natgillin/translations-raw huggingface dataset:
20 Middel procentændring i total atheromavolumen (primært studiekriterie) fra baseline er – 0, 4% (p=0, 98) i atorvastatingruppen, og +2, 7% (p=0, 001) i pravastatingruppen (n=249).
The median percent change, from baseline, in total atheroma volume (the primary study criteria) was - 0.4% (p=0.98) in the atorvastatin group and +2.7% (p=0.001) in the pravastatin group (n=249).
Effekten af atorvastatin er statistisk signifikant (p=0, 02) ved sammenligning med pravastatin.
When compared to pravastatin the effects of atorvastatin were statistically significant (p=0.02).
Effekten af intensiv lipidsænkning på kardiovaskulære endepunkter (dvs. behov for revaskularisering, ikke- fatalt myokardieinfarkt, koronardød) blev ikke undersøgt i dette studie.
The effect of intensive lipid lowering on cardiovascular endpoints (e. g. need for revascularisation, non fatal myocardial infarction, coronary death) was not investigated in this study.
I atorvastatingruppen reduceres LDL- kolesterol til et gennemsnit på 2, 04 mmol/ l ±0, 8 (78, 9 mg/ dl ±30) fra baseline 3, 98 mmol/ l ±0, 7 (150 mg/ dl ±28) og i pravastatingruppen til et gennemsnit på 2, 85 mmol/ l ± 0, 7 (110 mg/ dl ±26) fra baseline 3, 89 mmol/ l ± 0, 7 (150 mg/ dl ±26) (p < 0, 0001).
In the atorvastatin group, LDL-C was reduced to a mean of 2.04 mmol/ L ± 0.8 (78.9 mg/ dl ± 30) from baseline 3.89 mmol/ l ± 0.7 (150 mg/ dl ± 28) and in the pravastatin group, LDL-C was reduced to a mean of 2.85 mmol/ l ± 0.7 (110 mg/ dl ± 26) from baseline 3.89 mmol/ l ± 0.7 (150 mg/ dl ± 26) (p < 0.0001).
Atorvastatin reducerer også signifikant gennemsnit total- kolesterol (TC) med 34, 1% (pravastatin: - 18, 4%, p < 0, 0001), gennemsnit triglycerid (TG) niveauer med 20% (pravastatin: - 6, 8%, p < 0, 0009), og gennemsnit apolipoprotein B med 39, 1% pravastatin: - 22, 0%, p < 0, 0001).
Atorvastatin also significantly reduced mean TC by 34.1% (pravastatin: -18.4%, p < 0.0001), mean TG levels by 20% (pravastatin: -6.8%, p < 0.0009), and mean apolipoprotein B by 39.1% (pravastatin: -22.0%, p < 0.0001).
Atorvastatin øger gennemsnit HDL- kolesterol med 2, 9% (pravastatin: +5, 6%, p=NS).
Atorvastatin increased mean HDL-C by 2.9% (pravastatin: +5.6%, p=NS).
Der er 36, 4% gennemsnits reduktion i CRP i atorvastatingruppen sammenlignet med 5, 2% reduktion i pravastatingruppen (p < 0, 0001).
There was a 36.4% mean reduction in CRP in the atorvastatin group compared to a 5.2% reduction in the pravastatin group (p < 0.0001).
Studieresultaterne blev opnået for styrken 80 mg, hvorfor disse ikke kan ekstrapoleres til de lavere doser.
Therefore, they cannot be extrapolated to the lower dose strengths.
Sikkerheds - og tolerabilitetsprofilen er sammenlignelig i de 2 grupper.
The safety and tolerability profiles of the two treatment groups were comparable.
Akut koronarsyndrom
21 Acute coronary syndrome
I MIRACL- studiet blev atorvastatin 80 mg vurderet i 3086 patienter (atorvastatin n=1538; placebo n=1548) med akut koronarsyndrom (non- Q- tak MI eller ustabil angina).
In the MIRACL study, atorvastatin 80 mg has been evaluated in 3,086 patients (atorvastatin n=1,538; placebo n=1,548) with an acute coronary syndrome (non Q-wave MI or unstable angina).
Behandling med atorvastatin 80 mg dagligt forlængede tiden til forekomst af kombineret primært endepunkt, defineret som død af enhver årsag, ikke- fatal MI, genoplivet efter hjertestop, eller angina pectoris med tegn på myokardieiskæmi, der kræver hospitalsindlæggelse, med en risikoreduktion på 16% (p=0, 048).
Treatment with atorvastatin 80 mg/ day increased the time to occurrence of the combined primary endpoint, defined as death from any cause, nonfatal MI, resuscitated cardiac arrest, or angina pectoris with evidence of myocardial ischaemia requiring hospitalization, indicating a risk reduction by 16% (p=0.048).
Dette skyldes primært en risikoreduktion på 26% i genindlæggelse for angina pectoris med tegn på myokardieiskæmi (p=0, 018).
This was mainly due to a 26% reduction in re-hospitalisation for angina pectoris with evidence of myocardial ischaemia (p=0.018).
De øvrige sekundære endepunkter var ikke selvstændigt signifikante (samlet: placebo:
Placebo:
22, 2%, atorvastatin:
22.2%, Atorvastatin:
4. 8.
The safety profile of atorvastatin in the MIRACL study was consistent with what is described in Section 4.8.
I et randomiseret, dobbelt- blindt, placebokontrolleret studie, Anglo- Scandinavian Cardiac Outcomes Trial Lipid Lowering Arm (ASCOT- LLA) blev effekten af atorvastatin på fatal og ikke- fatal iskæmisk hjertesygdom undersøgt hos patienter med hypertension i alderen 40- 79 år, uden tidligere myokardieinfarkt eller i behandling for angina, og som havde total- kolesterol på ≤6, 5 mmol/ l (251 mg/ dl).
The effect of atorvastatin on fatal and non-fatal coronary heart disease was assessed in a randomized, double-blind, placebo-controlled study, the Anglo-Scandinavian Cardiac Outcomes Trial Lipid Lowering Arm (ASCOT-LLA).
Alle patienter havde mindst 3 af de foruddefinerede kardiovaskulære risikofaktorer: mand, alder ≥55 år, ryger, diabetes, iskæmisk hjertesygdom hos 1. grads slægtning, total- kolesterol:
Patients were hypertensive, 40-79 years of age, with no previous myocardial infarction or treatment for angina, and with TC levels ≤ 6.5 mmol/ l (251 mg/ dl).
HDL > 6, perifer vaskulær sygdom, venstresidig hjertehypertrofi, tidligere cerebrovaskulær sygdom, specifikke EKG- forandringer, proteinuri/ albuminuri.
All patients had at least 3 of the pre-defined cardiovascular risk factors: male gender, age ≥ 55 years, smoking, diabetes, history of CHD in a first-degree relative, TC: HDL-C > 6, peripheral vascular disease, left ventricular hypertrophy, prior cerebrovascular event, specific ECG abnormality, proteinuria/ albuminuria.
Ikke alle inkluderede patienter var vurderet til at have en høj risiko for debut af kardiovaskulær hændelse.
Not all included patients were estimated to have a high risk for a first cardiovascular event.
Patienterne fik antihypertensiv behandling (enten behandling med amlodipin eller atenolol) og enten atorvastatin 10 mg dagligt (n=5. 168) eller placebo (n=5. 137).
Patients were treated with anti-hypertensive therapy (either amlodipine or atenolol-based regimen) and either atorvastatin 10 mg daily (n=5,168) or placebo (n=5,137).
21 Den absolutte og relative risikoreduktion med atorvastatin er følgende:
The absolute and relative risk reduction effect of atorvastatin was as follows:
Hændelse
Relative Risk
Relativ risiko - reduktion (%)
No. of Events (Atorvastatin
Antal hændelser (Atorvastatin vs.
Absolute Risk
Placebo)
vs Placebo)
Absolut risiko - reduktion1 (%)
Reduction1
Fatal iskæmisk hjertesygdom og ikke- fatal myokardieinfarkt
Fatal CHD plus non-fatal MI Total cardiovascular events and revascularization procedures Total coronary events
36%
36% 20%
154
154 389 vs.
1, 9%
1.1% 1.9%
0, 0008
0.0005 0.0008
Totale koronare hændelser 1
1
247
178 vs 247
På baggrund af forskelle i de samlede hændelseshyppigheder opstået over en middelopfølgningsperiode på 3, 3 år
CHD = coronary heart disease; MI = myocardial infarction.
Mortaliteten af alle årsager og den kardiovaskulære mortalitet blev ikke signifikant nedsat (185 vs.
Total mortality and cardiovascular mortality were not significantly reduced (185 vs.
212 hændelser, p=0, 17 og 74 vs.
212 events, p=0.17 and 74 vs.
82 hændelser, p=0, 51).
82 events, p=0.51).
I undergruppeanalyserne af køn (81% mænd, 19% kvinder) blev atorvastatins gavnlige effekt bekræftet blandt mænd, men ikke blandt kvinder, muligvis på grund af det lille antal observerede hændelser hos kvinder i undergruppen.
In the subgroup analyses by gender (81% males, 19% females), a beneficial effect of atorvastatin was seen in males but could not be established in females possibly due to the low event rate in the female subgroup.
Samlet mortalitet og kardiovaskulær mortalitet var numerisk højere hos kvinder (38 vs.
Overall and cardiovascular mortality were numerically higher in the female patients (38 vs.
30 og 17 vs.
30 and 17 vs.
12), men det var ikke statistisk signifikant.
12), but this was not statistically significant.
Det primære endepunkt (fatal iskæmisk hjertesygdom samt ikke- fatal myokardieinfarkt blev signifikant nedsat af atorvastatin hos patienter behandlet med amlodipin (HR 0, 47 (0, 32- 0, 69) p=0, 00008), men ikke hos dem behandlet med atenolol (HR 0, 83 (0, 59- 1, 17), p=0, 287).
The primary endpoint (fatal CHD plus non-fatal MI) was significantly reduced by atorvastatin in patients treated with Amlodipine (HR 0.47 (0.32-0.69), p=0.00008), but not in those treated with Atenolol (HR 0.83 (0.59-1.17), p=0.287).
I et randomiseret, dobbelt- blindt, multicenter, placebokontrolleret studie, Collaborative Atorvastatin Diabetes Study (CARDS) blev effekten af atorvastatin på fatal og ikke- fatal kardiovaskulær sygdom også vurderet hos patienter med type 2 diabetes i alderen 40- 75 år, uden kardiovaskulær sygdom i anamnesen og med LDL- kolesterol ≤4, 14 mmol/ l (160 mg/ dl) og triglycerid ≤6, 78 mmol/ l (600 mg/ dl).
The effect of atorvastatin on fatal and non-fatal cardiovascular disease was also assessed in a randomized, double-blind, multicenter, placebo-controlled trial, the Collaborative Atorvastatin Diabetes Study (CARDS) in patients with type 2 diabetes, 40-75 years of age, without prior history of
Patienterne blev behandlet med enten atorvastatin 10 mg dagligt (n=1. 428) eller placebo (n=1. 410) med en middelopfølgningsperiode på 3, 9 år.
Patients were treated with either atorvastatin 10 mg daily (n=1,428) or placebo (n=1,410) for a median follow-up of 3.9 years.
Den absolutte og relative risikoreduktion med atorvastatin er følgende:
The absolute and relative risk reduction effect of atorvastatin was as follows:
Antal
Relative Risk
Absolut
No. of Events (Atorvastatin
p- værdi
Absolute Risk
Hændelse
Reduction
reduktion (%)
vs Placebo)
hændelser (Atorvastatin
Reduction1
risiko -
Event
vs.
(%)
Placebo)
(%)
Reduktion1 (%)
p-value
Større kardiovaskulære hændelser (fatal og ikke - fatal AMI, tavs MI, akut dødelig CHD, ustabil angina, CABG, PTCA, revaskularisering, slagtilfælde)
Major cardiovascular events (fatal and non-fatal AMI, silent MI, acute CHD death, unstable angina, CABG, PTCA, revascularization, stroke)
MI (fatal og ikke- fatal AMI, tavs MI)
MI (fatal and non-fatal AMI, silent MI)
64
38 vs 64
Slagtilfælde (fatal og ikke -
Strokes (Fatal and non-fatal) 1
22 fatal) 1 På baggrund af forskelle i de samlede hændelseshyppigheder opstået over en middelopfølgningsperiode på 3, 9 år.
Based on difference in crude events rates occurring over a median follow-up of 3.9 years.
Der var ikke bevis for en forskel i effekten af behandlingen med hensyn til patienternes køn, alder eller baseline- værdien for LDL- kolesterol.
There was no evidence of a difference in the treatment effect by patient’ s gender, age, or baseline LDL-C level.
Der er set en favorabel tendens med hensyn til mortalitetsrate (82 dødsfald i placebogruppen vs.
A favourable trend was observed regarding the mortality rate (82 deaths in the placebo group vs.
61 dødsfald i atorvastatingruppen, p=0, 0592).
61 deaths in the atorvastatin group, p=0.0592).
Atorvastatin absorberes hurtigt efter oral indgift; maksimal plamakoncentration (Cmax) nås inden for 1- 2 timer.
Atorvastatin is rapidly absorbed after oral administration; maximum plasma concentrations (Cmax) occur within 1 to 2 hours.
Biotilgængeligheden af atorvastatin filmovertrukne tabletter er 95- 99% sammenlignet med den orale opløsning.
After oral administration, atorvastatin film-coated tablets are 95% to 99% bioavailable compared to the oral solution.
30%.
The absolute bioavailability of atorvastatin is approximately 12% and the systemic availability of HMG-CoA reductase inhibitory activity is approximately 30%.
Den lave systemiske tilgængelighed skyldes præsystemisk clearance i gastrointestinal mucosa og/ eller first- pass metabolisme i leveren.
The low systemic availability is attributed to presystemic clearance in gastrointestinal mucosa and/ or hepatic first-pass metabolism
Distribution
23 Distribution
381 l.
Mean volume of distribution of atorvastatin is approximately 381 l.
Atorvastatin er bundet ≥98% eller mere til plasmaproteiner.
Atorvastatin is ≥ 98% bound to plasma proteins.
Atorvastatin metaboliseres via cytokrom P450 3A4 til orto - og parahydroxylerede derivater og forskellige beta- oxidationsprodukter.
Atorvastatin is metabolized by cytochrome P450 3A4 to ortho- and parahydroxylated derivatives and various beta-oxidation products.
Ca.
In vitro, inhibition of HMG-CoA reductase by ortho- and parahydroxylated metabolites is equivalent to that of atorvastatin.
70% af hæmningen af HMG- CoA- reduktase skyldes aktive metabolitter.
Approximately 70% of circulating inhibitory activity for HMG-CoA reductase is attributed to active metabolites.
Atorvastatin udskilles primært i galden efter metabolisering i eller uden for leveren.
Atorvastatin is eliminated primarily in bile following hepatic and/ or extrahepatic metabolism.
14 timer.
Mean plasma elimination half-life of atorvastatin in humans is approximately 14 hours.
20- 30 timer.
The half-life of inhibitory activity for HMG-CoA reductase is approximately 20 to 30 hours due to the contribution of active metabolites.
Særlige patientgrupper
Special populations − Geriatric:
Plasmakoncentrationer af atorvastatin og dets aktive metabolitter er højere hos raske ældre
Plasma concentrations of atorvastatin and its active metabolites are higher in healthy elderly subjects than in young adults while the lipid effects were comparable to those seen in younger patient populations. − Paediatric:
Der findes ikke farmakokinetiske data hos børn.
Pharmacokinetic data in the paediatric population are not available. − Gender:
Koncentrationen af atorvastatin og dets aktive metabolitter hos kvinder afviger (ca.
Concentrations of atorvastatin and its active metabolites in women differ from those in men (Women: approx.
20% højere
20% higher for Cmax and approx.
for Cmax og 10% lavere for AUC) fra koncentrationerne hos mænd.
10% lower for AUC).
Disse forskelle har ingen klinisk betydning og resulterer ikke i nogen klinisk signifikante forskelle i den lipidregulerende virkning mellem kønnene.
These differences were of no clinical significance, resulting in no clinically significant differences in lipid effects among men and women. − Renal insufficiency:
plasmakoncentration eller på deres effekt på lipiderne.
Renal disease has no influence on the plasma concentrations or lipid effects of atorvastatin and its active metabolites. − Hepatic insufficiency:
forhøjede (ca.
Plasma concentrations of atorvastatin and its active metabolites are markedly increased (approx.
16 gange for Cmax og ca.
16-fold in Cmax and approx.
11 gange for AUC) hos patienter med kronisk alkoholisk leversygdom (Childs- Pugh B).
11-fold in AUC) in patients with chronic alcoholic liver disease (Childs-Pugh B).
Den maksimale dosis var 63 gange højere end den højeste humane dosis (80 mg/ døgn) udregnet på baggrund af mg/ kg legemsvægt og 8- 16 gange højere baseret på AUC( 0- 24) bestemt ved total hæmmende aktivitet.
The maximum dose used was 63-fold higher than the highest human dose (80 mg/ day) on a mg/ kg body-weight basis and 8- to 16-fold higher based on AUC(0-24) values as determined by total inhibitory activity.
Den maksimale dosis var 250 gange højere end den højeste humane dosis udregnet på baggrund af mg/ kg legemsvægt.
In a 2-year study in mice, incidences of hepatocellular adenoma in males and hepatocellular carcinomas in females were increased at the maximum dose used, and the maximum dose used was 250-fold higher than the highest human dose on a mg/ kg body-weight basis.
Den systemiske eksponering var 6- 11 gange højere baseret på AUC( 0- 24).
Systemic exposure was 6- to 11-fold higher based on AUC(0-24).
I dyreforsøg havde atorvastatin ingen effekt på hanners eller hunners fertilitet i doser op til henholdsvis 175 og 225 mg/ kg dagligt; atorvastatin havde ingen teratogen virkning.
In animal studies atorvastatin had no effect on male or female fertility at doses up to 175 and 225 mg/ kg/ day, respectively, and was not teratogenic.
Calciumcarbonat Mikrokrystallinsk cellulose Lactosemonohydrat Croscarmellosenatrium Polysorbat 80 Hyprolose Magnesiumstearat.
Calcium carbonate Microcrystalline cellulose Lactose monohydrate Croscarmellose sodium Polysorbate 80 Hyprolose Magnesium stearate
Hypromellose Macrogol Titandioxid (E171) Talkum Simethicon Stearat emulgatorer Sorbinsyre Candelilla
Hypromellose Polyethylene glycol Titanium dioxide (E171) Talc Simethicone Stearate emulsifiers Sorbic acid Candelilla wax
24 Blisterformen består af polyamid/ aluminium folie/ polyvinylchlorid og blisterfolien består af enten af varmeforsegling med papir/ polyester/ aluminium folie/ vinyl eller aluminium folie/ vinyl.
The blisters consist of a forming film made of polyamide/ aluminum foil/ polyvinyl chloride and a backing made of either paper/ polyester/ aluminum foil/ vinyl heat-seal coating or aluminum foil/ vinyl heat-seal coating.
< [Se bilag I - Udfyldes nationalt] > [For referral procedures]
< [To be completed nationally] >
{Navn og adresse} < {tlf} > < {fax} > < {email} >
{Name and address }< {tel }> < {fax }> < {e-mail }>
November 21, 1996/ October 31, 2001
< [To be completed nationally] >
< [Se bilag I - Udfyldes nationalt] > [For referral procedures] {(Sær) navn} 20 mg filmovertrukne tabletter
< [See Annex I - To be completed nationally] > [For referral procedures] {PRODUCT NAME} 20mg film-coated tablet
1 filmovertrukken tablet indeholder 20 mg atorvastatin (som atorvastatincalciumtrihydrat).
Each film-coated tablet contains 20 mg atorvastatin (as atorvastatin calcium (trihydrate)).
1 {(Sær) navn} 20 mg filmovertrukken tablet indeholder 65, 61 mg lactosemonohydrat.
Each {PRODUCT NAME} 20 mg film-coated tablet contains 65.61 mg lactose monohydrate.
Filmovertrukne tabletter Hvide elipseformet filmovertrukne tabletter præget med "20 ” på den ene side og" PD156 ” på den anden side
White elliptical, film-coated tablets debossed "20" on one side and "PD 156" on the other.
26 Hos patienter med manifest iskæmisk hjertesygdom eller andre patienter med øget risiko for iskæmiske hændelser er behandlingsmålet LDL- kolesterol < 3 mmol/ l (eller < 115 mg/ dl) og total- kolesterol < 5 mmol/ l (eller < 190 mg/ dl).
27 For patients with established coronary heart disease or other patients at increased risk of ischemic events, the treatment goal is LDL-C < 3 mmol/ l (or < 115 mg/ dl) and total cholesterol < 5 mmol/ l (or < 190 mg/ dl).
I de primære forebyggelsesstudier var dosis 10 mg/ døgn.
In the primary prevention trials, the dose was 10 mg/ day.
27 4. 3 Kontraindikationer
4.3 Contraindications
- med overfølsomhed over for det aktive stof eller over for et eller flere af hjælpestofferne i dette
28 {PRODUCT NAME} is contraindicated in patients: − with hypersensitivity to the active substance or to any of the excipients of this medication − with active liver disease or unexplained persistent elevations of serum transaminases exceeding 3 times the upper limit of normal − with myopathy − during pregnancy − while breast-feeding − in women of child-bearing potential not using appropriate contraceptive measures.
Hvis CK- værdien er signifikant forhøjet (> 5 gange den øvre referenceværdi) ved baseline, bør behandlingen ikke startes.
If CPK levels are significantly elevated (> 5 times ULN) at baseline, treatment should not be started.
Kreatininfosfokinase (CK) måling CK bør ikke måles efter kraftig fysisk anstrengelse, eller hvis der er en alternativ grund til at CK er forhøjet, da det vanskeliggør fortolkningen af værdien.
Creatine phosphokinase measurement Creatine phosphokinase (CPK) should not be measured following strenuous exercise or in the presence of any plausible alternative cause of CPK increase as this makes value interpretation difficult.
Hvis CK- værdien er signifikant forhøjet ved baseline (> 5 gange den øvre referenceværdi), bør den måles igen inden for 5- 7 dage for at bekræfte resultatet.
If CPK levels are significantly elevated at baseline (> 5 times ULN), levels should be remeasured within 5 to 7 days later to confirm the results.
- Patienter skal opfordres til omgående at rapportere muskelsmerter, kramper eller svaghed, især hvis
Whilst on treatment − Patients must be asked to promptly report muscle pain, cramps, or weakness especially if accompanied by malaise or fever.
Hvis
29 − If such symptoms occur whilst a patient is receiving treatment with atorvastatin, their CPK levels should be measured.
denne værdi findes signifikant forhøjet (> 5 gange den øvre referenceværdi), bør behandlingen stoppes.
If these levels are found to be significantly elevated (> 5 times ULN), treatment should be stopped. − If muscular symptoms are severe and cause daily discomfort, even if the CPK levels are elevated to ≤ 5 x ULN, treatment discontinuation should be considered. − If symptoms resolve and CPK levels return to normal, then re-introduction of atorvastatin or introduction of an alternative statin may be considered at the lowest dose and with close monitoring. − Atorvastatin must be discontinued if clinically significant elevation of CPK levels (> 10 x ULN) occur, or if rhabdomyolysis is diagnosed or suspected.
29 Proteasehæmmere
Protease inhibitors
Grapefrugtjuice
30 Grapefruit juice
Cholestipol Plasmakoncentrationer af atorvastatin og dets aktive metabolitter var lavere (ca.
31 Colestipol Plasma concentrations of atorvastatin and its active metabolites were lower (by approx.
30 Fenazon Samtidig anvendelse af gentagne doser {(Sær) navn} og fenazon viste kun lidt eller ingen synlig effekt på fenazon- clearance.
Phenazone Coadministration of multiple doses of {PRODUCT NAME} and phenazone showed little or no detectable effect in the clearance of phenazone.
4. 6 Graviditet og amning
4.8 Pregnancy and lactation
4. 8 Bivirkninger
32 4.8 Undesirable effects
31 Lidelser i immunsystemet
Immune system disorders
Muskuloskeletale lidelser
33 Musculoskeletal disorders
32 Forhøjet serum- kreatininfosfokinase (CK) niveau på mere end 3 gange den øvre referenceværdi er set hos 2, 5% af de patienter, som behandles med {(Sær) navn}, hvilket svarer til andre HMG- CoA - reduktasehæmmere i kliniske studier.
Elevated serum creatine phosphokinase (CPK) levels greater than 3 times upper limit of normal occurred in 2.5% of patients on {PRODUCT NAME}, similar to other HMG-CoA reductase inhibitors in clinical trials.
Atorvastatin reducerer effektivt LDL- kolesterol hos patienter med homozygot familiær hyperkolesterolæmi, en patientgruppe, som ikke sædvanligvis responderer på lipidsænkende behandling.
34 homozygous familial hypercholesterolaemia, a population that has not usually responded to lipid- lowering medication.
33 Middel procentændring i total atheromavolumen (primært studiekriterie) fra baseline er – 0, 4% (p=0, 98) i atorvastatingruppen, og +2, 7% (p=0, 001) i pravastatingruppen (n=249).
The median percent change, from baseline, in total atheroma volume (the primary study criteria) was - 0.4% (p=0.98) in the atorvastatin group and +2.7% (p=0.001) in the pravastatin group (n=249).
I atorvastatingruppen reduceres LDL- kolesterol til et gennemsnit på 2, 04 mmol/ l ±0, 8 (78, 9 mg/ dl ±30) fra baseline 3, 98 mmol/ l ±0, 7 (150 mg/ dl ±28) og i pravastatingruppen til et gennemsnit på 2, 85 mmol/ l ± 0, 7 (110 mg/ dl ±26) fra baseline 3, 89 mmol/ l ±0, 7 (150 mg/ dl ±26) (p < 0, 0001).
In the atorvastatin group, LDL-C was reduced to a mean of 2.04 mmol/ l ± 0.8 (78.9 mg/ dl ± 30) from baseline 3.89 mmol/ l ± 0.7 (150 mg/ dl ± 28) and in the pravastatin group, LDL-C was reduced to a mean of 2.85 mmol/ l ± 0.7 (110 mg/ dl ± 26) from baseline 3.89 mmol/ l ± 0.7 (150 mg/ dl ± 26) (p < 0.0001).
Akut koronarsyndrom
35 Acute coronary syndrome
Patienterne fik antihypertensiv behandling (enten behandling med amlodipin eller atenolol) og enten atorvastatin 10 mg dagligt (n = 5. 168) eller placebo (n = 5. 137).
Patients were treated with anti-hypertensive therapy (either amlodipine or atenolol-based regimen) and either atorvastatin 10 mg daily (n=5,168) or placebo (n=5,137).
34 Den absolutte og relative risikoreduktion med atorvastatin er følgende:
The absolute and relative risk reduction effect of atorvastatin was as follows: