| 1 |
Editorial Cognitive impairment and blood pressure: quo usque tandem abutere patientia nostra? free! 2004
Staessen JA, Birkenhäger WH. · No affiliation provided · Hypertension. · Pubmed #15466658 links to free full text
This publication has no abstract.
|
| 2 |
Review Less atherosclerosis and lower blood pressure for a meaningful life perspective with more brain. free! 2007
Staessen JA, Richart T, Birkenhäger WH. · Studies Coordinating Centre, Division of Hypertension and Cardiovascular Rehabilitation, Department of Cardiovascular Diseases, University of Leuven, Leuven, Belgium. · Hypertension. · Pubmed #17283254 links to free full text
This publication has no abstract.
|
| 3 |
Review Progress in cardiovascular diseases: cognitive function in essential hypertension. 2006
Birkenhäger WH, Staessen JA. · Erasmus University, Rotterdam, the Netherlands. · Prog Cardiovasc Dis. · Pubmed #16867845 No free full text.
Abstract: Essential hypertension has rather recently become recognized as a major factor in the development of the 2 main types of dementia, that is, no longer merely vascular dementia but Alzheimer disease as well. The relationship between high blood pressure (BP) and the dementias is quite a complicated one, given a wide variability in temporal courses. The interval between the respective manifestations of hypertension and cognitive deterioration may vary from a few years to several decades. Moreover, temporal relationships may be obscured because of the observation that BP tends to fall in the face of imminent Alzheimer disease. Although the cause-and-effect sequence of this relationship has not been established, it may suggest that a low BP in this phase of life could be equally harmful as hypertension in the preceding period. Individual monitoring of BP and drug titration in the hypertensive elderly may well become mandatory in the highest age group. The question whether some antihypertensive drug categories might act more effectively in preventing cognitive deterioration than others, irrespective of their antihypertensive potential, remains. A modest meta-analysis on our part seems to suggest that suppression of the renin-angiotensin-aldosterone system (RAAS) would fail to offer such protection, in contrast to certain dihydropyridine (DHP) calcium-channel blockers. Unfortunately, recently published comparative prospective megatrials (Anti-hypertensive and Lipid-lowering Treatment to Prevent Heart Attack Trial and Anglo-Scandinavian Cardiac Outcomes Trial-Blood Pressure Lowering Arm) failed to carry any record on the mental status of the study populations, thereby missing a golden opportunity to resolve the above issue. Consequently, there remains an urgent need for further blinded long-term comparative hypertension trials, including follow-up evaluation of cognitive functions in relation to the course of BP.
|
| 4 |
Review Blood pressure and dementia. 2004
Birkenhäger WH, Staessen JA. · Erasmus University, Rotterdam, the Netherlands. · Panminerva Med. · Pubmed #15876979 No free full text.
Abstract: Hypertension has proven to be a major predisposing factor for the development of both vascular and degenerative (Alzheimer's) dementias, either following stroke or gradually through more insidious microcerebrovascular processes. In the latter case the interval between the respective manifestations of hypertension and dementia may vary between a few years and several decades. The temporal relationships may become complicated by the finding that blood pressure tends to fall shortly before the onset of overt Alzheimers' disease. Whether or not timely antihypertensive regimens may delay or even prevent the development of dementias later in life is still an ''educated'' guess, as long there has been no comprehensive trial comparing the potential of the different antihypertensive drug classes in this regard. Until then, the class of dihydropyridine calcium antagonists (exemplified by nitrendipine in the Syst-Eur trial) is the only category having statistically been proven to be of substantial value for prevention of Alzheimer's disease.
|
| 5 |
Review Blood pressure, cognitive functions, and prevention of dementias in older patients with hypertension. free! 2001
Birkenhäger WH, Forette F, Seux ML, Wang JG, Staessen JA. · Faculty of Medicine, Erasmus University Rotterdam, The Netherlands. · Arch Intern Med. · Pubmed #11176727 links to free full text
Abstract: The prevalence and incidence of degenerative and vascular dementias increase exponentially with age, from 70 years onward. In view of the increasing longevity of humans, both varieties are bound to evolve into a major problem worldwide. According to several longitudinal studies, hypertension appears to predispose individuals to the development of cognitive impairment and ensuing dementia, after a period varying from a few years to several decades. Antihypertensive drug treatment, according to preliminary evidence, may serve to reduce the rates of such events. Such findings await to be confirmed by formal therapeutic trials against a backdrop of "historical" observational sources.
|
| 6 |
Clinical Conference The prevention of dementia with antihypertensive treatment: new evidence from the Systolic Hypertension in Europe (Syst-Eur) study. free! 2002
Forette F, Seux ML, Staessen JA, Thijs L, Babarskiene MR, Babeanu S, Bossini A, Fagard R, Gil-Extremera B, Laks T, Kobalava Z, Sarti C, Tuomilehto J, Vanhanen H, Webster J, Yodfat Y, Birkenhäger WH, Anonymous00263. · Department of Geriatrics, Hôpital Broca, CHU Cochin, University of Paris V, 54-56 rue Pascal, 75013 Paris, France. · Arch Intern Med. · Pubmed #12374512 links to free full text
Abstract: BACKGROUND: After the double-blind, placebo-controlled Systolic Hypertension in Europe (Syst-Eur) trial ended in February 1997, randomized patients were offered active study medication for a further period of observation. OBJECTIVE: To refine the estimates of the long-term effects of antihypertensive therapy on the incidence of dementia. METHODS: Eligible patients had no dementia and were at least 60 years old. Their systolic blood pressure at entry was 160 to 219 mm Hg, with diastolic blood pressure below 95 mm Hg. Antihypertensive therapy was started immediately after randomization in the active treatment group, but only after termination of the double-blind trial in the control patients. Treatment consisted of nitrendipine (10-40 mg/d), with the possible addition of enalapril maleate (5-20 mg/d), hydrochlorothiazide (12.5-25 mg/d), or both add-on drugs. RESULTS: Median follow-up increased from 2.0 years in the double-blind trial to 3.9 years overall. The incidence of dementia doubled from 32 to 64 cases, 41 of whom had Alzheimer disease. Throughout follow-up, systolic/diastolic blood pressure was 7.0/3.2 mm Hg higher in the 1417 control patients than in the 1485 subjects randomized to active treatment. At the last examination, the blood pressure difference was still 4.2/2.9 mm Hg; 48.1%, 26.4%, and 11.4% of the control patients were taking nitrendipine, enalapril, and/or hydrochlorothiazide, whereas in the active treatment group these proportions were 70.2%, 35.4%, and 18.4%, respectively. Compared with the controls, long-term antihypertensive therapy reduced the risk of dementia by 55%, from 7.4 to 3.3 cases per 1000 patient-years (43 vs 21 cases, P<.001). After adjustment for sex, age, education, and entry blood pressure, the relative hazard rate associated with the use of nitrendipine was 0.38 (95% confidence interval, 0.23-0.64; P<.001). Treatment of 1000 patients for 5 years can prevent 20 cases of dementia (95% confidence interval, 7-33). CONCLUSION: The extended follow-up of Syst-Eur patients reinforces the evidence that blood pressure-lowering therapy initiated with a long-acting dihydropyridine protects against dementia in older patients with systolic hypertension.
|
| 7 |
Minor Antihypertensives for prevention of Alzheimer's disease. 2006
Birkenhäger WH, Staessen JA. · No affiliation provided · Lancet Neurol. · Pubmed #16713914 No free full text.
This publication has no abstract.
|
| 8 |
Minor Convergence of atherosclerosis and Alzheimer's disease. 2004
Birkenhäger WH, Staessen JA. · No affiliation provided · Lancet. · Pubmed #15207973 No free full text.
This publication has no abstract.
|
| 9 |
Minor Is angiogenesis a plausible hypothesis in Alzheimer's disease? 2003
Birkenhäger WH, Staessen JA. · No affiliation provided · J Hypertens. · Pubmed #12817194 No free full text.
This publication has no abstract.
|
|
|