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Aud Høieggen

Researcher at Oslo University Hospital

Publications -  93
Citations -  2331

Aud Høieggen is an academic researcher from Oslo University Hospital. The author has contributed to research in topics: Blood pressure & Insulin. The author has an hindex of 24, co-authored 83 publications receiving 2149 citations. Previous affiliations of Aud Høieggen include University Hospital of North Norway & University of Oslo.

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The impact of serum uric acid on cardiovascular outcomes in the LIFE study

TL;DR: The increase in SUA over 4.8years in the LIFE study was attenuated by losartan compared with atenolol treatment, appearing to explain 29% of the treatment effect on the primary composite end point.
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Adjusted Drug Treatment Is Superior to Renal Sympathetic Denervation in Patients With True Treatment-Resistant Hypertension

TL;DR: The data suggest that adjusted drug treatment has superior BP lowering effects compared with RDN in patients with true TRH, and Ambulatory BPs changed in parallel to office BPs.
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Evaluation of Adherence Should Become an Integral Part of Assessment of Patients With Apparently Treatment-Resistant Hypertension.

TL;DR: The highly variable BP response to renal denervation (RDN) prompted to a more rigorous evaluation of eligible patients, with the goal to exclude false resistant hypertension, because of poor adherence to drug treatment.
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Renal sympathetic denervation in patients with treatment-resistant hypertension after witnessed intake of medication before qualifying ambulatory blood pressure.

TL;DR: The findings question whether BP falls in response to RDN in patients with true treatment-resistant hypertension, and additional research must aim to verify potential BP lowering effect and identify a priori responders toRDN before this invasive method can routinely be applied to patients with drug- resistant hypertension.
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Whole-blood viscosity and the insulin-resistance syndrome.

TL;DR: Whole-blood viscosity contributes to the total peripheral resistance, and these results support the hypothesis that insulin resistance has a hemodynamic basis.