natgillin/translations-raw huggingface dataset:
Atorvastatin, like other HMG-CoA reductase inhibitors, may in rare occasions affect the skeletal muscle and cause myalgia, myositis, and myopathy that may progress to rhabdomyolysis, a potentially life-threatening condition characterised by markedly elevated CPK levels (> 10 times ULN), myoglobinaemia and myoglobinuria which may lead to renal failure.
Tako kot drugi zaviralci HMG- CoA reduktaze, lahko tudi atorvastatin v redkih primerih prizadene skeletne mišice in povzroči mialgijo, miozitis in miopatijo, ki lahko napreduje v rabdomiolizo - ta je lahko smrtno nevarna, značilni zanjo pa so izrazito zvišanje vrednosti CPK (> 10- kratna ZNM) - mioglobinemija in mioglobinurija, ki lahko povzroči odpoved ledvic.
Before the treatment Atorvastatin should be prescribed with caution in patients with pre-disposing factors for rhabdomyolysis.
Pred zdravljenjem Atorvastatin je treba previdno dajati bolnikom, ki imajo predispozicijske dejavnike za rabdomiolizo.
A creatine phosphokinase (CPK) level should be measured before starting statin treatment in the following situations: − Renal impairment − Hypothyroidism − Personal or familial history of hereditary muscular disorders − Previous history of muscular toxicity with a statin or fibrate − Previous history of liver disease and/ or where substantial quantities of alcohol are consumed − In elderly (age > 70 years), the necessity of such measurement should be considered, according to the presence of other predisposing factors for rhabdomyolysis
Vrednost kreatin fosfokinaze (CPK) je treba pred začetkom zdravljenja določiti v primeru: – okvare ledvic – hipotiroidizma – osebne ali družinske anamneze o podedovanih mišičnih motnjah – toksični učinki statinov ali fibratov na mišice v anamnezi – bolezni jeter in/ ali čezmerno uživanje alkohola v anamnezi – pri starejših bolnikih (starost > 70 let) je treba potrebo po takšnem merjenju oceniti glede na prisotnost drugih predispozicijskih dejavnikov za rabdomiolizo.
If CPK levels are significantly elevated (> 5 times ULN) at baseline, treatment should not be started.
Če je vrednost CPK izhodiščno zelo velika (> 5- kratna ZNM), zdravljenja ne začnemo.
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.
Merjenje kreatin fosfokinaze Kreatin fosfokinaze (CPK) ne smemo meriti po naporni telesni dejavnosti ali v prisotnosti drugih verjetnih vzrokov za zvišanje CPK, kajti v takšnem primeru je tolmačenje vrednosti težavno.
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.
Če je vrednost CPK izhodiščno zelo velika (> 5- kratna ZNM), je treba CPK za potrditev izvida ponovno izmeriti čez 5 do 7 dni.
Whilst on treatment − Patients must be asked to promptly report muscle pain, cramps, or weakness especially if accompanied by malaise or fever.
Med zdravljenjem – Bolnikom je treba naročiti, naj zdravnika takoj obvestijo o bolečinah v mišicah, krčih ali šibkosti mišic, zlasti če te simptome spremlja splošno slabo počutje ali zvišana telesna temperatura.
29 − If such symptoms occur whilst a patient is receiving treatment with atorvastatin, their CPK levels should be measured.
15 – Če se takšni simptomi pojavijo med zdravljenjem z atorvastatinom, je treba določiti CPK.
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.
Če je vrednost CPK pomembno zvišana (> 5- kratna ZNM), je treba zdravljenje prekiniti. – Če so mišični simptomi hudi in povzročajo težave v vsakodnevnem življenju, je treba razmisliti o prekinitvi zdravljenja tudi, če je vrednost CPK ≤ 5- kratna ZNM. – Če simptomi minejo in se CPK normalizira, pretehtamo možnost ponovne uvedbe atorvastatina ali uvedbe kakšnega drugega statina v najmanjšem odmerku in ob natančnem nadzoru. – Če se pojavi klinično pomembno zvišanje CPK (> 10- kratna ZNM), če je diagnosticirana rabdomioliza, ali če obstaja sum nanjo, je treba uporabo atorvastatina prekiniti.
Risk of rhabdomyolysis is increased when atorvastatin is administered concomitantly with certain medicaments such as: ciclosporin, erythromycin, clarithromycin, itraconazole, ketoconazole, nefazodone, niacin, gemfibrozil, other fibric acid derivates or HIV-protease inhibitors (see section 4.5 and section 4.8).
Tveganje za rabdomiolizo se zveča, če je atorvastatin uporabljen sočasno z določenimi zdravili, kakršna so npr.: ciklosporin, eritromicin, klaritromicin, itrakonazol, ketokonazol, nefazodon, niacin, gemfibrozil, drugi fibrati ali zaviralci HIV- proteaze (glejte poglavji 4. 5 in 4. 8).
Patients with rare hereditary problems of galactose intolerance, Lapp lactose deficiency or glucose- galactose malabsorption should not take this medicine.
Bolniki z redkimi dednimi težavami, kot so galaktozna intoleranca, Lappovo pomanjkanje laktaze ali glukozno- galaktozna malabsorpcija, ne smejo jemati tega zdravila.
Therefore, the benefit and the risk of concurrent treatment should be carefully weighed (see section 4.4).
Zato je treba natančno pretehtati koristi in tveganja sočasnega zdravljenja (glejte poglavje 4. 4).
Interaction may occur when {PRODUCT NAME} is administered with inhibitors of cytochrome P450 3A4 (e. g. ciclosporin, macrolide antibiotics including erythromycin and clarithromycin, nefazodone, azole antifungals including itraconazole and HIV protease inhibitors).
Medsebojno delovanje se lahko pojavi, če {(Lastniško) ime} uporabljamo sočasno z zaviralci citokroma P450 3A4 (npr. ciklosporinom, makrolidnimi antibiotiki, vključno z eritromicinom in klaritromicinom, nefazodonom, azolnimi antimikotiki vključno z itrakonazolom in zaviralci HIV proteaze).
Therefore, special caution should be exercised when atorvastatin is used in combination with such medicinal agents (see section 4.4).
Zato je med sočasno uporabo atorvastatina v kombinaciji s takšnimi zdravili potrebna posebna previdnost (glejte tudi poglavje 4. 4).
Atorvastatin and atorvastatin-metabolites are substrates of P-glycoprotein.
Atorvastatin in njegovi presnovki so substrati glikoproteina P.
Inhibitors of the P- glycoprotein (e. g. ciclosporin) can increase the bioavailability of atorvastatin.
Zaviralci glikoproteina P (npr. ciklosporin) lahko zvečajo biološko uporabnost atorvastatina.
Coadministration of atorvastatin 10 mg OD and erythromycin (500 mg QID), or atorvastatin 10 mg OD and clarithromycin (500 mg BID), known inhibitors of cytochrome P450 3A4, were associated with higher plasma concentrations of atorvastatin.
Sočasno uporabo 10 mg atorvastatina enkrat na dan in eritromicina (500 mg štirikrat na dan) oz. klaritromicina (500 mg dvakrat na dan) – oba sta znana zaviralca citokroma P450 3A4 – je spremljalo zvečanje koncentracije atorvastatina v plazmi.
Concomitant administration of atorvastatin 40 mg and itraconazole 200 mg daily resulted in a 3-fold increase in atorvastatin AUC.
Sočasna uporaba 40 mg atorvastatina in 200 mg itrakonazola na dan je povzročila 3- kratno zvečanje AUC atorvastatina.
30 Grapefruit juice
16 Grenivkin sok
Intake of one 240 ml glass of grapefruit juice resulted in an increase in atorvastatin AUC of 37% and a decreased AUC of 20.4% for the active orthohydroxy metabolite.
Zaužitje 240- ml kozarca grenivkinega soka je AUC atorvastatina zvečalo za 37%, AUC aktivnega ortohidroksi presnovka pa zmanjšalo za 20, 4%.
However, large quantities of grapefruit juice (over 1.2 l daily for 5 days) increased AUC of atorvastatin 2.5 fold and AUC of active (atorvastatin and metabolites) HMG-CoA reductase inhibitors 1.3 fold.
Vendar pa so velike količine zaužitega grenivkinega soka (več kot 1, 2 litra na dan pet dni) AUC atorvastatina zvečale za 2, 5- krat in AUC aktivnih zaviralcev HMG CoA reduktaze (atorvastatina in metabolitov) za 1, 3- krat.
The effect of inducers of cytochrome P450 3A4 (e. g. rifampicin or phenytoin) on {PRODUCT NAME} is unknown.
Vpliv induktorjev citokroma P450 3A4 (npr. rifampicina ali fenitoina) na {(Lastniško) ime} ni znan.
Gemfibrozil / fibric acid derivatives The risk of atorvastatin-induced myopathy may be increased with the concomitant use of fibric acid derivatives.
Gemfibrozil / fibrati Sočasna uporaba fibratov lahko zveča tveganje za nastanek z atorvastatinom povezane miopatije.
This may possibly lead to increased plasma levels of atorvastatin (see section 4.4).
To bi lahko povzročilo zvišano koncentracijo atorvastatina v plazmi (glejte tudi poglavje 4. 4).
However, digoxin concentrations increased approximately 20% following administration of digoxin with 80 mg atorvastatin daily.
Digoksin Med sočasno uporabo večkratnih odmerkov digoksina in 10 mg atorvastatina se koncentracija digoksina v stanju dinamičnega ravnovesja ni spremenila, med uporabo digoksina in 80 mg atorvastatina na dan pa se je zvečala za približno 20%.
This interaction may be explained by an inhibition of the membrane transport protein, P-glycoprotein.
To medsebojno delovanje je mogoče pojasniti z zavrtjem membranske transportne beljakovine, glikoproteina P.
Patients taking digoxin should be monitored appropriately.
Bolnike, ki jemljejo digoksin, je treba ustrezno nadzorovati.
Oral contraceptives Coadministration of {PRODUCT NAME} with an oral contraceptive produced increases in plasma concentrations of norethindrone and ethinyl oestradiol.
Peroralni kontraceptivi Sočasna uporaba {(Lastniško) ime} in peroralnih kontraceptivov je zvečala koncentracijo noretindrona in etilnilestradiola v plazmi.
25%) when colestipol was coadministered with {PRODUCT NAME}.
Holestipol Če je bil holestipol uporabljen sočasno s {(Lastniško) ime}, so bile koncentracije atorvastatina in njegovih aktivnih presnovkov nižje za približno 25%.
35%; however, LDL-C reduction was not altered.
Antacidi Sočasna uporaba {(Lastniško) ime} s peroralno antacidno suspenzijo, ki je vsebovala magnezijev in aluminijev hidroksid, je zmanjšala plazemsko koncentracijo atorvastatina in njegovih aktivnih presnovkov v plazmi za približno 35%, vendar na znižanje holesterola LDL ni vplivala.
Warfarin Coadministration of {PRODUCT NAME} and warfarin caused a small decrease in prothrombin time during the first days of dosing which returned to normal within 15 days of {PRODUCT NAME} treatment.
Varfarin Sočasna uporaba {(Lastniško) ime} in varfarina je v prvih dneh uporabe povzročila majhno skrajšanje protrombinskega časa; protrombinski čas se je normaliziral v 15 dneh uporabe {(Lastniško) ime}.
Phenazone Coadministration of multiple doses of {PRODUCT NAME} and phenazone showed little or no detectable effect in the clearance of phenazone.
Fenazon Sočasna uporaba večkratnih odmerkov {(Lastniško) ime} in fenazona je na očistek fenazona vplivala malo ali nič.
Cimetidine An interaction study with cimetidine and {PRODUCT NAME} was conducted, and no interaction was seen.
17 Cimetidin Raziskava interakcij cimetidina in {(Lastniško) ime} ni pokazala nobenega medsebojnega delovanja.
Amlodipine Atorvastatin pharmacokinetics were not altered by the coadministration of atorvastatin 80 mg and amlodipine 10 mg at steady state.
Amlodipin Sočasna uporaba 80 mg atorvastatina in 10 mg amlodipina v stanju dinamičnega ravnovesja ni spremenila farmakokinetike atorvastatina.
Other In clinical studies in which {PRODUCT NAME} was administered with antihypertensives or hypoglycaemic agents no clinically significant interactions were seen.
Drugo V kliničnih raziskavah, v katerih so {(Lastniško) ime} uporabljali hkrati z antihipertenzivi ali antidiabetiki, niso ugotovili klinično pomembnih interakcij.
4.8 Pregnancy and lactation
4. 6 Nosečnost in dojenje
{PRODUCT NAME} is contraindicated in pregnancy and while breast feeding.
{(Lastniško) ime} je med nosečnostjo in dojenjem kontraindiciran.
Women of child- bearing potential should use appropriate contraceptive measures.
Ženske v rodni dobi morajo uporabljati primerno kontracepcijsko zaščito.
The development of rat offspring was delayed and post-natal survival reduced during exposure of the dams to atorvastatin at doses above 20 mg/ kg/ day (the clinical systemic exposure).
Če so breje samice dobivale atorvastatin v odmerkih nad 20 mg/ kg/ dan (klinična sistemska izpostavljenost), je bil razvoj mladičev upočasnjen, preživetje neposredno po rojstvu pa manjše.
{PRODUCT NAME} has negligible influence on the ability to drive and use machines.
{(Lastniško) ime} ima zanemarljiv vpliv na sposobnost vožnje in upravljanja s stroji.
The most commonly expected adverse events are mainly gastrointestinal, including constipation, flatulence, dyspepsia, abdominal pain and usually ameliorate on continued treatment.
Med nadaljevanjem zdravljenja se ponavadi izboljšajo.
Estimated frequencies of events are ranked according to the following convention: common (≥ 1/ 100, < 1/ 10); uncommon (≥ 1/ 1,000, < 1/ 100); rare (≥ 1/ 10,000, < 1/ 1,000); very rare (≤ 1/ 10,000).
Ocenjene pogostnosti neželenih učinkov so po dogovoru razvrščene, kot sledi: pogosti (≥ 1/ 100, < 1/ 10); občasni (≥ 1/ 1000, < 1/ 100); redki (≥ 1/ 10000, < 1/ 1000); zelo redki (≤ 1/ 10000).
Uncommon: thrombocytopenia.
Občasno: trombocitopenija.
Very rare: anaphylaxis.
Zelo redko: anafilaksija.
Endocrine disorders
18 Bolezni endokrinega sistema
Common: insomnia.
Pogosto: nespečnost.
Uncommon: peripheral neuropathy.
Pogosto: glavobol, omotica, parestezije, hipestezija Nepogoste: periferna nevropatija.
Skin/ Appendages
Bolezni kože in podkožja
Skin rash, pruritus.
Pogosto: kožni izpuščaj, pruritus.
Uncommon: urticaria.
Občasno: urtikarija.
Very rare: angioneurotic oedema, bullous rashes (including erythema multiforme, Stevens-Johnson syndrome and toxic epidermal necrolysis).
Zelo redko: angionevrotski edem, bulozni izpuščaji (vključno z multiformnim eritemom, Stevens - Johnsonovim sindromom in toksično epidermalno nekrolizo).
33 Musculoskeletal disorders
Bolezni mišično- skeletnega sistema in vezivnega tkiva
Common: myalgia, arthralgia.
Pogosto: mialgija, artralgija.
Clinically important (> 3 times upper normal limit) elevations in serum transaminases occurred in 0.8% patients on {PRODUCT NAME}.
Klinično pomembno zvišanje (> 3- kratna ZNM) serumskih transaminaz se je pojavilo pri 0, 8% bolnikov, ki so jemali {(Lastniško) ime}.
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.
Zvišanje kreatin fosfokinaze (CPK), ki je presegalo 3- kratno ZNM, se je pojavilo pri 2, 5% bolnikov, ki so jemali {(Lastniško) ime}, kar je podobno kot v kliničnih raziskavah z drugimi zaviralci HMG CoA reduktaze.
Levels above 10 times the normal upper range occurred in 0.4% {PRODUCT NAME}-treated patients (see section 4.4).
Zvišanje nad 10- kratno ZNM se je pojavilo pri 0, 4% bolnikov, zdravljenih s {(Lastniško) ime} (glejte poglavje 4. 4).
Should an overdose occur, the patient should be treated symptomatically and supportive measures instituted, as required.
Specifičnega zdravljenja za preveliko odmerjanje {(Lastniško) ime} ni. V primeru prevelikega odmerjanja, je treba bolnika zdraviti siptomatsko in uvesti podporne ukrepe, kot je potrebno.
HMG-CoA-reductase inhibitors, ATC code:
Farmakoterapevtska skupina: zaviralci HMG CoA reduktaze, oznaka ATC:
Atorvastatin is a selective, competitive inhibitor of HMG-CoA reductase, the rate-limiting enzyme responsible for the conversion of 3-hydroxy-3-methyl-glutaryl-coenzyme A to mevalonate, a precursor of sterols, including cholesterol.
Atorvastatin je selektivni, kompetitivni zaviralec HMG CoA reduktaze, encima, ki omejuje hitrost pretvorbe 3- hidroksi- 3- metil- glutaril- koencima A v mevalonat, ki je predhodnik sterolov, vključno s holesterolom.
Low- density lipoprotein (LDL) is formed from VLDL and is catabolized primarily through the receptor with high affinity to LDL (LDL receptor).
Razgradijo se predvsem prek receptorja z veliko afiniteto za LDL (receptor LDL).
Atorvastatin lowers plasma cholesterol and lipoprotein serum concentrations by inhibiting HMG-CoA reductase and subsequently cholesterol biosynthesis in the liver and increases the number of hepatic LDL receptors on the cell surface for enhanced uptake and catabolism of LDL.
Zveča tudi število jetrnih receptorjev LDL na površini celic in s tem vstopanje LDL v celico in njegovo razgradnjo.
34 homozygous familial hypercholesterolaemia, a population that has not usually responded to lipid- lowering medication.
Atorvastatin učinkovito zniža holesterol LDL pri bolnikih s homozigotno familiarno hiperholesterolemijo, se pravi v populaciji, ki se ponavadi ne odzove na zdravljenje s hipolipemičnimi zdravili.
Atorvastatin has been shown to reduce concentrations of total-C (30% - 46%), LDL-C (41% - 61%), apolipoprotein B (34% - 50%), and triglycerides (14% - 33%) while producing variable increases in HDL-C and apolipoprotein A1 in a dose response study.
V raziskavi odzivanja na odmerjanje je atorvastatin zmanjšal koncentracijo celotnega holesterola (za 30- 46%), holesterola LDL (za 41- 61%), apolipoproteina B (za 34- 50%) in trigliceridov (za 14- 33%) obenem pa različno močno zvišal holesterol HDL in apolipoprotein A1.
In the Reversing Atherosclerosis with Aggressive Lipid- Lowering Study (REVERSAL), the effect of intensive lipid lowering with atorvastatin 80 mg and standard degree of lipid lowering with pravastatin 40 mg on coronary atherosclerosis was assessed by intravascular ultrasound (IVUS), during angiography, in patients with coronary heart disease.
V študiji REVERSAL (Reversing Atherosclerosis with Aggressive lipid- Lowering Study) so pri bolnikih s koronarno srčno boleznijo uporabili preiskavo z intravaskularnim ultrazvokom (IVUZ) in z njo med angiografijo ocenili učinek intenzivnega nižanja lipidov z 80 mg atorvastatina in standardnega nižanja lipidov s 40 mg pravastatina na koronarno aterosklerozo.
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).
Mediani odstotek spremembe celotnega volumna ateroma (ki je bil v študiji primarno merilo) od izhodišča je bil v skupini z atorvastatinom - 0, 4% (p=0, 98) in v skupini s pravastatinom + 2, 7% (p=0, 001) (n=249).
When compared to pravastatin the effects of atorvastatin were statistically significant (p=0.02).
Učinki atorvastatina so bili v primerjavi z učinki pravastatina statistično pomembni (p=0, 02).
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.
V študiji niso raziskovali učinka intenzivnega nižanja lipidov na kardiovaskularni opazovani dogodek (tj. potrebo po revaskularizaciji, miokarden infarkt brez smrtnega izida, koronarno smrt).
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).
20 V skupini z atorvastatinom se je holesterol LDL z izhodiščnih 3, 89 mmol/ l ± 0, 7 (150 mg/ dL ± 28) znižal na povprečno 2, 04 mmol/ L ± 0, 8 (78, 9 mg/ dL ± 30), v skupini s pravastatinom pa z izhodiščnih 3, 89 mmol/ l ± 0, 7 (150 mg/ dL ± 26) na povprečno 2, 85 mmol/ L ± 0, 7 (110 mg/ dL ± 26) (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 je tudi pomembno znižal povprečni celotni holesterol za 34, 1% (pravastatin: – 18, 4%, p < 0, 0001), povprečno koncentracijo trigliceridov za 20% (pravastatin: – 6, 8%, p < 0, 0009) in povprečni apolipoprotein B za 39, 1% (pravastatin: – 22, 0%, p < 0, 0001).
Atorvastatin increased mean HDL-C by 2.9% (pravastatin: +5.6%, p=NS).
Atorvastatin je zvišal povprečni holesterol HDL za 2, 9% (pravastatin: +5, 6%, p=NZ).
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).
V skupini z atorvastatinom se je CRP v povprečju znižal za 36, 4%, vskupini s pravastatinom pa za 5, 2% (p < 0, 0001).
Therefore, they cannot be extrapolated to the lower dose strengths.
Rezultate študije so dobili z odmerkom 80 mg, zato jih ni mogoče ekstrapolirati na nižje odmerke.
35 Acute coronary syndrome
Akutni koronarni sindrom
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).
V raziskavi MIRACL so pri 3086 bolnikih (atorvastatin n=1538; placebo n=1548) z akutnim koronarnim sindromom (miokardni infarkt brez zobca Q in nestabilna angina pektoris) ovrednotili zdravljenje z atorvastatinom 80 mg.
Treatment was initiated during the acute phase after hospital admission and lasted for a period of 16 weeks.
Z zdravljenjem so pričeli med akutno fazo po sprejemu v bolnišnico in je trajalo 16 tednov.
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).
Zdravljenje z atorvastatinom 80 mg dnevno je podaljšalo čas do nastopa sestavljenega primarnega opazovanega dogodka, ki je bil definiran kot smrt zaradi kateregakoli razloga, miokardni infarkt brez smrtnega izida, uspešno oživljanje po zastoju srca ali angina pektoris z znaki ishemije miokarda, zaradi katere je potrebna hospitalizacija, kar kaže na 16 - odstotno zmanjšanje tveganja (p=0, 048).
This was mainly due to a 26% reduction in re-hospitalisation for angina pectoris with evidence of myocardial ischaemia (p=0.018).
Razlog za to je bilo predvsem 26- odstotno zmanjšanje števila ponovnih hospitalizacij zaradi angine pektoris z znaki ishemije miokarda (p=0, 018).
22.4%).
Ostali sekundarni opazovani dogodki sami niso bili statistično pomembni (skupno: placebo 22, 2%, atorvastatin 22, 4%).
The safety profile of atorvastatin in the MIRACL study was consistent with what is described in Section 4.8.
Varnostni profil atorvastatina je bil v študiji MIRACL skladen z navedbami v poglavju 4. 8.
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).
Učinek atorvastatina na koronarno bolezen s smrtnim izidom in brez njega so ocenili v randomiziranem, dvojno slepi, s placebom kontrolirani študiji ASCOT- LLA (Anglo- Scandinavian Cardiac Outcomes Trial Lipid Lowering Arm).
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).
Bolniki so bili hipertenzivni, stari od 40 do 79 let, pred tem niso imeli miokardnega infarkta, se niso zdravili zaradi angine pektoris in so imeli koncentracijo trigliceridov ≤ 6, 5 mmol/ l (251 mg/ dl).