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Hypertension and cognitive function: pathophysiologic effects of hypertension on the brain
Manolio TA, Olson J, Longstreth WT.. Current hypertension reports, 2003-06-01
Topic: Risk, prevention and care in population studies
Accumulating evidence supports a causal role of hypertension for cognitive decline above and beyond its relationship to frank stroke. Hypertension-associated pathologic changes in the brain and its vasculature include vascular remodeling, impaired cerebral autoregulation, cerebral microbleeds, white matter lesions, unrecognized lacunar infarcts, and Alzheimer-like changes such as amyloid angiopathy and cerebral atrophy. White matter lesions and retinal vascular changes, both of which can be imaged noninvasively, may reveal the general condition of the cerebral vasculature or the presence of arteriosclerotic or hypertensive encephalopathy. These noninvasive indicators may also identify a subgroup in whom infarct prevention, particularly via blood pressure reduction, is of paramount importance. Optimal control of blood pressure on a population-wide basis, but particularly in those prone to cognitive loss, is thus a critically important but as yet elusive goal that should be fully exploited for its potential to reduce future cognitive impairment.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Manolio, T. A., Olson, J., & Longstreth, W. T. (2003). Hypertension and cognitive function: pathophysiologic effects of hypertension on the brain. Current hypertension reports. https://doi.org/10.1007/s11906-003-0029-6
Vancouver
Manolio TA, Olson J, Longstreth WT. Hypertension and cognitive function: pathophysiologic effects of hypertension on the brain. Current hypertension reports. 2003. doi:10.1007/s11906-003-0029-6. PMID: 12724059.
BibTeX
@article{manolio2003-12724059,
author = {Manolio, T. A. and Olson, J. and Longstreth, W. T.},
title = {{Hypertension and cognitive function: pathophysiologic effects of hypertension on the brain}},
journal = {Current hypertension reports},
year = {2003},
doi = {10.1007/s11906-003-0029-6},
pmid = {12724059},
url = {https://doi.org/10.1007/s11906-003-0029-6}
}
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Key findings
- Accumulating evidence supports a causal role of hypertension for cognitive decline above and beyond its relationship to frank stroke.
- Hypertension-associated pathologic changes in the brain and its vasculature include vascular remodeling, impaired cerebral autoregulation, cerebral microbleeds, white matter lesions, unrecognized lacunar infarcts, and Alzheimer-like changes such as amyloid angiopathy and cerebral atrophy.
- White matter lesions and retinal vascular changes, both of which can be imaged noninvasively, may reveal the general condition of the cerebral vasculature or the presence of arteriosclerotic or hypertensive encephalopathy.
- These noninvasive indicators may also identify a subgroup in whom infarct prevention, particularly via blood pressure reduction, is of paramount importance.
- Optimal control of blood pressure on a population-wide basis, but particularly in those prone to cognitive loss, is thus a critically important but as yet elusive goal that should be fully exploited for its potential to reduce future cognitive impairment.
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Study details
- Evidence strengthLow
How this study scored 36/100
Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported, studied in people and randomised / blinded because the record does not state it. We have no data on journal's citation record, times cited, citations per year, impact for its field and year, cited by studies here, still being cited, senior author's track record, institution's track record and multi-centre collaboration, so those were left out: it earned 21 of the 58 points we could judge it on, which is 36 out of 100.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Current hypertension reports) |
| Journal's citation record | — / 4 | No journal record from OpenAlex — left out of this score |
| Study design | 0 / 12 | No study design recorded — scores zero, not guessed (not stated in the record — scored 0) |
| Strength of evidence | 1 / 5 | Rated “low” in our summary |
| Peer-review validation | 10 / 10 | Peer-reviewed. Published as an article in a named peer-reviewed journal. |
| How recent | 1 / 5 | 2003 — older than 20 years, still counted |
| Sample size | 0 / 4 | Participant count not stated — scores zero (not stated in the record — scored 0) |
| Effect reported | 0 / 3 | No effect size reported — scores zero (not stated in the record — scored 0) |
| Studied in people | 0 / 3 | Not stated whether this was studied in people — scores zero (not stated in the record — scored 0) |
| Randomised / blinded | 0 / 2 | No randomisation or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | — / 7 | No citation count (not found in OpenAlex) — left out of this score |
| Citations per year | — / 5 | No citation count or no year — left out of this score |
| Impact for its field and year | — / 6 | No field-weighted citation impact (OpenAlex has none yet) — left out of this score |
| Cited by studies here | — / 6 | Not yet checked against this library's citation graph — left out of this score |
| Still being cited | — / 4 | No yearly citation counts — left out of this score |
| Senior author's track record | — / 4 | Senior author's record not available — left out of this score |
| Institution's track record | — / 3 | No institution listed in OpenAlex — left out of this score |
| Multi-centre collaboration | — / 3 | Institutions not listed — left out of this score |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 12724059) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Points | 21 / 58 | Scored on 11 of 20 parts. We have no data for the rest, so they are left out: 21 of the 58 points we could judge it on is 36 out of 100. |
| Total | 36 / 100 | — |
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