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unstabil angina, aortaklapregur- gitation, aterosklerose af koronararterier, sinusbradykardi, ventrikulær hypertrofi
angina unstable, aortic valve incompetence, coronary artery atherosclerosis, sinus bradycardia, ventricular hypertropy
de påviste risikofaktorer hos disse patienter var anamnestisk aterosklerose og/eller myokardieinfarkt eller kongestivt hjertesvigt.
identified risk factors among these patients were a medical history of atherosclerotic disease and/or myocardial infarction, or of congestive heart failure.
prasugrels farmakokinetik er ens hos raske forsøgspersoner, patienter med stabil aterosklerose og patienter, som gennemgår perkutant koronarindgreb.
prasugrel’s pharmacokinetics are similar in healthy subjects, patients with stable atherosclerosis, and patients undergoing percutaneous coronary intervention.
foruden leversygdom oplever patienter med lal-mangel en øget risiko for hjerte-karsygdomme og accelereret aterosklerose.
in addition to liver disease, patients with lal deficiency experience increased risk for cardiovascular disease and accelerated atherosclerosis.
hvis du lider af åreforkalkning ("aterosklerose"), er der en øget risiko for, at der dannes blodpropper i dine blodårer.
if you suffer from hardening of the arteries (“atherosclerosis”) there is an increased risk of a blood clot forming in your blood vessels.
i begge tilfælde blev der for 89% af de raske forsøgspersoner og patienter med stabil aterosklerose opnået mindst 50% hæmning af trombocytaggregering efter 1 time.
the maximum inhibition by prasugrel of adp-induced platelet aggregation is 83% with 5 µm adp and 79% with 20 µm adp, in both cases with 89% of healthy subjects and patients with stable atherosclerosis achieving at least 50% inhibition of platelet aggregation by 1 hour.
det antages, at hdl deltager i transporten af kolesterol fra vævene tilbage til leveren for at hæmme vaskulær inflammation, der er forbundet med aterosklerose, og for at have antioxidativ og antitrombotisk effekt.
hdl is hypothesised to participate in the transport of cholesterol from tissues back to the liver, to suppress vascular inflammation associated with atherosclerosis, and to have anti-oxidative and anti-thrombotic effects.
hos raske forsøgspersoner, patienter med stabil aterosklerose og patienter med aks, som fik efient, gav genetisk variation i cyp3a5, cyp2b6, cyp2c9 eller cyp2c19 ingen relevant virkning på prasugrels farmakokinetik eller dets hæmning af trombocytaggregeringen.
in healthy subjects, patients with stable atherosclerosis, and patients with acs receiving efient, there was no relevant effect of genetic variation in cyp3a5, cyp2b6, cyp2c9, or cyp2c19 on the pharmacokinetics of prasugrel or its inhibition of platelet aggregation.
et-1 koncentrationer i væv og plasma er forhøjede ved flere kardiovaskulære sygdomme og bindevævssygdomme, inklusive pulmonal arteriel hypertension, sklerodermi, akut og kronisk hjerteinsufficiens, myokardieiskæmi, systemisk hypertension og aterosklerose, hvilket kunne tyde på, at et- 1 spiller en patogen rolle i forbindelse med disse sygdomme.
et-1 concentrations in tissues and plasma are increased in several cardiovascular disorders and connective tissue diseases, including pulmonary arterial hypertension, scleroderma, acute and chronic heart failure, myocardial ischaemia, systemic hypertension and atherosclerosis, suggesting a pathogenic role of et-1 in these diseases.
