by 75 mg once daily) were treated for a median of 14.5 months (maximum of 15 months with a minimum of 6 months follow-up).
Bolniki, ki so bili randomizirani, da prejmejo prasugrel (60 mg polnilni odmerek, ki mu sledi 10 mg vzdrževalni odmerek enkrat na dan) ali klopidogrel (300 mg polnilni odmerek, ki mu sledi 75 mg vzdrževalni odmerek enkrat na dan) so bili zdravljeni z mediano 14, 5 mececev (največ 15 mesecev z najmanj 6 mesečnim obdobjem sledenja).
Other therapies, such as heparin and GPIIb/ IIIa inhibitors, were administered at the discretion of the physician.
Druge terapije, kot je heparin in zaviralci GPIIb/ IIIa, so bile uporabljene po odločitvi zdravnika.
Approximately 40% of patients (in each of the treatment groups) received GPIIb/ IIIa inhibitors in support of PCI (no information available regarding the type of GP IIb/ IIIa inhibitor used).
Približno 40% bolnikov (v vsaki skupini zdravljenja) je prejelo zaviralce GPIIb/ IIIa, kot podporo PCI (podatkov o uporabljenem tipu zaviralca GPIIb/ IIIa ni na voljo).
Approximately 98% of patients (in each of the treatment groups) received antithrombins (heparin, low molecular weight heparin, bivalirudin, or other agent) directly in support of PCI.
Približno 98% bolnikov (v vsaki skupini zdravljenja) je prejelo antitrombine (heparin, nizko molekularni heparin, bivalirudin ali druga zdravila) neposredno, kot podporo PCI.
The trial’ s primary outcome measure was the time to first occurrence of cardiovascular (CV) death, non-fatal myocardial infarction (MI), or non-fatal stroke.
Primarno merilo izida preskušanja je bil čas do pojava srčnožilne (CV) smrti, ne- smrtnega miokardnega infarkta (MI) ali ne- smrtne kapi.
Analysis of the composite endpoint in the All ACS population (combined UA/ NSTEMI and STEMI cohorts) was contingent on showing statistical superiority of prasugrel versus clopidogrel in the UA/ NSTEMI cohort (p < 0.05).
Analiza sestavljenega cilja študije v celotni ACS populaciji (kombinacija UA/ NSTEMI in STEMI skupin) je kazala možno statistično superiornost prasugrela proti klopidogrelu v skupini UA/ NSTEMI (p < 0, 05).
Efient showed superior efficacy compared to clopidogrel in reducing the primary composite outcome events as well as the pre-specified secondary outcome events, including stent thrombosis (see Table 3).
Zdravilo Efient je pokazalo superiorno učinkovitost v primerjavi s klopidogrelom pri znižanju primarnih sestavljenih izidov kot tudi pred- določenih sekundarnih izidov, vključno s trombozo žilne opornice (glejte Preglednico 3).
The superior efficacy was accompanied by an increase in major bleeding (see sections 4.4 and 4.8).
Superiorno učinkovitost je spremljalo povečano pojavljanje večje krvavitve (glejte poglavji 4. 4 in 4. 8).
The patient population was 92% Caucasian, 26% female, and 39% ≥ 65 years of age.
Populacija bolnikov je bila 92% belcev, 26% žensk in 39% ≥ 65 let starosti.
The benefits associated with prasugrel were independent of the use of other acute and long-term cardiovascular therapies, including heparin/ low molecular weight heparin, bivalirudin, intravenous GPIIb/ IIIa inhibitors, lipid-lowering medicinal products, beta-blockers, and angiotensin converting enzyme inhibitors.
Koristi, povezane s prasugrelom, so bile neodvisne od uporabe drugih akutnih in dolgotrajnih srčnožilnih terapij, vključno s heparinom/ nizko molekularnim heparinom, bivalirudinom, intravenskimi zaviralci GPIIb/ IIIa, zdravili za znižanje lipidov, beta- blokatorji in zaviralci encima angiotenzin konvertaze.
The use of oral anticoagulants, non-study antiplatelet medicinal products and chronic NSAIDs was not allowed in TRITON.
Uporaba peroralnih antikoagulantov, ne- preiskovanih zdravil proti trombocitom in kronično zdravljenje z NSAIDs v študiji TRITON niso bili dovoljeni.
In the All ACS population, prasugrel was associated with a lower incidence of CV death, non-fatal MI, or non-fatal stroke compared to clopidogrel, regardless of baseline characteristics such as age, sex, body weight, geographical region, use of GPIIb/ IIIa inhibitors, and stent type.
V celotni ACS populaciji, je bil prasugrel povezan z nižjo incidenco CV smrti, ne- smrtnega MI ali ne- smrtne kapi, v primerjavi s klopidogrelom, neodvisno od osnovnih značilnosti, kot so starost, spol, telesna masa, geografsko področje, uporaba zaviralcev GPIIb/ IIIa in tip žilne opornice.
The benefit was primarily due to a significant decrease in non-fatal MI (see table 3).
Korist je bila primarno posledica signifikantnega znižanja ne- smrtnega MI (glejte Preglednico 3).
9 The observed benefit of prasugrel in patients ≥ 75 years was less than that observed in patients < 75 years.
Opazovane koristi prasugrela pri bolnikih ≥ 75 let so bile manjše, kot pri bolnikih < 75 let.