Función cognitiva y demencia en la hipertensión arterial

As a consequence of aging of the population, cognitive function disorders and dementias are increasing. A total of 90 % correspond to Alzheimer's disease and vascular dementias. For the former, the risk factors are age, family background of dementia and E4 allele of the apolipoprotein E gene. For the vascular dementia one, they are age, male gender, HBP, coronary disease, diabetes, generalized atherosclerosis, smoking, elevated lipid concentration and previous history of stroke. Diagnosis of dementia and cognitive deterioration is based on clinical criteria and tests that lack adequate accuracy. In this sense, modern neuroimaging techniques (CT scan and MRI) are supplying very valuable information, as it relates lacunar infarction and white substance lesions not only to HBP and other cardiovascular risk factors but also to the appearance of dementia. Based on the presently available information, it has been hypothesized that an initially elevated systolic BP would lead to multiple lacunar infarctions and to lesions of the brain white substance that would lead to progressive cognitive deterioration and to a later reduction of BP. Although the benefits of controlling BP on longevity are firmly established, the costs that it may have on cognitive function have not been determined. Observational studies in general have demonstrated improvement of cognitive function when HPB is treated. Regarding drug treatment, the results must be interpreted with care. In general, diuretics and beta blockers do not worsen or improve cognitive function. The antagonists of angiotensin II, ACE inhibitors and calcium antagonist have a positive affect on cognitive function. The large clinical trials (evidence A grade), with more appropriate population samples and duration time have shown a reduction of dementia with dihydropyridine calcium antagonists (nitrendipine) and with the ACE inhibitor and diuretic combination (perindopril plus indapamide).