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effect on cardiac repolarisation
effett fuq ir-ripolarizzazzjoni kardijaka

cardiac conduction and repolarisation abnormalities:
anomalitajiet fit-trasmissjoni u fir-polarizzazzjoni mill-ġdid tal-qalb:

ventricular repolarisation abnormalities may have been contributory factors.
anormalitajiet ta’ polarizzazzjoni mill-ġdid tal-ventrikulu setgħu kienu fatturi li kkontribwixxew għal dan.

general physical condition abnormal electrocardiogram repolarisation abnormality electrocardiogram t wave inversion
kundizzjoni fiżika ġenerali mhux normali anormalità fir- ripolarizzazzjoni tal- elettrokardjogramma inverżjoni tal-mewġa t tal- elettrokardjogramma

a qtc study in healthy volunteers dosed 150 mg eltrombopag per day did not show a clinically significant effect on cardiac repolarisation.
studju tal-qtc f’voluntiera b’saħħithom li kienu qed jirċievu doża ta’ 150 mg eltrombopag kuljum ma weriex effett klinikament sinifikanti fuq ir-ripolarizzazzjoni kardijaka.

in contrast, similar concentrations of lopinavir/ritonavir demonstrated no repolarisation delay in the canine cardiac purkinje fibres.
b’kuntrast, konċentrazzjonijiet simili ta’ lopinavir/ritonavir ma’ urew l-ebda dewmien fir-ripolarizzazjoni fil-fibri kardijaċi purkinje tal-klieb.

non clinical in vitro and in vivo studies have evidenced the potential of toremifene and its metabolite to prolong cardiac repolarisation and this can be attributed to the blockade of herg channels.
studji in vitro u in vivo li mhumiex kliniċi taw evidenza tal-potenzjal ta’ toremifene u l-metabolit tiegħu biex itawlu r-ripolarizzazzjoni tal-qalb u dan jista’ jiġi attribwit għall-imblokk tal-kanali herg.

additionally, the ability of vernakalant to block the late component of the sodium current limits effects on ventricular repolarisation induced by blockade of potassium currents in the ventricle.
barra minn hekk, l-abbiltà ta’ vernakalant li jimblokka l-komponent tardiv tal-kurrent tas-sodju, tillimita l- effetti fuq ir-ripolarizzazzjoni ventrikolari kkawżata mill-imblokk tal-kurrenti ta’ potassju fil- ventrikolu.

dasatinib activity in vitro in herg and purkinje fiber assays suggested a potential for prolongation of cardiac ventricular repolarisation (qt interval).
l-attività in vitro ta’ dasatinib f’analiżi herg u purkinje fiber issuġġeriet potenzjal għal titwil tar-ripolarizzazzjoni ventrikulari kardijaka (intervall qt).

the cardiac effects are specific to the sinus node with no effect on intra-atrial, atrioventricular or intraventricular conduction times, nor on myocardial contractility or ventricular repolarisation.
l-effetti kardijaċi huma speċifiċi fuq is- sinus node b’ebda effett fuq il-ħin biex jgħaddi l-istimulu intra-atrijali, atrijuventrikulari jew intraventrikulari, la fuq it-tagħfis mijokardijaku u lanqas fuq ir-ripolarizzazzjoni ventrikulari.

a study of the effect of teysuno on cardiac repolarisation conducted in advanced cancer patients met the definition for a negative study according to international conference on harmonisation (ich) guidelines.
studju dwar l-effett ta' teysuno fuq ripolarizzazzjoni kardijaka li saret f'pazjenti b'kanċer avvanzat issodisfat it-tifsira għal studju negattiv skont il-linji gwida tal-konferenza internazzjonali dwar l-armonizzazzjoni (ich).

in a thorough qt study in healthy subjects, there was no indication of a qt/qtc prolonging effect of ruxolitinib in single doses up to a supratherapeutic dose of 200 mg, indicating that ruxolitinib has no effect on cardiac repolarisation.
waqt studju profond tal-qt f’pazjenti b’saħħithom, ma kienx hemm indikazzjoni li l-effett ta' qt/qtc twal minn dożi singoli sa doża supraterapewtika b'ruxolitinib ta' 200 mg, u dan jindika li ruxolitinib m’għandu l-ebda effett fuq ir-ripolarizzazzjoni kardijaka.

supratherapeutic concentrations of the active metabolite of fesoterodine, have been shown to inhibit k+ current in cloned human ether-à-go-go-related gene (herg) channels and prolong action potential duration (70% and 90% repolarisation) in canine isolated purkinje fibres.
konċentrazzjonijiet supraterapewtiċi tal-metabolit attiv ta’ fesoterodine, urew li jimpedixxu l-kurrent k+ f’kanali fil-ġene uman ikklownjat ether-à-go-go (herg) u wkoll żieda fit-tul ta’ l-azzjoni potenzjali (ripolariżazzjoni 70% u 90%) fil-fibri ta’ purkinje iżolati mill-klieb.