natgillin/translations-raw huggingface dataset:
• Overfølsomhed over for det aktive stof eller over for et eller flere af hjælpestofferne. • Stærkt nedsat leverfunktion. • Aktiv patologisk blødning såsom peptisk ulcus eller intrakraniel blødning.
• Hypersensitivity to the active substance or to any of the excipients. • Severe liver impairment. • Active pathological bleeding such as peptic ulcer or intracranial haemorrhage.
4. 8).
Due to the risk of bleeding and haematological undesirable effects, blood cell count determination and/ or other appropriate testing should be promptly considered whenever clinical symptoms suggestive of bleeding arise during the course of treatment (see section 4.8).
Ligesom andre antitrombotiske midler skal clopidogrel anvendes med forsigtighed til patienter med risiko for tiltagende blødninger pga. traumer, kirurgi eller andre patologiske tilstande samt til patienter, der samtidigt behandles med ASA, heparin, glykoprotein IIb/ IIIa - hæmmere eller nonsteroide antiinflammatoriske lægemidler inklusive cox- 2 hæmmere.
As with other antiplatelet agents, clopidogrel should be used with caution in patients who may be at risk of increased bleeding from trauma, surgery or other pathological conditions and in patients receiving treatment with ASA, heparin, glycoprotein IIb/ IIIa inhibitors or non-steroidal anti-inflammatory drugs including Cox-2 inhibitors.
Patienterne skal kontrolleres omhyggeligt for tegn på blødninger, herunder okkulte blødninger, især i behandlingens første uger og/ eller efter invasive hjerteindgreb eller - kirurgi.
Patients should be followed carefully for any signs of bleeding including occult bleeding, especially during the first weeks of treatment and/ or after invasive cardiac procedures or surgery.
4. 5).
The concomitant administration of clopidogrel with oral anticoagulants is not recommended since it may increase the intensity of bleedings (see section 4.5).
4. 2).
Therefore clopidogrel should be used with caution in these patients (see section 4.2).
Der er begrænset erfaring med clopidogrel til patienter med moderat leversygdom, som kan have blødningstendens.
3 Experience is limited in patients with moderate hepatic disease who may have bleeding diatheses.
4. 2).
Clopidogrel should therefore be used with caution in this population (see section 4.2).
Patienter med sjældne arvelige problemer med galactoseintolerans, Lapp lactase deficiency eller glucose - og/ eller galactosemalabsorption, bør ikke anvende dette lægemiddel.
Patients with rare hereditary problems of galactose intolerance, the Lapp lactase deficiency or glucose-galactose malabsorption should not take this medicinal product.
Dette produkt indeholder hydrogeneret ricinusolie, der kan give maveproblemer og diarré.
This product contains hydrogenated castor oil which may cause stomach upset and diarrhoea.
4. 4).
Oral anticoagulants: the concomitant administration of clopidogrel with oral anticoagulants is not recommended since it may increase the intensity of bleedings (see section 4.4).
4. 4).
Glycoprotein IIb/ IIIa inhibitors: clopidogrel should be used with caution in patients who may be at risk of increased bleeding from trauma, surgery or other pathological conditions that receive concomitant glycoprotein IIb/ IIIa inhibitors (see section 4.4).
ASA ændrede ikke på, at clopidogrel hæmmer den trombocytaggregation som ADP inducerer, men clopidogrel forstærkede virkningen af ASA den trombocytaggregation som kollagen inducerer.
ASA did not modify the clopidogrel-mediated inhibition of ADP-induced platelet aggregation, but clopidogrel potentiated the effect of ASA on collagen-induced platelet aggregation.
5. 1).
However, clopidogrel and ASA have been administered together for up to one year (see section 5.1).
I et klinisk forsøg med raske forsøgspersoner gav clopidogrel ikke anledning til ændring af heparindosis og det forandrede ikke heparins virkning på koagulationen.
Heparin: in a clinical study conducted in healthy subjects, clopidogrel did not necessitate modification of the heparin dose or alter the effect of heparin on coagulation.
4. 4).
Therefore, concomitant use should be undertaken with caution (see section 4.4).
Sikkerheden ved samtidig administration af clopidogrel, fibrin eller non- fibrinspecifikke trombolytiske midler og hepariner blev bedømt hos patienter med akut myokardieinfarkt.
Thrombolytics: the safety of the concomitant administration of clopidogrel, fibrin or non-fibrin specific thrombolytic agents and heparins was assessed in patients with acute myocardial infarction.
I et klinisk forsøg foretaget på raske forsøgspersoner øgede den samtidige administration af clopidogrel og naproxen okkult gastrointestinalt blodtab.
Non-Steroidal Anti-Inflammatory Drugs (NSAIDs): in a clinical study conducted in healthy volunteers, the concomitant administration of clopidogrel and naproxen increased occult gastrointestinal blood loss.
Imidlertid er det på grund af manglen på interaktionsforsøg med andre NSAID’ er ikke umiddelbart klart, om der er øget risiko for gastrointestinal blødning med alle NSAID- præparater.
However, due to the lack of interaction studies with other NSAIDs it is presently unclear whether there is an increased risk of gastrointestinal bleeding with all NSAIDs.
4. 4).
Consequently, NSAIDs including Cox-2 inhibitors and clopidogrel should be co-administered with caution (see section 4.4).
Der er gennemført en række andre kliniske forsøg med clopidogrel og anden samtidig medicinering for at undersøge muligheden for farmakodynamisk og farmakokinetisk interaktion.
Other concomitant therapy: a number of other clinical studies have been conducted with clopidogrel and other concomitant medicinal products to investigate the potential for pharmacodynamic and pharmacokinetic interactions.
Herudover blev clopidogrels farmakodynamiske aktivitet ikke påvirket signifikant af samtidig administration af phenobarbital, cimetidin eller østrogen.
Furthermore, the pharmacodynamic activity of clopidogrel was not significantly influenced by the co- administration of phenobarbital, cimetidine, or oestrogen.
Dette kunne muligvis føre til forhøjede plasmaniveauer af lægemidler som phenytoin og tolbutamid samt de NSAID’ er, som metaboliseres af cytochrom P450 2C9.
This could potentially lead to increased plasma levels of medicinal products such as phenytoin and tolbutamide and the NSAIDs, which are
Data fra CAPRIE- undersøgelsen indikerer, at phenytoin og tolbotamid uden risiko kan administreres samtidig med clopidogrel.
Data from the CAPRIE study indicate that phenytoin and tolbutamide can be safely co-administered with clopidogrel.
Imidlertid fik de patienter, som indgik i kliniske forsøg med clopidogrel, en lang række ledsagende lægemidler såsom diuretika, beta- blokkere, ACE- hæmmere, calciumantagonister, kolesterolsænkende midler, dilatatorer med effekt på koronarkarrene, antidiabetika (inklusive insulin), antiepileptika samt GPIIb/ IIIa - hæmmere, uden at der blev påvist klinisk signifikante uønskede interaktioner.
However, patients entered into clinical trials with clopidogrel received a variety of concomitant medicinal products including diuretics, beta blockers, ACEI, calcium antagonists, cholesterol lowering agents, coronary vasodilators, antidiabetic agents (including insulin), antiepileptic agents, and GPIIb/ IIIa antagonists without evidence of clinically significant adverse interactions.
Clopidogrel er blevet evalueret sikkerhedsmæssigt hos mere end 42. 000 patienter, der har deltaget i kliniske studier, inklusive over 9. 000 patienter, der blev behandlet i mindst 1 år.
Clopidogrel has been evaluated for safety in more than 42,000 patients who have participated in clinical studies, including over 9,000 patients treated for 1 year or more.
De klinisk relevante bivirkninger observeret i CAPRIE -, CURE -, CLARITY - og COMMIT- undersøgelserne beskrives nedenfor.
The clinically relevant adverse reactions observed in the CAPRIE, CURE, CLARITY and COMMIT studies are discussed below.
Samlet set var clopidogrel 75 mg/ dag sammenligneligt med ASA 325 mg/ dag i CAPRIE, uden hensyntagen til alder, køn eller race.
Overall, clopidogrel 75 mg/ day was comparable to ASA 325 mg/ day in CAPRIE regardless of age, gender and race.
Blødning er den mest almindeligt indrapporterede bivirkning fra både kliniske studier, såvel som fra post - marketing erfaring, hvor den mestendels blev indrapporteret i løbet af behandlingens første måned.
Bleeding is the most common reaction reported both in clinical studies as well as in post-marketing experience where it was mostly reported during the first month of treatment.
I CAPRIE var den generelle forekomst af blødninger 9, 3% hos patienter behandlet med enten clopidogrel eller ASA.
In CAPRIE, in patients treated with either clopidogrel or ASA, the overall incidence of any bleeding was 9.3%.
Forekomsten af svære tilfælde var 1, 4% for clopidogrel og 1, 6% for ASA.
The incidence of severe cases was 1.4% for clopidogrel and 1.6% for ASA.
I CURE var forekomsten af større blødninger med clopidogrel+ASA dosisafhængig for ASA (< 100 mg 2, 6%; 100- 200 mg:
2.6%; 100-200mg:
3, 5%; > 200mg:
3.5%; > 200mg:
4, 9%), ligeledes var forekomsten af større blødninger for placebo+ASA (< 100 mg:
4.9%) as was the major bleeding event rate for placebo+ASA (< 100mg:
Risikoen for blødninger (livstruende, større, mindre, andre) faldt under forsøgsforløbet:
The risk of bleeding (life-threatening, major, minor, other) decreased during the course of the trial:
0- 1 måned (clopidogrel:
0-1 months (clopidogrel:
9, 6%; placebo:
9.6%; placebo:
6, 6%), 1- 3 måneder (clopidogrel:
6.6%), 1-3 months (clopidogrel:
4, 5%; placebo 2, 3%), 3- 6 måneder (clopidogrel 3, 8%; placebo:
3.8%; placebo:
1, 6%), 6- 9 måneder (clopidogrel:
1.6%), 6-9 months (clopidogrel:
3, 2%; placebo 1, 5%), 9- 12 måneder (clopidogrel 1, 9%; placebo 1, 0%).
1.9%; placebo:
Der forekom ikke overrepræsentation af større blødninger med clopidogrel + ASA inden for 7 dage efter koronar bypass hos patienter, der indstillede behandlingen mere end 5 dage før indgrebet (4, 4% clopidogrel+ASA versus 5, 3% placebo+ASA).
5.3% placebo+ASA).
Hos patienter, som fortsatte med behandlingen indtil 5 dage før bypassoperationen, var forekomsten 9, 6% for clopidogrel+ASA og 6, 3% for placebo+ASA.
In patients who remained on therapy within five days of bypass graft surgery, the event rate was 9.6% for clopidogrel+ASA, and 6.3% for placebo+ASA.
I CLARITY var der en generel stigning i antallet af blødninger i clopidrogrel+ASA- gruppen (17, 4%) versus placebo+ASA- gruppen (12, 9%).
This was
Forekomsten af større blødninger var ensartet i de to grupper (1. 3% versus 1. 1% for hhv. clopidogrel+ASA - og placebo+ASA- gruppen.) Dette var ensartet blandt undergrupperne af patienter, defineret ved baseline karakterisktika og typen af fibrinolytika eller heparinbehandling.
5 consistent across subgroups of patients defined by baseline characteristics, and type of fibrinolytic or heparin therapy.
I COMMIT var den generelle forekomst af non- cerebrale større blødninger eller cerebrale blødninger lav og ensartet i begge grupper (0, 6% versus 0, 5% i hhv. clopidogrel+ASA og placebo+ASA- gruppen).
In COMMIT, the overall rate of noncerebral major bleeding or cerebral bleeding was low and similar in both groups (0.6% versus 0.5% in the clopidogrel + ASA and the placebo + ASA groups, respectively).
Hyppighed defineres i henhold til følgende konvention: almindelig (> 1/ 100 til < 1/ 10), ikke almindelig (> 1/ 1000 til < 1/ 100), sjælden (> 1/ 10000 til < 1/ 10000), meget sjælden < 1/ 10000).
Their frequency is defined using the following conventions: common (≥ 1/ 100 to < 1/ 10); uncommon (≥ 1/ 1,000 to < 1/ 100); rare (≥ 1/ 10,000 to < 1/ 1,000); very rare (< 1/ 10,000).
Trombotisk trombocytopenisk purpura (TTP) (se afsnit 4. 4), aplastisk anæmi, pancytopeni, agranulocytose, alvorlig trombocytopeni, granulocytopeni, anæmi
Thrombotic thrombocytopenic purpura (TTP) (see section 4.4), aplastic anaemia, pancytopenia, agranulocytosis, severe thrombocytopenia, granulocytopenia, anaemia
Intrakraniel blødning (nogle med fatal udgang), hovedpine, paræstesi, svimmelhed
Intracranial bleeding (some cases were
Øjne
reported with fatal outcome), headache, paraesthesia, dizziness Eye disorders
Blødning i luftvejene (hæmoptyse, pulmonær
Respiratory tract bleeding (haemoptysis, pulmonary haemorrhage), bronchospasm, interstitial pneumonitis
blødning), bronkospasmer, interstitiel pneumoni Mave- tarmkanalen
Gastrointestinal Gastrointestinal
Gastrointestinal blødning, diarré, mavesmerter, dyspepsi
Retroperitoneal Gastrointestinal and
Mavesår og duodenalt ulcus gastritis, opkastning, kvalme, forstoppelse, flatulens
haemorrhage, diarrhoea, abdominal pain, dyspepsia
Retroperitoneal blødning
duodenal ulcer, haemorrhage gastritis, vomiting, nausea, constipation, flatulence
Gastrointestinal og retroperitoneal blødning med fatalt udfald, bugspytkirtelbetændelse, colitis (inklusive ulcerosa eller lymfocytisk colitis), stomatitis
retroperitoneal haemorrhage with fatal outcome, pancreatitis, colitis (including ulcerative or lymphocytic colitis), stomatitis
Trombocytfunktionshæmmende midler eksklusive heparin, ATC- kode:
Pharmacotherapeutic group: platelet aggregation inhibitors excl. heparin, ATC Code:
Clopidogrel hæmmer selektivt, at adenosindiphosphat (ADP) bindes til dets trombocytreceptor og som følge deraf, at ADP aktiverer GBIIb- IIIa- komplekset og derved hæmmer clopidogrel trombocytaggregation.
Clopidogrel selectively inhibits the binding of adenosine diphosphate (ADP) to its platelet receptor, and the subsequent ADP-mediated activation of the GPIIb/ IIIa complex, thereby inhibiting platelet aggregation.
Biotransformation af clopidogrel er nødvendig for at hæmme trombocytaggregationen.
Biotransformation of clopidogrel is necessary to produce inhibition of platelet aggregation.
Clopidogrel hæmmer også den trombocytaggregation, som andre agonister inducerer ved at blokere for, at frigjort ADP forstærker trombocytaktiveringen.
Clopidogrel also inhibits platelet aggregation induced by other agonists by blocking the
Clopidogrel virker ved irreversibel modifikation af trombocytternes ADP- receptor.
Clopidogrel acts by irreversibly modifying the platelet ADP receptor.
Derfor påvirkes trombocytter, der har været udsat for clopidogrel, i resten af deres levetid, og normal trombocytfunktion generhvervelse med den hastighed, hvormed trombocytterne omsættes.
Consequently, platelets exposed to clopidogrel are affected for the remainder of their lifespan and recovery of normal platelet function occurs at a rate consistent with platelet turnover.
Ved steady state var den hæmningsgrad, der blev iagttaget med en dosis på 75 mg/ dag, mellem 40% og 60%.
At steady state, the average inhibition level observed with a dose of 75 mg per day was between 40% and 60%.
Sikkerheden og effekten af clopidrogrel er blevet evalueret i 4 dobbeltblindede forsøg, der omfattede mere end 80. 000 patienter i CAPRIE- undersøgelsen, hvor clopidogrel sammenlignes med ASA, og CURE, CLARITY og COMMIT- undersøgelserne, hvor clopidogrel sammenlignes med placebo, og hvor begge lægemidler gives i kombination med ASA eller anden standardterapi.
The safety and efficacy of clopidogrel have been evaluated in 4 double-blind studies involving over 80,000 patients: the CAPRIE study, a comparison of clopidogrel to ASA, and the CURE, CLARITY and COMMIT studies comparing clopidogrel to placebo, both medicinal products given in combination with ASA and other standard therapy.
CAPRIE- undersøgelsen omfattede 19. 185 patienter med aterotrombose manifesteret ved nyligt myokardieinfarkt (< 35 dage), nyligt iskæmisk slagtilfælde (mellem 7 dage og 6 måneder) eller påviste perifere kredsløbsforstyrrelser (PAD).
The CAPRIE study included 19,185 patients with atherothrombosis as manifested by recent myocardial infarction (< 35 days), recent ischaemic stroke (between 7 days and 6 months) or established peripheral arterial disease (PAD).
Patienterne blev randomiseret til clopidogrel 75 mg/ dag eller ASA 325 mg/ dag og blev kontrolleret i 1- 3 år.
Patients were randomised to clopidogrel 75 mg/ day or ASA 325 mg/ day, and were followed for 1 to 3 years.
I intention- to- treat- analysen blev der observeret 939 tilfælde i clopidogrelgruppen og 1. 020 tilfælde i ASA - gruppen (relativ risikoreduktion (RRR) 8, 7% [95% CI:
In the intention to treat analysis, 939 events were observed in the clopidogrel group and 1,020 events with ASA (relative risk reduction (RRR) 8.7%, [95% CI:
0, 2- 16, 4], p=0, 045), hvilket for hver 1000 patienter, der blev behandlet i 2 år, svarer til, at yderligere 10 [CI:
0.2 to 16.4]; p = 0.045), which corresponds, for every 1,000 patients treated for 2 years, to 10 [CI:
0- 20] patienter beskyttes mod et nyt iskæmisk tilfælde.
0 to 20] additional patients being prevented from experiencing a new ischaemic event.
En analyse med total mortalitet som sekundært endpoint viste ingen signifikant forskel mellem clopidogrel (5, 8%) og ASA (6, 0%).
Analysis of total mortality as a secondary endpoint did not show any significant difference between clopidogrel (5.8%) and ASA (6.0%).
I en delgruppeanalyse af inklusionsgrupperne (myokardieinfarkt, iskæmisk slagtilfælde og PAD) syntes udbyttet at være størst (dvs. den opnåede statisk signifikans ved p=0, 003) hos patienter, som indgik på grund af PAD (især de patienter, som tidligere også havde haft et myokardieinfarkt) (RRR = 23, 7%, CI:
In a subgroup analysis by qualifying condition (myocardial infarction, ischaemic stroke, and PAD) the benefit appeared to be strongest (achieving statistical significance at p = 0.003) in patients enrolled due to PAD (especially those who also had a history of myocardial infarction) (RRR = 23.7%; CI:
8, 9 til 36, 2) og mindst (= afveg ikke signifikant fra ASA) hos patienter med slagtilfælde (RRR = 7, 3%, CI: - 5, 7 til 18, 7 [p=0, 258]).
8.9 to 36.2) and weaker (not significantly different from ASA) in stroke patients (RRR = 7.3%; CI: -5.7 to 18.7 [p=0.258]).
Hos de patienter, som alene indgik i undersøgelsen på grund af et nyligt myokardieinfarkt, lå clopidogrel numerisk lavere, men ikke statistisk forskelligt fra ASA (RRR = 4, 0%, CI: - 22, 5 til 11, 7 [p=0, 639]).
In patients who were enrolled in the trial on the sole basis of a recent myocardial infarction, clopidogrel was numerically inferior, but not statistically different from ASA (RRR = -4.0%; CI: -22.5 to 11.7 [p=0.639]).
Endvidere tydede en analyse af aldersbaserede delgrupper på, at fordelen ved clopidogrel hos patienter over 75 år var mindre end hos patienter ≤75 år.
In addition, a subgroup analysis by age suggested that the benefit of clopidogrel in patients over 75 years was less than that observed in patients ≤ 75 years.
Da CAPRIE- undersøgelsen imidlertid ikke havde statistisk styrke til at evaluere virkningen i de enkelte delgrupper, kan det ikke udledes, hvorvidt forskellene i relativ risikoreduktion på tværs af inklusionskriterierne er reelle eller tilfældige.
Since the CAPRIE trial was not powered to evaluate efficacy of individual subgroups, it is not clear whether the differences in relative risk reduction across qualifying conditions are real, or a result of chance.
CURE- undersøgelsen omfattede 12. 562 patienter med akut koronarsyndrom uden forhøjelse af ST- segmentet (ustabil angina pectoris eller myokardieinfarkt uden forekomst af Q- takker), som indfandt sig inden for 24 timer efter starten på den seneste periode med brystsmerter eller symptomer der svarede til iskæmi.
The CURE study included 12,562 patients with non-ST segment elevation acute coronary syndrome (unstable angina or non-Q-wave myocardial infarction), and presenting within 24 hours of onset of the most recent episode of chest pain or symptoms consistent with ischaemia.
Patienterne skulle have enten EKG- forandringer, som var kompatible med ny iskæmi, eller forhøjede værdier af hjerteenzymer eller troponin I eller T på mindst 2 x øvre grænse for normalområdet.
Patients were required to have either ECG changes compatible with new ischaemia or elevated cardiac enzymes or troponin I or T to at least twice the upper limit of normal.
Patienterne blev randomiseret til clopidogrel (300 mg initial stabiliseringsdosis efterfulgt af 75 mg/ dag, N=6. 259) eller placebo (N=6. 303), begge i kombination med ASA (75- 325 mg en gang daglig) samt anden standard - behandling.
Patients were randomised to clopidogrel (300 mg loading dose followed by 75 mg/ day, N=6,259) or placebo (N=6,303), both given in combination with ASA (75-325 mg once daily) and other standard therapies.
I CURE blev 823 (6, 6%) patienter samtidig behandlet med GPIIb/ IIIa- hæmmere.
In CURE, 823 (6.6%) patients received concomitant GPIIb/ IIIa receptor antagonist therapy.
Heparin blev givet til over 90% af patienterne, og den relative blødningsforekomst i clopidogrel - og placebogruppen blev ikke signifikant påvirket af den ledsagende heparinbehandling.
Heparins were administered in more than 90% of the patients and the relative rate of bleeding between clopidogrel and placebo was not significantly affected by the concomitant heparin therapy.
10% - 28%; p=0, 00009) for clopidogrelgruppen (en relativ risikoreduktion på 17%, når patienterne fik konservativ behandling, 29%, når de fik perkutan transluminal koronar angioplasti (PTCA) med eller uden stent, og 10%, når de fik koronar bypassoperation (CABG)).
8 The number of patients experiencing the primary endpoint [cardiovascular (CV) death, myocardial infarction (MI), or stroke] was 582 (9.3%) in the clopidogrel-treated group and 719 (11.4%) in the placebo-treated group, a 20% relative risk reduction (95% CI of 10%-28%; p=0.00009) for the clopidogrel-treated group (17% relative risk reduction when patients were treated conservatively, 29% when they underwent percutaneous transluminal coronary angioplasty (PTCA) with or without stent and 10% when they underwent coronary artery bypass graft (CABG)).
Nye kardiovaskulære hændelser (primært endpoint) blev forebygget med relative risikoreduktioner på 22% (CI:
New cardiovascular events (primary endpoint) were prevented, with relative risk reductions of 22% (CI:
8, 6, 33, 4) 32% (CI:
8.6, 33.4), 32% (CI:
12, 8, 46, 4), 4% (CI: - 26, 9, 26, 7), 6% (CI: - 33, 5, 34, 3) og 14% (CI: - 31, 6, 44, 2), i løbet af forsøgets intervaller på henholdsvis 0- 1, 1- 3, 3- 6, 6- 9 og 9- 12 måneder.
12.8, 46.4), 4% (CI: -26.9, 26.7), 6% (CI: -33.5, 34.3) and 14% (CI: -31.6, 44.2), during the 0-1, 1-3, 3-6, 6-9 and 9-12 month study intervals, respectively.
I CURE var anvendelse af clopidogrel forbundet med et aftagende behov for behandling med trombolytika (RRR = 43, 3%, CI:
The use of clopidogrel in CURE was associated with a decrease in the need of thrombolytic therapy (RRR = 43.3%; CI:
24, 3%, 57, 5%) og GPIIb/ IIIa- hæmmere (RRR = 18, 2%, CI:
24.3%, 57.5%) and GPIIb/ IIIa inhibitors (RRR = 18.2%; CI:
6% - 21%; p=0, 00005) for clopidogrelgruppen.
The number of patients experiencing the co-primary endpoint (CV death, MI, stroke or refractory ischaemia) was 1,035 (16.5%) in the clopidogrel-treated group and 1,187 (18.8%) in the placebo- treated group, a 14% relative risk reduction (95% CI of 6%-21%, p=0.0005) for the clopidogrel- treated group.
Fordelen må hovedsageligt tilskrives den statistisk signifikante reduktion i forekomsten af myokardieinfarkt [287 (4, 6%) i clopidogrelgruppen og 363 (5, 8%) i placebogruppen].
This benefit was mostly driven by the statistically significant reduction in the incidence of MI [287 (4.6%) in the clopidogrel treated group and 363 (5.8%) in the placebo treated group].
De resultater, som blev opnået i populationer med forskellige karakteristika (fx ustabil angina pectoris eller myokardieinfarkt uden forekomst af Q- takker, høj - eller lavrisikogruppe, diabetes, behov for revaskularisering, alder, køn, osv.) svarede til den primære analyses resultater.
The results obtained in populations with different characteristics (e. g. unstable angina or non-Q-wave MI, low to high risk levels, diabetes, need for revascularisation, age, gender, etc.) were consistent with the results of the primary analysis.