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| Fältnamn | Indikatorer | Metadata |
|---|---|---|
| 000 | 06833naa a2201249 4500 | |
| 001 | oai:gup.ub.gu.se/284857 | |
| 003 | SwePub | |
| 008 | 240528s2019 | |||||||||||000 ||eng| | |
| 024 | 7 | a https://gup.ub.gu.se/publication/2848572 URI |
| 024 | 7 | a https://doi.org/10.1161/jaha.119.0119382 DOI |
| 040 | a (SwePub)gu | |
| 041 | a eng | |
| 042 | 9 SwePub | |
| 072 | 7 | a ref2 swepub-contenttype |
| 072 | 7 | a art2 swepub-publicationtype |
| 100 | 1 | a de Heus, R. A. A.4 aut |
| 245 | 1 0 | a Blood Pressure Lowering With Nilvadipine in Patients With Mild-to-Moderate Alzheimer Disease Does Not Increase the Prevalence of Orthostatic Hypotension |
| 264 | 1 | b Ovid Technologies (Wolters Kluwer Health),c 2019 |
| 520 | a Background-Hypertension is common among patients with Alzheimer disease. Because this group has been excluded from hypertension trials, evidence regarding safety of treatment is lacking. This secondary analysis of a randomized controlled trial assessed whether antihypertensive treatment increases the prevalence of orthostatic hypotension (OH) in patients with Alzheimer disease. Methods and Results-Four hundred seventy-seven patients with mild-to-moderate Alzheimer disease were randomized to the calcium-channel blocker nilvadipine 8 mg/day or placebo for 78 weeks. Presence of OH (blood pressure drop >= 20/>= 10 mm Hg after 1 minute of standing) and OH-related adverse events (dizziness, syncope, falls, and fractures) was determined at 7 follow-up visits. Mean age of the study population was 72.2 +/- 8.2 years and mean Mini-Mental State Examination score was 20.4 +/- 3.8. Baseline blood pressure was 137.8 +/- 14.0/77.0 +/- 8.6 mm Hg. Grade I hypertension was present in 53.4% (n=255). After 13 weeks, blood pressure had fallen by -7.8/-3.9 mm Hg for nilvadipine and by -0.4/-0.8 mm Hg for placebo (P<0.001). Across the 78-week intervention period, there was no difference between groups in the proportion of patients with OH at a study visit (odds ratio [95% CI] 1.1 [0.8-1.5], P 0.62), nor in the proportion of visits where a patient met criteria for OH, corrected for number of visits (7.7 +/- 13.8% versus 7.3 +/- 11.6%). OH-related adverse events were not more often reported in the intervention group compared with placebo. Results were similar for those with baseline hypertension. Conclusions-This study suggests that initiation of a low dose of antihypertensive treatment does not significantly increase the risk of OH in patients with mild-to-moderate Alzheimer disease. | |
| 650 | 7 | a MEDICIN OCH HÄLSOVETENSKAPx Klinisk medicin0 (SwePub)3022 hsv//swe |
| 650 | 7 | a MEDICAL AND HEALTH SCIENCESx Clinical Medicine0 (SwePub)3022 hsv//eng |
| 653 | a adverse drug event | |
| 653 | a Alzheimer disease | |
| 653 | a antihypertensive agent | |
| 653 | a calcium channel blocker | |
| 653 | a orthostatic | |
| 653 | a antihypertensive treatment | |
| 653 | a cognitive impairment | |
| 653 | a consensus statement | |
| 653 | a cardiovascular risk | |
| 653 | a european-society | |
| 653 | a hypertension | |
| 653 | a association | |
| 653 | a management | |
| 653 | a older | |
| 653 | a dementia | |
| 700 | 1 | a Donders, R.4 aut |
| 700 | 1 | a Santoso, A. M. M.4 aut |
| 700 | 1 | a Rikkert, Mgmo4 aut |
| 700 | 1 | a Lawlor, B. A.4 aut |
| 700 | 1 | a Claassen, Jahr4 aut |
| 700 | 1 | a Segurado, R.4 aut |
| 700 | 1 | a Kennelly, S.4 aut |
| 700 | 1 | a Howard, R.4 aut |
| 700 | 1 | a Pasquier, F.4 aut |
| 700 | 1 | a Börjesson-Hanson, Anne,d 1959u Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi, sektionen för psykiatri och neurokemi,Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry4 aut0 (Swepub:gu)xborja |
| 700 | 1 | a Tsolaki, M.4 aut |
| 700 | 1 | a Lucca, U.4 aut |
| 700 | 1 | a Molloy, D. W.4 aut |
| 700 | 1 | a Coen, R.4 aut |
| 700 | 1 | a Riepe, M. W.4 aut |
| 700 | 1 | a Kalman, J.4 aut |
| 700 | 1 | a Kenny, R. A.4 aut |
| 700 | 1 | a Cregg, F.4 aut |
| 700 | 1 | a O'Dwyer, S.4 aut |
| 700 | 1 | a Walsh, C.4 aut |
| 700 | 1 | a Adams, J.4 aut |
| 700 | 1 | a Banzi, R.4 aut |
| 700 | 1 | a Breuilh, L.4 aut |
| 700 | 1 | a Daly, L.4 aut |
| 700 | 1 | a Hendrix, S.4 aut |
| 700 | 1 | a Aisen, P.4 aut |
| 700 | 1 | a Gaynor, S.4 aut |
| 700 | 1 | a Sheikhi, A.4 aut |
| 700 | 1 | a Taekema, D. G.4 aut |
| 700 | 1 | a Verhey, F. R.4 aut |
| 700 | 1 | a Nemni, R.4 aut |
| 700 | 1 | a Nobili, F.4 aut |
| 700 | 1 | a Franceschi, M.4 aut |
| 700 | 1 | a Zanetti, O.4 aut |
| 700 | 1 | a Konsta, A.4 aut |
| 700 | 1 | a Anastasios, O.4 aut |
| 700 | 1 | a Nenopoulou, S.4 aut |
| 700 | 1 | a Tsolaki-Tagarak, F.4 aut |
| 700 | 1 | a Pakaski, M.4 aut |
| 700 | 1 | a Dereeper, O.4 aut |
| 700 | 1 | a de la Sayette, V.4 aut |
| 700 | 1 | a Senechal, O.4 aut |
| 700 | 1 | a Lavenu, I.4 aut |
| 700 | 1 | a Devendeville, A.4 aut |
| 700 | 1 | a Calais, G.4 aut |
| 700 | 1 | a Crawford, F.4 aut |
| 700 | 1 | a Mullan, M.4 aut |
| 700 | 1 | a Aalten, P.4 aut |
| 700 | 1 | a Berglund, M. A.4 aut |
| 700 | 1 | a de Jong, D. L. K.4 aut |
| 700 | 1 | a Godefroy, O.4 aut |
| 700 | 1 | a Hutchinso, S.4 aut |
| 700 | 1 | a Loannou, A.4 aut |
| 700 | 1 | a Jonsson, Michael,d 1955u Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi, sektionen för psykiatri och neurokemi,Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry4 aut0 (Swepub:gu)xjonmi |
| 700 | 1 | a Kent, A.4 aut |
| 700 | 1 | a Kern, Jürgenu Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi, sektionen för psykiatri och neurokemi,Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry4 aut0 (Swepub:gu)xkerju |
| 700 | 1 | a Nemtsas, P.4 aut |
| 700 | 1 | a Panidou, M. K.4 aut |
| 700 | 1 | a Abdullah, L.4 aut |
| 700 | 1 | a Paris, D.4 aut |
| 700 | 1 | a van Spijker, G. J.4 aut |
| 700 | 1 | a Spiliotou, M.4 aut |
| 700 | 1 | a Thomoglou, G.4 aut |
| 700 | 1 | a Wallin, Anders,d 1950u Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi, sektionen för psykiatri och neurokemi,Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry4 aut0 (Swepub:gu)xwaand |
| 700 | 1 | a Frisoni, G.4 aut |
| 700 | 1 | a Nilvad Study, Grp4 aut |
| 710 | 2 | a Göteborgs universitetb Institutionen för neurovetenskap och fysiologi, sektionen för psykiatri och neurokemi4 org |
| 773 | 0 | t Journal of the American Heart Associationd : Ovid Technologies (Wolters Kluwer Health)g 8:10q 8:10x 2047-9980 |
| 856 | 4 | u https://www.ahajournals.org/doi/pdf/10.1161/JAHA.119.011938 |
| 856 | 4 8 | u https://gup.ub.gu.se/publication/284857 |
| 856 | 4 8 | u https://doi.org/10.1161/jaha.119.011938 |
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- Cregg, F.
- O'Dwyer, S.
- Walsh, C.
- Adams, J.
- Banzi, R.
- Breuilh, L.
- Daly, L.
- Hendrix, S.
- Aisen, P.
- Gaynor, S.
- Sheikhi, A.
- Taekema, D. G.
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- Nemni, R.
- Nobili, F.
- Franceschi, M.
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- Konsta, A.
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