qanastek/EMEA-V3 huggingface dataset:
Hepatic impairment In patients with mild to moderate hepatic impairment without cholestasis, Diovan should be used with caution (see sections 4.2 and 5.2).
Indeboliment epatiku Diovan għandu jintuża b’ kawtela f’ pazjenti b’ indeboliment epatiku ħafif sa moderat mingħajr kolestasi (ara sezzjonijiet 4. 2 u 5. 2).
Pregnancy Angiotensin II Receptor Antagonists (AIIRAs) should not be initiated during pregnancy.
Tqala Antagonisti tar- Riċetturi ta ’ Angiotensin II (AIIRAs) m’ għandhomx jinbdew waqt it- tqala.
Unless continued AIIRAs therapy is considered essential, patients planning pregnancy should be changed to alternative anti-hypertensive treatments which have an established safety profile for use in pregnancy.
Sakemm terapija kontinwata b’ AIIRAs mhux ikkunsidrata essenzjali, pazjenti li qed jippjanaw tqala għandhom jinqalbu għall- kura oħra li tbaxxi l- pressjoni li għandha profil ta ’ sigurtà stabbilit għal użu waqt it - tqala.
When pregnancy is diagnosed, treatment with AIIRAs should be stopped immediately, and, if appropriate, alternative therapy should be started (see sections 4.3 and 4.6).
Meta ssir dijanjosi ta ’ tqala, kura b’ AIIRAs għandha titwaqqaf minnufih, u, jekk xieraq, għandha tinbeda terapija alternattiva (ara sezzjonijiet 4. 3 u 4. 6).
Recent myocardial infarction The combination of captopril and valsartan has shown no additional clinical benefit, instead the risk for adverse events increased compared to treatment with the respective therapies (see sections 4.2 and 5.1).
Infart mijokardijaku reċenti It- taħlita ta ’ captopril u valsartan ma wriet l- ebda benefiċċju kliniku addizzjonali, minflok ir- riskju għal avvenimenti avversi żdied meta mqabbel ma ’ kura bit- terapiji rispettivi (ara sezzjonijiet 4. 2 u 5. 1).
Therefore, the combination of valsartan with an ACE inhibitor is not recommended.
Għalhekk, it- taħlita ta ’ valsartan ma ’ inibitur ta ’ ACE mhux irrakkomandata.
Caution should be observed when initiating therapy in post-myocardial infarction patients.
Għandu jkun hemm kawtela meta tinbeda terapija f’ pazjenti li kellhom infart mijokardijaku.
Evaluation of post-myocardial infarction patients should always include assessment of renal function (see section 4.2).
Valutazzjoni ta ’ pazjenti wara infart mijokardijaku għandha dejjem tinkludi valutazzjoni tal- funzjoni renali (ara sezzjoni 4. 2).
Use of Diovan in post-myocardial infarction patients commonly results in some reduction in blood pressure, but discontinuation of therapy because of continuing symptomatic hypotension is not usually necessary provided dosing instructions are followed (see section 4.2).
31 L- użu ta ’ Diovan f’ pazjenti wara infart mijokardijaku b’ mod komuni jwassal għal xi tnaqqis fil - pressjoni tad- demm, iżda twaqqif tat- terapija minħabba pressjoni baxxa sintomatika li tippersisti ġeneralment ma jkunx neċessarju dejjem jekk jiġu segwiti l- istruzzjonijiet dwar id- dożaġġ (ara sezzjoni 4. 2).
Heart Failure In patients with heart failure, the triple combination of an ACE inhibitor, a beta blocker and Diovan has not shown any clinical benefit (see section 5.1).
Insuffiċjenza tal- Qalb F’ pazjenti b’ insuffiċjenza tal- qalb, it- taħlita tripla ta ’ inibitur ta ’ ACE, imblokkatur tar- riċetturi beta u Diovan ma wriet l- ebda benefiċċju kliniku (ara sezzjoni 5. 1).
This combination apparently increases the risk for adverse events and is therefore not recommended.
Din it- taħlita jidher li żżid ir- riskju ta ’ avvenimenti avversi u għalhekk mhux irrakkomandata.
Caution should be observed when initiating therapy in patients with heart failure.
Għandu jkun hemm kawtela meta tinbeda terapija f’ pazjenti b’ insuffiċjenza tal- qalb.
Evaluation of patients with heart failure should always include assessment of renal function (see section 4.2).
Valutazzjoni ta ’ pazjenti b’ insuffiċjenza tal- qalb għandha dejjem tinkludi valutazzjoni tal- funzjoni renali (ara sezzjoni 4. 2).
33 Use of Diovan in patients with heart failure commonly results in some reduction in blood pressure, but discontinuation of therapy because of continuing symptomatic hypotension is not usually necessary provided dosing instructions are followed (see section 4.2).
L- użu ta ’ Diovan f’ pazjenti b’ insuffiċjenza tal- qalb b’ mod komuni jwassal għal xi tnaqqis fil- pressjoni tad- demm, iżda twaqqif tat- terapija minħabba pressjoni baxxa sintomatika li tippersisti ġeneralment ma jkunx neċessarju dejjem jekk jiġu segwiti l- istruzzjonijiet dwar id- dożaġġ (ara sezzjoni 4. 2).
In patients whose renal function may depend on the activity of the renin-angiotensin system (e. g patients with severe congestive heart failure), treatment with angiotensin converting enzyme inhibitors has been associated with oliguria and/ or progressive azotaemia and in rare cases with acute renal failure and/ or death.
F’ pazjenti li l- funzjoni renali tagħhom tista ’ tiddependi fuq l- attività tas- sistema renin- angiotensin (eż. pazjenti b’ insuffiċjenza konġestiva tal- qalb severa), kura b’ inibituri ta ’ angiotensin converting enzyme kienet assoċjata ma ’ oligurja u/ jew ażotemja progressiva u f’ każijiet rari ma ’ insuffiċjenza renali akuta u/ jew mewt.
As valsartan is an angiotensin II antagonist, it cannot be excluded that the use of Diovan may be associated with impairment of the renal function.
Peress li valsartan huwa antagonist ta ’ angiotensin II, ma jistax jiġi eskluż li l- użu ta ’ Diovan jista ’ jkun assoċjat ma ’ indeboliment fil- funzjoni renali.
Use of Diovan in post-myocardial infarction patients commonly results in some reduction in blood pressure, but discontinuation of therapy because of continuing symptomatic hypotension is not usually necessary provided dosing instructions are followed (see section 4.2).
L- użu ta ’ Diovan f’ pazjenti wara infart mijokardijaku b’ mod komuni jwassal għal xi tnaqqis fil - pressjoni tad- demm, iżda twaqqif tat- terapija minħabba pressjoni baxxa sintomatika li tippersisti ġeneralment ma jkunx neċessarju dejjem jekk jiġu segwiti l- istruzzjonijiet dwar id- dożaġġ (ara sezzjoni 4. 2).
Use of Diovan in patients with heart failure commonly results in some reduction in blood pressure, but discontinuation of therapy because of continuing symptomatic hypotension is not usually necessary provided dosing instructions are followed (see section 4.2).
L- użu ta ’ Diovan f’ pazjenti b’ insuffiċjenza tal- qalb b’ mod komuni jwassal għal xi tnaqqis fil- pressjoni tad- demm, iżda twaqqif tat- terapija minħabba pressjoni baxxa sintomatika li tippersisti ġeneralment ma jkunx neċessarju dejjem jekk jiġu segwiti l- istruzzjonijiet dwar id- dożaġġ (ara sezzjoni 4. 2).
Other conditions with stimulation of the renin-angiotensin system In patients whose renal function may depend on the activity of the renin-angiotensin system (e. g patients with severe congestive heart failure), treatment with angiotensin converting enzyme inhibitors has been associated with oliguria and/ or progressive azotaemia and in rare cases with acute renal failure and/ or death.
Kundizzjonijiet oħra bi stimulazzjoni tas- sistema renin- angiotensin F’ pazjenti li l- funzjoni renali tagħhom tista ’ tiddependi fuq l- attività tas- sistema renin- angiotensin (eż. pazjenti b’ insuffiċjenza konġestiva tal- qalb severa), kura b’ inibituri ta ’ angiotensin converting enzyme kienet assoċjata ma ’ oligurja u/ jew ażotemja progressiva u f’ każijiet rari ma ’ insuffiċjenza renali akuta u/ jew mewt.
As valsartan is an angiotensin II antagonist, it cannot be excluded that the use of Diovan may be associated with impairment of the renal function.
Peress li valsartan huwa antagonist ta ’ angiotensin II, ma jistax jiġi eskluż li l- użu ta ’ Diovan jista ’ jiġi assoċjat ma ’ indeboliment fil- funzjoni renali.
4.5 Interaction with other medicinal products and other forms of interaction
32 4. 5 Prodotti mediċinali oħra li ma jaqblux ma ’ dan il- prodott u affarijiet oħra li jistgħu jibdlu l- effett farmaċewtiku tal- prodott
Concomitant use not recommended
L- użu flimkien mhux irrakkomandat
Lithium Reversible increases in serum lithium concentrations and toxicity have been reported during concurrent use of ACE inhibitors.
Lithium Waqt l- użu fl- istess waqt ta ’ inibituri ta ’ ACE, kienet irrapportata żjieda riversibbli fil - konċentrazzjonijiet fis- serum u fit- tossiċità ta ’ lithium.
Due to the lack of experience with concomitant use of valsartan and lithium, this combination is not recommended.
Minħabba n- nuqqas ta ’ esperjenza bl- użu flimkien ta ’ valsartan u lithium, din it- taħlita mhijiex irrakkomandata.
If the combination proves necessary, careful monitoring of serum lithium levels is recommended.
Jekk it- taħlita tkun neċessarja, hija rrakkomandata sorveljanza b’ attenzjoni tal- livelli ta ’ lithium fis- serum.
Potassium-sparing diuretics, potassium supplements, salt substitutes containing potassium and other substances that may increase potassium levels If a medicinal product that affects potassium levels is considered necessary in combination with valsartan, monitoring of potassium plasma levels is advised.
Jekk prodott mediċinali li jaffettwa l- livelli ta ’ potassium huwa kkunsidrat neċessarju flimkien ma ’ valsartan, hija rrakkomandata sorveljanza tal- livelli ta ’ potassium fil- plażma.
34 Caution required with concomitant use
Ħtieġa ta ’ kawtela ma ’ l- użu flimkien
Non-steroidal anti-inflammatory medicines (NSAIDs), including selective COX-2 inhibitors, acetylsalicylic acid > 3 g/ day), and non-selective NSAIDs When angiotensin II antagonists are administered simultaneously with NSAIDs, attenuation of the antihypertensive effect may occur.
Mediċini anti- infjammatorji mhux sterojdi (NSAIDs), inkluż inibituri selettivi ta ’ COX- 2, acetylsalicylic acid > 3 g/ kuljum, u NSAIDs mhux selettivi Meta antagonisti ta ’ angiotensin II jingħataw flimkien ma ’ NSAIDs, jista ’ jkun hemm tnaqqis tal- effett li jbaxxi l- pressjoni.
Furthermore, concomitant use of angiotensin II antagonists and NSAIDs may lead to an increased risk of worsening of renal function and an increase in serum potassium.
Barra dan, l- użu ta ’ antagonisti ta ’ angiotensin II flimkien ma ’ NSAIDs jista ’ jwassal għal żjieda fir- riskju ta ’ rkadar tal- funzjoni renali u żjieda fil- potassium fis- serum.
Therefore, monitoring of renal function at the beginning of the treatment is recommended, as well as adequate hydration of the patient.
Għalhekk fil- bidu tal- kura hija rrakkomandata sorveljanza tal- funzjoni renali, kif ukoll idratazzjoni adegwata tal - pazjent.
Others In drug interaction studies with valsartan, no interactions of clinical significance have been found with valsartan or any of the following substances: cimetidine, warfarin, furosemide, digoxin, atenolol, indometacin, hydrochlorothiazide, amlodipine, glibenclamide.
Oħrajn Fi studji dwar l- interazzjoni tal- mediċina b’ valsartan, ma nstabet l- ebda interazzjoni ta ’ sinifikanza klinika b’ valsartan jew b’ xi wieħed mis- sustanzi li ġejjin: cimetidine, warfarin, furosemide, digoxin, atenolol, indometacin, hydrochlorothiazide, amlodipine, glibenclamide.
The use of Angiotensin II Receptor Antagonists (AIIRAs) is not recommended during the first trimester of pregnancy (see section 4.4).
L- użu ta ’ Antagonisti tar- Riċettur ta ’ Angiotensin II (AIIRAs) mhux irrakkomandat waqt l- ewwel trimestru tat- tqala (ara sezzjoni 4. 4).
The use of AIIRAs is contra-indicated during the second and third trimester of pregnancy (see sections 4.3 and 4.4).
L- użu ta ’ AIIRAs huwa kontra- indikat waqt it- tieni u t- tielet trimestru tat- tqala (ara sezzjonijiet 4. 3 u 4. 4).
Epidemiological evidence regarding the risk of teratogenicity following exposure to ACE inhibitors during the first trimester of pregnancy has not been conclusive; however, a small increase in risk cannot be excluded.
Evidenza epidemjoloġika dwar ir- riskju ta ’ teratoġeniċità wara espożizzjoni għall- inibituri ta ’ ACE waqt l- ewwel trimestru tat- tqala ma kinetx konklużiva; madankollu, ma tistax tiġi eskluża żjieda żgħira fir- riskju.
Whilst there is no controlled epidemiological data on the risk with AIIRAs, similar risks may exist for this class of drugs.
Filwaqt li m’ hemmx tagħrif epidemjoloġiku kkontrollat dwar ir- riskju b’ AIIRAs, jistgħu jeżistu riskji simili għal din il- klassi ta ’ mediċini.
Unless continued AIIRA therapy is considered essential, patients planning pregnancy should be changed to alternative anti-hypertensive treatments which have an established safety profile for use in pregnancy.
Sakemm terapija kontinwa b’ AIIRA mhux ikkunsidrata bħala essenzjali, pazjenti li qed jippjanaw tqala għandhom jinqalbu għall- kura alternattiva li tbaxxi l- pressjoni għolja li għandha profil ta ’ sigurtà stabbilit għall- użu waqt it- tqala.
When pregnancy is diagnosed, treatment with AIIRAs should be stopped immediately, and, if appropriate, alternative therapy should be started.
Meta ssir dijanjosi ta ’ tqala kura b’ AIIRAs għandha titwaqqaf minnufih, u jekk xieraq għandha tinbeda terapija alternattiva.
AIIRAs therapy exposure during the second and third trimesters is known to induce human fetotoxicity (decreased renal function, oligohydramnios, skull ossification retardation) and neonatal toxicity (renal failure, hypotension, hyperkalemia); see also section 5.3 “ Preclinical safety data”.
Espożizzjoni għal terapija b’ AIIRAs waqt it- tieni u t- tielet trimestru hija magħrufa li tinduċi tossiċità lill- fetu uman (funzjoni renali mnaqqsa, fluwidu amnjotiku mhux suffiċjenti, ittardjar ta ’ l - ossifikazzjoni tal- qorriegħa tar- ras) u tossiċità neonatali (insuffiċjenza renali, pressjoni baxxa, iperkalimja); ara wkoll sezzjoni 5. 3 “ Tagħrif ta ’ qabel l- użu kliniku dwar is- sigurtà tal- mediċina ”.
Should exposure to AIIRAs have occurred from the second trimester of pregnancy, ultrasound check of renal function and skull is recommended.
Jekk ikun hemm espożizzjoni għal AIIRAs mit- tieni trimestru tat- tqala, hija rrakkomandata valutazzjoni tal- funzjoni renali u tal- qorriegħa tar- ras b’ ultrasound.
Infants whose mothers have taken AIIRAs should be closely observed for hypotension (see also sections 4.3 and 4.4).
Trabi ta ’ ommijiet li ħadu AIIRAs għandhom jiġu osservati mill- qrib għall- pressjoni baxxa (ara wkoll sezzjoni 4. 3 u 4. 4).
Lactation Because no information is available regarding the use of valsartan during breastfeeding, Diovan is not recommended and alternative treatments with better established safety profiles during breast-feeding are preferable, especially while nursing a newborn or preterm infant.
33 Treddigħ Peress li m’ hemmx informazzjoni disponibbli dwar l- użu ta ’ valsartan waqt it- treddigħ, Diovan mhux irrakkomandat u kura alternattiva li għandha profil ta ’ sigurtà stabbilit aħjar għall- użu waqt it- treddigħ hija preferibbli, speċjalment waqt treddigħ ta ’ tarbija tat- twelid jew tarbija li twieldet qabel iż- żmien.
No studies on the effects on the ability to drive have been performed.
Ma sarux studji dwar l- effetti fuq il- ħila biex issuq jew tħaddem magni.
When driving vehicles or operating machines it should be taken into account that occasionally dizziness or weariness may occur.
Waqt is- sewqan jew tħaddim ta ’ magni wieħed għandu jikkunsidra li xi kultant jista ’ jkun hemm sturdament jew għeja.
In controlled clinical studies in patients with hypertension, the overall incidence of adverse reactions (ADRs) was comparable with placebo and is consistent with the pharmacology of valsartan.
Fi studji kliniċi kkontrollati f’ pazjenti bi pressjoni għolja, l- inċidenza globali ta ’ reazzjonijiet avversi (ADRs) kienet komparabbli mal- plaċebo u hija konsistenti mal- farmakoloġija ta ’ valsartan.
The incidence of ADRs did not appear to be related to dose or treatment duration and also showed no association with gender, age or race.
L - inċidenza ta’ ADRs ma dehritx li hija relata mad- doża jew mat- tul tal- kura u ma kienet osservata l- ebda assoċjazzjoni ma ’ sess, età jew razza.
35 The ADRs reported from clinical studies, post-marketing experience and laboratory findings are listed below according to system organ class.
L- ADRs irrapportati mill- istudji kliniċi, mill- esperjenza ta ’ wara t- tqegħid fis- suq u minn sejbiet tal - laboratorju huma mniżżla hawn taħt skond is- sistema tal- klassifika tal- organi.
Adverse reactions are ranked by frequency, the most frequent first, using the following convention: very common (≥ 1/ 10); 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), including isolated reports.
Ir- reazzjonijet avversi huma mniżżla skond il- frekwenza, bl- aktar frekwenti l- ewwel, bl- użu tal - konvenzjoni li ġejja: komuni ħafna (≥ 1/ 10); komuni (≥ 1/ 100 sa < 1/ 10); mhux komuni (≥ 1/ 1, 000 sa < 1/ 100); rari (≥ 1/ 10, 000 sa < 1/ 1, 000) rari ħafna (< 1/ 10, 000), inkluż rapporti iżolati.
Within each frequency grouping, adverse reactions are ranked in order of decreasing seriousness.
F’ kull sezzjoni ta ’ frekwenza, r- reazzjonijet avversi għandhom jitniżżlu skond is- serjetà tagħhom, bl- aktar serji jitniżżlu l- ewwel.
For all the ADRs reported from post-marketing experience and laboratory findings, it is not possible to apply any ADR frequency and therefore they are mentioned with a "not known" frequency.
Għall- ADRs kollha rrapportati mill- esperjenza ta ’ wara t- tqegħid fis- suq u mis- sejbiet tal- laboratorju, l- frekwenza ta ’ l- ADR mhux possibli li tiġi applikata u għalhekk huma msemmija bi frekwenza "mhux magħrufa".
 Hypertension
Pressjoni għolja
Blood and lymphatic system disorders Not known Immune system disorders
Disturbi tad- demm u tas- sistema limfatika Mhux magħrufa Disturbi fis- sistema immuni
Decrease in haemoglobin, Decrease in haematocrit, Neutropenia, Thrombocytopenia
Tnaqqis fl- emoglobina, Tnaqqis fl- ematokrita, Newtropenija, Tromboċitopenija
Not known Metabolism and nutrition disorders
Mhux magħrufa Disturbi fil- metaboliżmu u n- nutrizzjoni
Hypersensitivity including serum sickness
Sensittività eċċessiva ikluż marda tas- serum
Not known Ear and labyrinth system disorders
Mhux magħrufa Disturbi fil- widnejn u fis- sistema labirintika
Increase of serum potassium
Żjieda fil- potassium fis- serum
Not known Respiratory, thoracic and mediastinal disorders
Mhux magħrufa Disturbi respiratorji, toraċiċi u medjastinali
Uncommon Gastrointestinal disorders
Mhux komuni Disturbi gastro- intestinali
Uncommon Hepato-biliary disorders
Mhux komuni Disturbi fil- fwied u fil- marrara
Not known Skin and subcutaneous tissue disorders
Mhux magħrufa Disturbi fil- ġilda u fit- tessuti ta ’ taħt il- ġilda
Elevation of liver function values including increase of serum bilirubin
Żjieda fil- valuri tal- funzjoni tal- fwied inkluż żjieda fil- bilirubin fis- serum
Not known Musculoskeletal and connective tissue disorders
Mhux magħrufa Disturbi muskolu- skeltrali u tal- connective tissue
Angioedema, Rash, Pruritus
Anġjoedima, Raxx, Ħakk
Not known Renal and urinary disorders
Mhux magħrufa
Renal failure and impairment, Elevation of serum creatinine
Insuffiċjenza u indeboliment renali, Żjieda fil - krejatinina fis- serum
General disorders and administration site conditions Uncommon
Disturbi ġenerali u kondizzjonijiet ta ’ mnejn jingħata Mhux komuni
The safety profile seen in controlled-clinical studies in patients with post-myocardial infarction and/ or heart failure varies from the overall safety profile seen in hypertensive patients.
insuffiċjenza tal- qalb ivarja mill- profil ta ’ sigurtà globali osservat f’ pazjenti bi pressjoni għolja.
This may relate to the patients underlying disease.
Dan jista ’ jkollu x’ jaqsam mal- marda li għandu l- pazjent.
ADRs that occurred in post-myocardial infarction and/ or heart failure patients are listed below:
ADRs li seħħew f’ pazjenti wara infart mijokardijaku u/ jew insuffiċjenza tal- qalb huma mniżżla isfel:
 Post-myocardial infarction and/ or heart failure
Wara infart mijokardijaku u/ jew insuffiċjenza tal- qalb
Thrombocytopenia
Tromboċitopenija
Uncommon Not known Nervous system disorders
Mhux komuni Mhux magħrufa Disturbi fis- sistema nervuża
Hyperkalaemia Increase of serum potassium
Iperkalimja Żjieda fil- potassium fis- serum
36 Common Uncommon Ear and labyrinth system disorders
Komuni Mhux komuni Disturbi fil- widnejn u fis- sistema labirintika
Dizziness, Postural dizziness Syncope, Headache
Sturdament, Sturdament mal- waqfien Sinkope, Uġigħ ta ’ ras
Uncommon Cardiac disorders
Mhux komuni Disturbi fil- qalb
Common Not known Respiratory, thoracic and mediastinal disorders
Komuni Mhux magħrufa Disturbi respiratorji, toraċiċi u medjastinali
Hypotension, Orthostatic hypotension Vasculitis
Pressjoni baxxa, Pressjoni ortostatika baxxa Vaskulite
Nausea, Diarrhoea
Tqalligħ, Dijarea
Elevation of liver function values
Żjieda fil- valuri tal- funzjoni tal- fwied
Uncommon Not known Musculoskeletal and connective tissue disorders
Mhux komuni Mhux magħrufa Disturbi muskolu- skeltrali u tal- connective tissue
Angioedema Rash, Pruritis
Anġjoedima Raxx, Ħakk
Not known Renal and urinary disorders
Mhux magħrufa Disturbi fil- kliewi u fis- sistema urinarja
Common Uncommon Not known
Mhux magħrufa
Renal failure and impairment Acute renal failure, Elevation of serum creatinine Increase in Blood Urea Nitrogen
Żjieda fin- Nitrogen fid- Demm mill- Urea
Asthenia, Fatigue
Astenja, Għeja
4.9 Overdose
Sintomi
Symptoms Overdose with Diovan may result in marked hypotension, which could lead to depressed level of consciousness, circulatory collapse and/ or shock.
35 Doża eċċessiva b’ Diovan tista ’ tikkawża pressjoni baxxa ħafna, li tista ’ twassal għall- livell depress ta ’ koxjenza, kollass taċ- ċirkolazzjoni u/ jew xokk.
Treatment The therapeutic measures depend on the time of ingestion and the type and severity of the symptoms; stabilisation of the circulatory condition is of prime importance.
Kura Il- miżuri terapewtiċi jiddependu fuq il- ħin ta ’ l- inġestjoni u fuq it- tip u s- severità tas- sintomi; stabilizzazzjoni tal- kundizzjoni ċirkolatorja hija ta ’ importanza ewlenija.
If hypotension occurs, the patient should be placed in a supine position and blood volume correction should be undertaken.
Jekk isseħħ pressjoni baxxa, il- pazjent għandu jitpoġġa f’ pożizzjoni mimduda u għandha ssir korrezzjoni tal- volum tad- demm.
Valsartan is unlikely to be removed by haemodialysis.
Valsartan mhux probabbli li jitneħħa permezz ta ’ emodijalisi.
Angiotensin II Antagonists, plain, ATC code:
Antagonisti ta ’ Angiotensin II, waħedhom, Kodiċi ATC:
Valsartan is an orally active, potent, and specific angiotensin II (Ang II) receptor antagonist.
Valsartan huwa antagonist qawwi u speċifiku tar- riċettur ta ’ angiotensin II (Ang II) attiv b’ mod orali.
It acts selectively on the AT 1 receptor subtype, which is responsible for the known actions of angiotensin II.
Huwa jaħdem b’ mod selettiv fuq is- sottotip ta ’ riċettur AT 1, li huwa responsabbli għall- azzjonijiet magħrufa ta ’ angiotensin II.
The increased plasma levels of Ang II following AT 1 receptor blockade with valsartan may stimulate the unblocked AT 2 receptor, which appears to counterbalance the effect of the AT 1 receptor.
Iż- żjieda fil- livelli fil- plażma ta ’ Ang II wara l- imblokk tar- riċettur AT 1 permezz ta ’ valsartan jista ’ jistimola r- riċettur AT 2 li mhux imblokkat, li jidher li jikkontrobilanċja l - effett tar- riċettur AT 1.
Valsartan does not exhibit any partial agonist activity at the AT 1 receptor and has much (about 20,000 fold) greater affinity for the AT 1 receptor than for the AT 2 receptor.
Valsartan ma jurix attività agonista parzjali fir- riċettur AT 1 u għandu affinità ferm aktar ogħla (madwar 20, 000 darba) għar- riċettur AT 1 milli għar- riċettur AT 2.
Valsartan is not known to bind to or block other hormone receptors or ion channels known to be important in cardiovascular regulation.
Valsartan mhux magħruf li jeħel jew jimblokka riċetturi ta ’ ormoni oħra jew kanali tal- joni magħrufa li huma importanti fir- regolazzjoni kardjovaskulari.
37 Valsartan does not inhibit ACE (also known as kininase II) which converts Ang I to Ang II and degrades bradykinin.
Valsartan ma jinibixxix ACE (magħruf ukoll bħala kininase II) li jaqleb Ang I għal Ang II u jiddegrada bradykinin.
Since there is no effect on ACE and no potentiation of bradykinin or substance P, angiotensin II antagonists are unlikely to be associated with coughing.
Peress li m’ hemmx effett fuq ACE u l- ebda żjieda fil- qawwa ta ’ bradykinin jew tas- sustanza P, antagonisti ta ’ angiotensin II mhux probabbli li jkunu assoċjati ma ’ sogħla.
In clinical trials where valsartan was compared with an ACE inhibitor, the incidence of dry cough was significantly (P < 0.05) less in patients treated with valsartan than in those treated with an ACE inhibitor (2.6% versus 7.9% respectively).
Fi provi kliniċi fejn valsartan kien imqabbel ma ’ inibitur ta ’ ACE, l- inċidenza ta ’ sogħla xotta kienet inqas b’ mod sinifikanti (P < 0. 05) f’ pazjenti kkurati b’ valsartan meta mqabbel ma ’ dawk ikkurati b’ inibitur ta ’ ACE (2. 6% kontra 7. 9% rispettivament).
In a clinical trial of patients with a history of dry cough during ACE inhibitor therapy, 19.5% of trial subjects receiving valsartan and 19.0% of those receiving a thiazide diuretic experienced cough compared to 68.5% of those treated with an ACE inhibitor (P < 0.05).
Fi prova klinika ta ’ pazjenti b’ passat ta ’ sogħla xotta waqt terapija b’ inibitur ta ’ ACE, 19. 5% ta ’ l- individwi fil- prova li rċevew valsartan u 19. 0% ta ’ dawk li rċevew dijuretiku thiazide kellhom esperjenza ta ’ sogħla meta mqabbel ma ’ 68. 5% ta ’ dawk ikkurati b’ inibitur ta ’ ACE (P < 0. 05).
Recent myocardial infarction The VALsartan In Acute myocardial iNfarcTion trial (VALIANT) was a randomised, controlled, multinational, double-blind study in 14,703 patients with acute myocardial infarction and signs, symptoms or radiological evidence of congestive heart failure and/ or evidence of left ventricular systolic dysfunction (manifested as an ejection fraction ≤ 40% by radionuclide ventriculography or ≤ 35% by echocardiography or ventricular contrast angiography).
Infart mijokardijaku reċenti Il- prova VALsartan In Acute myocardial iNfarcTion (VALIANT) kienet studju randomised, ikkontrollat, multinazzjonali u double- blind f’ 14, 703 pazjenti b’ infart mijokardijaku akut u sinjali, sintomi jew evidenza radjoloġika ta ’ insuffiċjenza konġestiva tal- qalb u/ jew disfunzjoni sistolika tal - ventriklu tax- xellug (manifestata bħala frazzjoni ta ’ tfigħ ’ il barra ta ’ ≤40% permezz ta ’ radionuclide ventriculography jew ta ’ ≤35% permezz ta ’ ekukardjografija jew anġjografija ventrikulari b’ kuntrast).
Patients were randomised within 12 hours to 10 days after the onset of myocardial infarction symptoms to valsartan, captopril, or the combination of both.
Pazjenti kienu randomised fi żmien 12- il siegħa sa għaxart ijiem wara l- bidu tas- sintomi ta ’ infart mijokardijaku għal valsartan, captopril, jew taħlita tat- tnejn.
The mean treatment duration was two years.
It- tul medju ta ’ kura kien ta ’ sentejn.
The primary endpoint was time to all-cause mortality.
Ir - riżultat tat- tmiem l- aktar importanti kien iż- żmien sa mortalità minn kull kawża.
Valsartan was as effective as captopril in reducing all-cause mortality after myocardial infarction.
Valsartan kien effettiv daqs captopril biex inaqqas il- mortalità minn kull kawża wara infart mijokardijaku.
All- cause mortality was similar in the valsartan (19.9%), captopril (19.5%), and valsartan + captopril (19.3%) groups.
Mortalità minn kull kawża kienet simili fil- gruppi ta ’ valsartan (19. 9%), captopril (19. 5%), u valsartan + captopril (19. 3%).
Combining valsartan with captopril did not add further benefit over captopril alone.
Taħlita ta ’ valsartan ma ’ captopril ma żiditx aktar benefiċċju fuq captopril waħdu.
There was no difference between valsartan and captopril in all-cause mortality based on age, gender, race, baseline therapies or underlying disease.
Ma kienx hemm differenza bejn valsartan u captopril fil- mortalità minn kull kawża bbażat fuq età, sess, razza, terapiji fil- linja bażi jew marda li hemm preżenti.
Valsartan was also effective in prolonging the time to and reducing cardiovascular mortality, hospitalisation for heart failure, recurrent myocardial infarction, resuscitated cardiac arrest, and non-fatal stroke (secondary composite endpoint).
Valsartan kien effettiv ukoll biex itawwal iż- żmien sa u biex inaqqas il- mortalità kardjovaskulari, teħid l- isptar għall - insuffiċjenza tal- qalb, infart mijokardijaku rikorrenti, arrest kardijaku risuxxitat, u puplesija mhux fatali (ir- riżultat tat- tmiem sekondarju kompost).
The safety profile of valsartan was consistent with the clinical course of patients treated in the post- myocardial infarction setting.
Il- profil ta ’ sigurtà ta ’ valsartan kien konsistenti mal- progressjoni klinika ta ’ pazjenti kkurati fl - ambjent ta ’ wara infart mijokardijaku.
Regarding renal function, doubling of serum creatinine was observed in 4.2% of valsartan-treated patients, 4.8% of valsartan+captopril-treated patients, and 3.4% of captopril- treated patients.
Dwar il- funzjoni renali, irduppjar tal- krejatinina fis- serum kien osservat f’ 4. 2% tal- pazjenti kkurati b’ valsartan, f’ 4. 8% tal- pazjenti kkurati b’ valsartan+captopril, u fi 3. 4% tal- pazjenti kkurati b’ captopril.
Discontinuations due to various types of renal dysfunction occurred in 1.1% of valsartan-treated patients, 1.3% in valsartan+captopril patients, and 0.8% of captopril patients.
36 f’ 1. 1% tal- pazjenti kkurati b’ valsartan, f’ 1. 3% tal- pazjenti kkurati b’ valsartan+captopril, u f’ 0. 8% tal - pazjenti kkurati b’ captopril.
An assessment of renal function should be included in the evaluation of patients post-myocardial infarction.
Valutazzjoni tal- pazjenti wara infart mijokardijaku għandha tinkludi valutazzjoni tal- funzjoni renali.
There was no difference in all-cause mortality, cardiovascular mortality or morbidity when beta blockers were administered together with the combination of valsartan + captopril, valsartan alone, or captopril alone.
Ma kienx hemm differenza fil- mortalità minn kull kawża, mortalità kardjovaskulari jew morbidità meta imblokkaturi tar- riċetturi beta ingħataw flimkien mat- taħlita ta ’ valsartan + captopril, valsartan waħdu, jew captopril waħdu.
Irrespective of treatment, mortality was lower in the group of patients treated with a beta blocker, suggesting that the known beta blocker benefit in this population was maintained in this trial.
Irrispettivament mill- kura, il- mortalità kienet aktar baxxa fil- grupp ta ’ pazjenti kkurati b’ imblokkatur tar- riċetturi beta, li jissuġġerixxi li l- benefiċċju magħruf ta ’ imblokkatur tar- riċetturi beta f’ din il- popolazzjoni nżamm f’ din il- prova.
Heart failure Val-HeFT was a randomised, controlled, multinational clinical trial of valsartan compared with placebo on morbidity and mortality in 5,010 NYHA class II (62%), III (36%) and IV (2%) heart failure patients receiving usual therapy with LVEF< 40% and left ventricular internal diastolic diameter (LVIDD) > 2.9 cm/m2.
Insuffiċjenza tal- qalb Val- HeFT kienet prova klinika multinazzjonali, randomised, ikkontrollata ta ’ valsartan imqabbel ma ’ plaċebo dwar il- morbidità u l- mortalità f’ 5, 010 pazjenti b’ insuffiċjenza tal- qalb ta ’ klassi NYHA II (62%), III (36%) u IV (2%) li rċevew it- terapija tas- soltu b’ LVEF ta ’ < 40% u b’ dijametru dijastoliku intern tal- ventriklu tax- xellug (LVIDD) ta ’ > 2. 9 cm/ m2.
Baseline therapy included ACE inhibitors (93%), diuretics (86%), digoxin (67%) and beta blockers (36%).
Terapija fil- linja bażi kienet tinkludi inibituri ta ’ ACE (93%), dijuretiċi (86%), digoxin (67%) u imblokkaturi tar- riċetturi beta (36%).
The mean duration of follow-up was nearly two years.
It- tul medju tal- vista ta ’ wara kien kważi sentejn.
The mean daily dose of Diovan in Val-HeFT was 254 mg.
Id- doża medja ta ’ kuljum ta ’ Diovan f’ Val- HeFT kienet ta ’ 254 mg.
The study had two primary endpoints: all cause mortality (time to death) and composite mortality and heart failure morbidity (time to first morbid event) defined as death, sudden death with resuscitation, hospitalisation for heart failure, or administration of intravenous inotropic or vasodilator agents for four hours or more without hospitalisation.
L- istudju kellu żewġ riżultati tat- tmiem l- aktar importanti: mortalità minn kull kawża (żmien sal- mewt) u mortalità komposta u morbidità kkawżata minn insuffiċjenza tal- qalb (żmien sa l- ewwel avveniment ta ’ morbidità) definit bħala mewt, mewt f’ daqqa b’ risuxxitazzjoni, dħul l- isptar minħabba insuffiċjenza tal- qalb, jew għoti ta ’ mediċini inotropiċi jew vażodilataturi ġol- vini għal erba ’ sigħat jew aktar mingħajr dħul l- isptar.
All cause mortality was similar (p=NS) in the valsartan (19.7%) and placebo (19.4%) groups.
Mortalità minn kull kawża kienet simili (p=NS) fil- gruppi ta ’ valsartan (19. 7%) u tal- plaċebo (19. 4%).
The primary benefit was a 27.5% (95% CI:
Il- benefiċċju l- aktar importanti kien tnaqqis ta ’ 27. 5% (95% CI:
17 to 37%) reduction in risk for time to first heart failure hospitalisation (13.9% vs.
17 sa 37%) fir- riskju għaż- żmien sa l - ewwel dħul fl- isptar minħabba insuffiċjenza tal- qalb (13. 9% vs.
18.5%).
18. 5%).
Results appearing to favour placebo (composite mortality and morbidity was 21.9% in placebo vs.
Riżultati li jidrhu jiffavorixxu plaċebo (mortalità u morbidità komposta kienu 21. 9% fil- plaċebo vs.
25.4% in valsartan group) were observed for those patients receiving the triple combination of an ACE inhibitor, a beta blocker and valsartan.
25. 4% fil- grupp ta ’ valsartan) kienu osservati għal dawk il- pazjenti li rċevew it- taħlita tripla ta ’ inibitur ta ’ ACE, imblokkatur tar - riċetturi beta u valsartan.
In this subgroup all-cause mortality was significantly reduced with valsartan compared to placebo by
Il- benefiċċji għall- morbidità kienu l- akbar f’ sottogrupp ta ’ pazjenti li ma kienux qed jirċievu inibitur ta ’ ACE (n=366).
38 33% (95% CI: – 6% to 58%) (17.3% valsartan vs.
F’ dan is- sottogrupp il- mortalità minn kull kawża kienet imnaqqsa b’ mod sinifikanti b’ valsartan bi 33% (95% CI: – 6% sa 58%) meta mqabbel mal- plaċebo (17. 3% valsartan vs.
42.5% placebo).
27. 1% plaċebo) u r- riskju kompost ta ’ mortalità u morbidità kien imnaqqas b’ mod sinifikanti b’ 44% (24. 9% valsartan vs.
In patients receiving an ACE inhibitor without a beta-blocker, all cause mortality was similar (p=NS) in the valsartan (21.8%) and placebo (22.5%) groups.
F’ pazjenti li rċevew inibitur ta ’ ACE mingħajr imblokkatur tar- riċetturi beta, il- mortalità minn kull kawża kienet simili (p=NS) fil- gruppi ta ’ valsartan (21. 8%) u plaċebo (22. 5%).
Composite mortality and morbidity risk was significantly reduced by 18.3% (95% CI:
Ir- riskju ta ’ mortalità u morbidità komposta kien imnaqqas b’ mod sinifikanti bi 18. 3% (95% CI:
8% to 28%) with valsartan compared with placebo (31.0% vs.
8% sa 28%) b’ valsartan meta mqabbel mal- plaċebo (31. 0% vs.
36.3%).
36. 3%).
In the overall Val-HeFT population, valsartan treated patients showed significant improvement in NYHA class, and heart failure signs and symptoms, including dyspnoea, fatigue, oedema and rales compared to placebo.
Fil- popolazzjoni globali Val- HeFT, pazjenti kkurati b’ valsartan urew titjib sinifikanti fil- klassi ta ’ NYHA, u fis- sinjali u sintomi ta ’ insuffiċjenza tal- qalb, inkluż qtugħ ta ’ nifs, għeja, edima u tħarħir meta mqabbel mal- plaċebo.
Patients treated with valsartan had a better quality of life as demonstrated by change in the Minnesota Living with Heart Failure Quality of Life score from baseline at endpoint than placebo.
Pazjenti kkurati b’ valsartan kellhom kwalità ta ’ ħajja aħjar kif muri mill - bidla fil- punteġġ Minnesota Living with Heart Failure Quality of Life mil- linja bażi fir- riżultat tat - tmiem meta mqabbel mal- plaċebo.
Ejection fraction in valsartan treated patients was significantly increased and LVIDD significantly reduced from baseline at endpoint compared to placebo.
Il- frazzjoni ta ’ tfiħ ’ il barra f’ pazjenti kkurati b’ valsartan kienet miżjuda b’ mod sinifikanti u LVIDD kien imnaqqas b’ mod sinifikanti mil- linja bażi fir- riżultat tat - tmiem meta mqabbel mal- plaċebo.
Hypertension Administration of Diovan to patients with hypertension results in reduction of blood pressure without affecting pulse rate.
Pressjoni għolja L- għoti ta ’ Diovan lill- pazjenti bi pressjoni għolja jwassal għal tnaqqis fil- pressjoni tad- demm mingħajr effett fuq ir- rata tal- polz.
In most patients, after administration of a single oral dose, onset of antihypertensive activity occurs within 2 hours, and the peak reduction of blood pressure is achieved within 4-6 hours.
Fil- biċċa l- kbira tal- pazjenti, wara l- għoti ta ’ doża orali waħda, il- bidu ta ’ l- attività li tbaxxi l- pressjoni għolja sseħħ fi żmien sagħtejn, u l- massimu ta ’ tnaqqis fil- pressjoni tad- demm jintlaħaq fi żmien 4 - 6 sigħat.
The antihypertensive effect persists over 24 hours after dosing.
L- effett li jbaxxi l- pressjoni għolja jippersisti għal aktar minn 24 siegħa wara d- dożaġġ.
During repeated dosing, the antihypertensive effect is substantially present within 2 weeks, and maximal effects are attained within 4 weeks and persist during long-term therapy.
Waqt dożaġġ ripetut, l- effett li jbaxxi l- pressjoni għolja huwa preżenti b’ mod sostanzjali fi żmien ġimagħtejn, u l- effetti massimi jintlaħqu fi żmien 4 ġimgħat u jippersistu waqt terapija fit- tul.
Combined with hydrochlorothiazide, a significant additional reduction in blood pressure is achieved.
F’ taħlita ma ’ hydrochlorothiazide, jintlaħaq tnaqqis addizzjonali sinifikanti fil- pressjoni tad- demm.
Abrupt withdrawal of Diovan has not been associated with rebound hypertension or other adverse clinical events.
Twaqqif f’ daqqa ta ’ Diovan ma kienx assoċjat ma ’ dehra mill- ġdid ta ’ pressjoni għolja jew avvenimenti kliniċi avversi oħra.
In hypertensive patients with type 2 diabetes and microalbuminuria, valsartan has been shown to reduce the urinary excretion of albumin.
F’ pazjenti bi pressjoni għolja b’ dijabete tat- tip 2 u b’ mikroalbuminurja, valsartan intwera li jnaqqas it - tneħħija ta ’ l- albumina fl- awrina.
The MARVAL (Micro Albuminuria Reduction with Valsartan) study assessed the reduction in urinary albumin excretion (UAE) with valsartan (80-160 mg/ od) versus amlodipine (5-10 mg/ od), in 332 type 2 diabetic patients (mean age:
37 ivvaluta t- tnaqqis fit- tneħħija ta ’ l- albumina fl- awrina (UAE) b’ valsartan (80- 160 mg/ od) kontra amlodipine (5- 10 mg/ od), f’ 332 pazjent b’ dijabete tat- tip 2 (età medja:
58 years; 265 men) with microalbuminuria (valsartan:
58 sena; 265 raġel) b’ mikroalbuminurja (valsartan:
55.4 µg/ min), normal or high blood pressure and with preserved renal function (blood creatinine < 120 µmol/ l).
55. 4 µg/ min), bi pressjoni tad- demm normali jew għolja u b’ funzjoni renali ppreservata (krejatinina fid- demm < 120 µmol/ l).
At 24 weeks, UAE was reduced (p < 0.001) by 42% (– 24.2 µg/ min; 95% CI: – 40.4 to – 19.1) with valsartan and approximately 3% (– 1.7 µg/ min; 95% CI: – 5.6 to 14.9) with amlodipine despite similar rates of blood pressure reduction in both groups.
Wara 24 ġimgħa, l - UAE kienet imnaqqsa (p < 0. 001) b’ 42% (– 24. 2 µg/ min; 95% CI: – 40. 4 sa – 19. 1) b’ valsartan u b’ madwar 3% (– 1. 7 µg/ min; 95% CI: – 5. 6 sa 14. 9) b’ amlodipine minkejja rati simili ta ’ tnaqqis fil - pressjoni tad- demm fiż- żewġ gruppi.
The Diovan Reduction of Proteinuria (DROP) study further examined the efficacy of valsartan in reducing UAE in 391 hypertensive patients (BP=150/ 88 mmHg) with type 2 diabetes, albuminuria (mean=102 µg/ min; 20-700 µg/ min) and preserved renal function (mean serum creatinine = 80 µmol/ l).
L- istudju Diovan Reduction of Proteinuria (DROP) kompla jeżamina l- effikaċja ta ’ valsartan biex inaqqas l- UAE f’ 391 pazjent bi pressjoni għolja (BP=150/ 88 mmHg) u b’ dijabete tat- tip 2, albuminurja (medja=102 µg/ min; 20- 700 µg/ min) u b’ funzjoni renali ppreservata (medja tal - krejatinina fis- serum = 80 µmol/ l).
Patients were randomized to one of 3 doses of valsartan (160, 320 and 640 mg/ od) and treated for 30 weeks.
Il- pazjenti kienu randomised għal waħda minn 3 dożi ta ’ valsartan (160, 320 u 640 mg/ od) u kkurati għal 30 ġimgħa.
The purpose of the study was to determine the optimal dose of valsartan for reducing UAE in hypertensive patients with type 2 diabetes.
L- iskop ta ’ l- istudju kien li jiddetermina l- aħjar doża ta ’ valsartan biex inaqqas l- UAE f’ pazjent bi pressjoni għolja b’ dijabete tat- tip 2.
At 30 weeks, the percentage change in UAE was significantly reduced by 36% from baseline with valsartan 160 mg (95%CI:
Wara 30 ġimgħa, il- persentaġġ tal- bidla fil- UAE kien imnaqqas b’ mod sinifikanti b’ 36% mil- linja bażi b’ valsartan 160 mg (95% CI:
22 to 47%), and by 44% with valsartan 320 mg (95%CI:
22 sa 47%), u b’ 44% b’ valsartan 320 mg (95% CI:
31 to 54%).
31 sa 54%).
It was concluded that 160-320 mg of valsartan produced clinically relevant reductions in UAE in hypertensive patients with type 2 diabetes.
Kien konkluż li 160- 320 mg ta ’ valsartan ipproduċa tnaqqis ta ’ rilevanza klinika fil- UAE f’ pazjent bi pressjoni għolja b’ dijabete tat- tip 2.
There was no difference between valsartan and captopril in all-cause mortality based on age, gender,
Ma kienx hemm differenza bejn valsartan u captopril fil- mortalità minn kull kawża bbażat fuq età, sess, razza, terapiji fil- linja bażi jew marda li hemm preżenti.
Discontinuations due to various types of renal dysfunction occurred in 1.1% of valsartan-treated patients, 1.3% in valsartan+captopril patients, and 0.8% of captopril patients.
Twaqqif minħabba tipi differenti ta ’ disfunzjoni renali seħħ f’ 1. 1% tal- pazjenti kkurati b’ valsartan, f’ 1. 3% tal- pazjenti kkurati b’ valsartan+captopril, u f’ 0. 8% tal - pazjenti kkurati b’ captopril.
Irrespective of treatment, mortality was lower in the group of patients treated with a beta blocker, suggesting that the known beta blocker benefit in this population was maintained in this trial.
Irrispettivament mill- kura, il- mortalità kienet aktar baxxa fil- grupp ta ’ pazjenti kkurati b’ imblokkatur tar- riċetturi beta, li jissuġġerixxi li l- benefiċċju magħruf ta ’ imblokkatur tar- riċetturi beta f’ din il- popolazzjoni inżamm f’ din il- prova.
Heart failure Val-HeFT was a randomised, controlled, multinational clinical trial of valsartan compared with placebo on morbidity and mortality in 5,010 NYHA class II (62%), III (36%) and IV (2%) heart failure patients receiving usual therapy with LVEF< 40% and left ventricular internal diastolic diameter (LVIDD) > 2.9 cm/m2.
Insuffiċjenza tal- qalb Val- HeFT kienet prova klinika multinazzjonali, randomised, ikkontrollata ta ’ valsartan imqabbel ma ’ plaċebo dwar il- morbidità u l- mortalità f’ 5, 010 pazjenti b’ insuffiċjenza tal- qalb ta ’ klassi NYHA II (62%), III (36%) u IV (2%) li rċevew it- terapija tas- soltu b’ LVEF ta ’ < 40% u b’ dijametru dijastoliku intern tal- ventriklu tax- xellug (LVIDD) ta ’ > 2. 9 ċm/ m2.
The mean daily dose of Diovan in Val-HeFT was 254 mg.
Id- doża medja ta ’ kuljum ta ’ Diovan f’ Val- HeFT kienet ta ’
In a subgroup of patients not receiving an ACE inhibitor (n=366), the morbidity benefits were greatest.
Il- benefiċċji għall- morbidità kienu l- akbar f’ sottogrupp ta ’ pazjenti li ma kienux qed jirċievu inibitur ta ’ ACE (n=366).
In this subgroup all-cause mortality was significantly reduced with valsartan compared to placebo by 33% (95% CI: – 6% to 58%) (17.3% valsartan vs.
F’ dan is- sottogrupp il- mortalità minn kull kawża kienet imnaqqsa b’ mod sinifikanti b’ valsartan bi 33% (95% CI: – 6% sa 58%) meta mqabbel mal- plaċebo (17. 3% valsartan vs.
42.5% placebo).
27. 1% plaċebo) u r- riskju kompost ta ’ mortalità u morbidità kien imnaqqsas b’ mod sinifikanti b’ 44% (24. 9% valsartan vs.
40 Abrupt withdrawal of Diovan has not been associated with rebound hypertension or other adverse clinical events.
Twaqqif f’ daqqa ta ’ Diovan ma kienx assoċjat ma ’ dehra mill- ġdid ta ’ pressjoni għolja jew avvenimenti kliniċi avversi oħra.
The MARVAL (Micro Albuminuria Reduction with Valsartan) study assessed the reduction in urinary albumin excretion (UAE) with valsartan (80-160 mg/ od) versus amlodipine (5-10 mg/ od), in 332 type 2 diabetic patients (mean age:
L- istudju MARVAL (Micro Albuminuria Reduction with Valsartan) ivvaluta t- tnaqqis fit- tneħħija ta ’ l- albumina fl- awrina (UAE) b’ valsartan (80- 160 mg/ od) kontra amlodipine (5- 10 mg/ od), f’ 332 pazjent b’ dijabete tat- tip 2 (età medja:
Patients were randomized to one of 3 doses of valsartan (160, 320 and 640 mg/ od) and treated for 30 weeks.
Il- pazjenti kienu randomised għal waħda minn 3 dożi ta ’ valsartan (160, 320 u 640 mg mg (95% CI:
5.2 Pharmacokinetic properties
39 5. 2 Tagħrif farmakokinetiku
Following oral administration of valsartan alone, peak plasma concentrations of valsartan are reached in 2– 4 hours.
Wara għoti orali ta ’ valsartan waħdu, il- konċentrazzjonijiet massimi ta ’ valsartan fil- plażma jintlaħqu fi żmien 2– 4 sigħat.
Mean absolute bioavailability is 23%.
Il- bijodisponibiltà assoluta medja hija ta ’ 23%.
Food decreases exposure (as measured by AUC) to valsartan by about 40% and peak plasma concentration (C max) by about 50%, although from about 8 h post dosing plasma valsartan concentrations are similar for the fed and fasted groups.
L- ikel inaqqas l- espożizzjoni (kif imkejjel mill- AUC) għal valsartan b’ madwar 40% u l- konċentrazzjoni massima fil- plażma (C max) b’ madwar 50%, għalkemm minn madwar 8 h wara d- dożaġġ konċentrazzjonijiet ta ’ valsartan fil - plażma huma simili għall- gruppi mitmuma u sajma.
This reduction in AUC is not, however, accompanied by a clinically significant reduction in the therapeutic effect, and valsartan can therefore be given either with or without food.
Madankollu, dan it- tnaqqis fl- AUC mhux akkompanjat minn tnaqqis ta ’ sinifikanza klinika fl- effett terapewtiku, u għalhekk valsartan jista ’ jingħata ma ’ l- ikel jew mingħajr ikel.
The steady-state volume of distribution of valsartan after intravenous administration is about 17 litres, indicating that valsartan does not distribute into tissues extensively.
Il- volum ta ’ distribuzzjoni fi stat fiss ta ’ valsartan wara għoti ġol- vini huwa ta ’ madwar 17- il litru, u dan jindika li ma sseħħx distribuzzjoni estensiva ta ’ valsartan fit- tessuti.
Valsartan is highly bound to serum proteins (94– 97%), mainly serum albumin.
Valsartan huwa mwaħħal ħafna mal- proteini fis- serum (94– 97%), l- aktar ma ’ l- albumina fis- serum.
Valsartan is not biotransformed to a high extent as only about 20% of dose is recovered as metabolites.
Valsartan ma jiġix bijotrasformat b’ mod estensiv peress li madwar 20% biss tad- doża hija rkuprata bħala metaboliti.
A hydroxy metabolite has been identified in plasma at low concentrations (less than 10% of the valsartan AUC).
Metabolit hydroxy kien identifikat fil- plażma f’ konċentrazzjonijiet baxxi (inqas minn 10% ta ’ l- AUC ta ’ valsartan).
This metabolite is pharmacologically inactive.
Dan il- metabolit mhux attiv farmakoloġikament.
Valsartan shows multiexponential decay kinetics (t ½α < 1 h and t ½ß about 9 h).
Valsartan juri kinetika ta ’ diżintegrazzjoni multiesponenzjali (t ½α < 1 h u t ½ß madwar 9 h).
Valsartan is primarily eliminated by biliary excretion in faeces (about 83% of dose) and renally in urine (about 13% of dose), mainly as unchanged drug.
Valsartan huwa eliminat primarjament permezz ta ’ eskrezzjoni biljari fl- ippurgar (madwar 83% tad- doża) u renali fl- awrina (madwar 13% tad- doża), l- aktar bħala mediċina mhux mibdula.
Following intravenous administration, plasma clearance of valsartan is about 2 l/ h and its renal clearance is 0.62 l/ h (about 30% of total clearance).
Wara għoti ġol- vini, tneħħija mill- plażma ta ’ valsartan hija madwar 2 l/ h u t- tneħħija renali tiegħu hija 0. 62 l/ h (madwar 30% tat- tneħħija totali).
The half-life of valsartan is 6 hours.
Il- half- life ta ’ valsartan hija 6 sigħat.
In Heart failure patients:
F’ pazjenti b’ insuffiċjenza tal- Qalb:
The average time to peak concentration and elimination half-life of valsartan in heart failure patients are similar to that observed in healthy volunteers.
Il- medja ta ’ ħin sal- konċentrazzjoni massima u l- half- life ta ’ l- eliminazzjoni ta ’ valsartan f’ pazjenti b’ insuffiċjenza tal- qalb huma simili għal dawk osservati f’ voluntiera b’ saħħithom.