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Biomedical subjects

A Hofman

Publications and source records attributed to A Hofman.

At least 469 records · Page 26Linked to original sources
PubMed1982

Blood pressure and haemodynamics in teenagers.

It has been suggested that a hyperkinetic circulatory state, with high cardiac output, causes high blood pressure in childhood and, secondarily, in adulthood. We studied blood pressure and cardiac output in 319 subjects aged 15 to 19. Blood pressure was measured with an automated device; cardiac output was estimated by M-mode echocardiography and indexed by body surface area. The distribution of cardiac output was stratified using quartiles. Mean arterial pressure was virtually constant over these strata, with boys and girls showing essentially the same pattern. Linear regression of mean arterial pressure on cardiac output yielded a coefficient which was not significantly different from zero. A history of high blood pressure in the parents was positively associated with mean arterial pressure, but unrelated to cardiac output, in the offspring. This evidence does not support the hypothesis that the hyperkinetic circulatory state causes high blood pressure in childhood; rather, raised blood pressure in adolescents appears to relate to increased peripheral vascular resistance. Therefore, our findings lend support to the view that change in blood pressure over time is caused by a gradual increase in peripheral resistance beginning early in life.

Adolescent↗
PubMed1981

Haemodynamics, plasma noradrenaline and plasma renin in hypertensive and normotensive teenagers.

1. Plasma noradrenaline, active and inactive plasma renin, cardiac index and total peripheral vascular resistance were studied in 41 subjects, initially aged 10-19 years, who were followed up for at least 2 years after a blood pressure reading of 140 and/or 90 mmHg or more (initial hypertensives) and in 41 normotensive control subjects selected from the same population and matched for age, sex and body-mass index. 2. The initial hypertensive subjects had a lower mean cardiac index (3.63 +/- SD 0.83 vs 4.00 +/- 0.89 litre min-1 m-2), a higher mean total peripheral resistance (26.8 +/- 5.7 vs 22.8 +/- 5.5 peripheral resistance (26.8 +/- 5.7 vs 22.8 +/- 5.5 units) and a higher mean plasma noradrenaline units) and a higher mean plasma noradrenaline concentration (336 +/- 146 vs 281 +/- 126 pg/ml) than the control subjects. 3. Mean plasma noradrenaline concentration was higher in initial hypertensive subjects with a high active renin concentration than in those with a normal renin concentration (442 +/- 70 vs 324 +/- 100 pg/ml). 4. A weight-adjusted standardized regression coefficient of 0.77 between active plasma renin concentration and left ventricular mass was found in normotensive control subjects. 5. These findings are at variance with the existence of a hyperkinetic phase in young hypertensive subjects and suggest that sympathetic overactivity may be related to early essential hypertension through increase of peripheral vascular resistance.

Adolescent↗
PubMed1980

Increased blood pressure in schoolchildren related to high sodium levels in drinking water.

The relationship between sodium in drinking water and blood pressure was examined in 348 schoolchildren aged 7.7 to 11.7 years. They were born and living in three areas with different levels of sodium in the public drinking water. Sodium content of the water was either long-term low, long-term high, or short-term high. The three communities are closely comparable according to demographic characteristics. The mean values of systolic and diastolic blood pressure were higher in the high sodium areas. After adjustment for dissimilarities in distributions of weight, height, pulse rate, age, family history of hypertension, and time of blood pressure measurement, these differences remained constant, ranging from 1.8 to 4.0 mm Hg. Girls and boys showed essentially the same differences. Mean 24-hour sodium excretion was somewhat higher in the long-term low area; no differences were found in sodium-creatinine ratio. The regression coefficients between sodium excretion and blood pressure were not significant. The findings from this retrospective follow-up study support the hypothesis that sodium intake influences blood pressure. The association seems to be of a relatively short-term nature, as no differences in blood pressure levels were found between the long-term and short-term high areas.

Blood Pressure↗
PubMed1979

Raised blood pressure and plasma noradrenaline concentrations in teenagers and young adults selected from an open population.

Plasma noradrenaline (PNA) concentrations were measured in 38 subjects aged 13-23, who were followed up for two to four years after an initial blood-pressure (BP) reading of 140/90 mm Hg or over was obtained, and in 39 age-matched controls from the same open population. Subjects who were hypertensive when the PNA concentration was measured had a significantly higher concentration (351 +/- SE 26 pg/ml) compared with their controls (248 +/- 29 pg/ml). Furthermore, in those subjects in whom the mean arterial pressure decreased by under 5% during the follow-up period the mean concentration was 363 +/- 27 pg/ml, compared with 271 +/- 29 pg/ml in their controls. PNA concentrations and systolic BP were positively correlated. A positive association between PNA concentrations and age was observed in the controls but not the subjects with hypertension, owing to the higher concentrations in younger hypertensive subjects.

Adolescent↗
PubMedDate not supplied

Costs and effects of long-term oral anticoagulant treatment after myocardial infarction.

OBJECTIVE: To investigate the costs and effects of long-term oral anticoagulant treatment after myocardial infarction. DESIGN: Cost-effectiveness analysis, based on a randomized, double-blind, placebo-controlled trial. SETTING: Sixty Dutch hospitals. PATIENTS: A total of 3404 hospital survivors of acute myocardial infarction randomized within a median period of 4 days after discharge to either oral anticoagulant treatment or placebo. The mean follow-up was 37 months. INTERVENTION: Oral anticoagulant treatment aimed at a target international normalized ratio of 2.8 to 4.8. MAIN OUTCOME MEASUREMENTS: Costs of hospital stay during readmissions, costs related to major cardiologic interventions, and costs of oral anticoagulant treatment. RESULTS: The costs of oral anticoagulant treatment were estimated at 394 Dutch guilders (Dfl) per patient-year (Dfl 1 = US $0.58). Placebo patients stayed 18,830 days in the hospital compared with 15,083 days for anticoagulation patients. Average costs per patient of medical care during follow-up were estimated at Dfl 10,784 for placebo patients and Dfl 9878 for anticoagulation patients. CONCLUSIONS: Costs of long-term anticoagulant treatment are outweighed by the costs of prevented clinical events.

Administration, Oral↗
PubMedDate not supplied

Decreased DNA repair capacity in familial, but not in sporadic Alzheimer's disease.

Using the alkaline filter elution technique we determined the induction and disappearance of DNA single-strand breaks (SSB) in freshly isolated peripheral blood lymphocytes (PBL) from 43 Alzheimer's disease (AD) patients and 48 normal, healthy age- and sex-matched control subjects following in vitro exposure to N-ethyl-N-nitrosourea (ENU). The mean percentage SSB disappearance in PBL from control subjects at 1 h after ENU treatment was 41.4 +/- 2.9%; this was not significantly different from that found in samples from AD patients which had no (n = 16) or one (n = 12) first-degree relative with dementia (42.5 +/- 8.2% and 43.0 +/- 4.4%, respectively; p greater than 0.75). However, in PBL of 15 AD patients with at least two first-degree relatives with dementia the mean percentage SSB disappearance was 23.6 +/- 5.8%, which was significantly lower than that found in controls (p less than 0.01) or in the other AD patients (p less than 0.02).

Aged↗
PubMedDate not supplied

Antihypertensive drugs and incidence of dementia: the Rotterdam Study.

There is increasing evidence that hypertension may contribute to the development of dementia. We investigated the relation of antihypertensive drug use and the risk of dementia in the cohort of the population based Rotterdam Study. The study cohort included 7046 elderly, free of dementia at baseline. Dementia was diagnosed in a stepwise procedure. Participants were first screened. Screen positives were further tested. Those suspected of dementia underwent a diagnostic work-up. Dementia and its subtypes were diagnosed according to prevailing criteria. A Cox proportional hazards model was used to estimate relative risks. After a mean follow-up of 2.2 years, subjects taking antihypertensive medication at baseline (n = 2015) had a reduced incidence of dementia (adjusted relative risk, 0.76; 95% confidence interval 0.52-1.12). This risk reduction was most pronounced for vascular dementia, (adjusted relative risk, 0.30; 95% confidence interval 0.11-0.99). For Alzheimer's disease the relative risk was 0.87, not significant. Dementia may be prevented by antihypertensive treatment. In order to confirm any relation in Alzheimer's disease larger observational studies with longer follow-up are needed.

Aged↗
PubMedDate not supplied

Incidence of dementia: does gender make a difference?

Several studies suggested that women are at higher risk of dementia than men. However, that was based on rather limited data. We investigated possible gender differences in the incidence of dementia, Alzheimer's disease and vascular dementia, in the Rotterdam Study, a large population based prospective cohort study in the Netherlands of 7,046 persons aged 55 years and older, free of dementia at baseline. In 40,441 person-years of follow-up (mean 5.7 years) we identified 395 new cases of dementia (overall incidence: 9.8 per 1,000 person-years). Alzheimer's disease was the most frequent subtype of dementia (293 cases; 7.2 per 1,000). Vascular dementia was diagnosed in 57 participants (1.5 per 1,000). Overall, dementia incidence was similar for men and women (rate ratio women versus men: 1.00, 95% CI: 0.80-1.24). However, after 90 years of age dementia incidence declined in men but not in women (rate ratio 2.61, 95% CI: 1.04-6.56), in particular for Alzheimer's disease (rate ratio 5.79, 95% CI: 1.40-23.90). The overall incidence of vascular dementia was lower in women than in men (rate ratio 0.57, 95% CI: 0.34-0.97). This large population-based study suggests no gender differences in the incidence of dementia up to high age. After 90 years of age the incidence of Alzheimer's disease is higher for women than for men. The incidence of vascular dementia is higher for men than for women in all age groups.

Age Distribution↗
PubMedDate not supplied

Histamine H2 blocking drugs and the risk for Alzheimer's disease: the Rotterdam Study.

We investigated the cross-sectional relation of the use of histamine H2 blocking drugs and the risk for AD in the population based Rotterdam Study. AD was clinically diagnosed according to DSM-IIIR and NINCDS-ADRDA criteria. Data on medication used in the past week were obtained by having subjects show vials of medications and were classified according to the Anatomical Therapeutic Chemical (ATC) index. There were 7276 subjects with complete data, including 208 with AD and 378 H2 users (ATC code A0BA). Compared to the total cohort of non-H2 users, the relative risk (estimated as the odds ratio) for AD among those taking H2 blockers was 0.95 (95% confidence interval (CI) 0.52-1.75), after controlling for age, education, sex, history of stroke, and use of benzodiazepines and nonsteroidal antiinflammatory drugs. To address unmeasured confounding (by (contra) indication), we compared the risk of AD in H2 users with a subset of subjects using topical medications (ATC code D and S; n = 436). The adjusted OR in this comparison was 1.24 (95% CI 0.52-2.98). These results do not support the hypothesis that use of histamine H2 blocking drugs protect against AD.

Aged↗
PubMedDate not supplied

Regional cerebral blood flow and cerebrovascular risk factors in the elderly population.

Regional cerebral blood flow (rCBF) was studied in 60 elderly persons (aged 65 to 84 years) recruited from a population-based study, with single photon emission computed tomography using technetium 99m-labeled hexamethylpropylene amine oxime. We investigated whether it is only age that affects rCBF or whether other factors can be indentified that explain this relationship. Using multiple linear regression analysis, increasing age was significantly associated with rCBF decrease in parietal, temporo-parietal, and temporal cortex, but not in frontal cortex. Adjustment with several risk factors for cerebrovascular disease, including hypertension, history of myocardial infarction, factor VIIc, factor VIIIc, cholesterol and HDL cholesterol, smoking, and diabetes mellitus had no influence on these relations. Conversely, the association between age and rCBF was no longer statistically significant after adjustment with fibrinogen and indicators of carotid atherosclerosis, including intima-media wall thickness of the carotid artery and plaques in the carotid artery. Correction with local ratings of cortical atrophy did not affect the relations between age and rCBF. The results suggest that in the elderly population rCBF declines with age in posterior cortical areas and that these changes may well be explained by the presence of atherosclerosis. Reduced contractility of the vascular muscle wall with increasing age resulting from atherosclerosis may be the underlying mechanism.

Aged↗
PubMedDate not supplied

NSAIDs and incident Alzheimer's disease. The Rotterdam Study.

Recent studies suggest that the use of nonsteroidal anti-inflammatory drugs (NSAIDs) may reduce the risk for Alzheimer's disease (AD). We investigated the relation of NSAID use over a 10-year period and the risk for incident AD using a nested case-control design in the population-based Rotterdam Study. The study was performed in 306 subjects; 74 Alzheimer patients diagnosed according to NINCDS-ADRDRA criteria and 232 age and sex-matched controls. NSAID use was abstracted from general practitioners' medical records and expressed as cumulative prescription days. The relative risk for AD associated with long-term use (> or = 2 months) was 0.95 (95% CI: 0.46-1.99) as compared to nonusers, after controlling for possible confounders. In a separate examination, subjects who had more than 6 months of prescription days had a reduced relative risk for AD (RR = 0.74 (95% CI: 0.20-2.72). In an age-stratified analysis the effect in long-term users was evident in those aged 85 and under; 0.53 (95% CI: 0.15-1.77). All risk estimates were lower when the last 2 years of exposure were excluded from the analyses. Our point estimates in subjects younger than 85 years and in subjects using NSAIDs for 6 months or more are consistent with the hypothesis that long-term use of NSAIDs reduces the risk for AD. However, overall there was no association between NSAID use and the risk for incident AD.

Aged↗
PubMedDate not supplied

Genetic association of the presenilin-1 regulatory region with early-onset Alzheimer's disease in a population-based sample.

Genetic association has been reported between a di-allelic polymorphism in intron 8 of presenilin-1 (PSEN1) and Alzheimer's disease (AD) in some studies but not in others. In a population-based series of 102 patients with early onset AD and 118 community controls we examined whether polymorphisms in linkage disequilibrium with intron8 of PSEN1 may explain the association. In addition to the intron 8 polymorphism (P = 0.05), a promoter polymorphism (P = 0.03) and the simple tandem repeat (STR) polymorphism D14S1028 located upstream of PSEN1 (P = 0.04) were found to be marginally significantly associated to AD. When excluding PSEN1 mutation cases (n = 6), the intron 8 association was explained by linkage disequilibrium to the dominant PSEN1 mutations. In the non-mutation cases, the weak associations between the polymorphisms in the regulatory region remained. Our study suggests that a polymorphism/mutation in the promoter or regulatory region of PSEN1 rather than the polymorphism in intron 8 of PSEN1 is associated with early onset AD.

Age of Onset↗