ReviewDrugs1998
[Pathogenesis and epidemiology of arterial hypertension].
Review in Drugs, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
4 citing papers in PubMed, 1 synthesis or guideline pooled it, 17 citations in OpenAlex.
- Association Between Cystatin C and the Risk of Ischemic Stroke: a Systematic Review and Meta-analysis.Journal of molecular neuroscience : MN · 2019Pooled it
- Comorbidity of hypertension and lung cancer: interplay of genetics and environment.Discover oncology · 2025Review
- Does the Composition of Gut Microbiota Affect Hypertension? Molecular Mechanisms Involved in Increasing Blood Pressure.International journal of molecular sciences · 2023Review
- Molecular Interactions of Arterial Hypertension in Its Target Organs.International journal of molecular sciences · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The pathogenesis of arterial hypertension is more clearly understood today because of the availability of data enabling identification of a certain number of precipitating factors. From a genetic standpoint, hypertension would appear to be a multifactorial polygenic disorder with a tendency to interact with certain environmental factors. The latter are mainly related to lifestyle and are potentially modifiable. Obesity during childhood and adolescence is the main predictive factor for hypertension. It has been suggested that the underlying mechanism could well be hyperinsulinaemia, which induces hyperactivity of the sympathetic nervous system. The mechanisms of the relationship between hypertension and alcohol are still unclear. However, in many countries, excessive alcohol consumption has been reported to be a significant factor in the development of arterial hypertension. The negative effect of a sedentary lifestyle on blood pressure has been widely demonstrated. In addition, it has also been shown that regular physical exercise under aerobic conditions leads to a reduction in blood pressure levels. An excessive sodium intake is also responsible for inducing arterial hypertension through increases in cardiac output and effects on vascular reactivity and contractility. Similarly, restricting sodium intake leads to a reduction in blood pressure levels. Smoking--namely, certain components of tobacco smoke--would appear to have both short and long term effects on blood pressure. These contributing factors all have specific effects on cardiac output and peripheral resistance in individuals. At the community level, the impact of hypertension is particularly significant. Prevalence is strongly influenced by the type of population studied, although it is generally estimated that this disease affects between 10 and 20% of the adult population and is responsible for 5.8% of all deaths worldwide. The direct and indirect costs of the disease are particularly high and are generally considered to be underestimated since a significant proportion of cardiac disease and stroke should also be included in any cost estimates, giving extremely high final figures. Hypertension-related morbidity and mortality principally result from cardiovascular complications and approximately 35% of atherosclerotic cardiovascular events can be attributed to hypertension. The highest risks are associated with stroke (relative risk: 3.8) and congestive heart failure in individuals with hypertension, in whom the risk is quadrupled. With regard to risk for an individual, the higher the blood pressure the greater the risk for the patient. However, the situation is very different if the entire population is being considered. In this instance, the highest risk is associated with mild hypertension since this involves the largest proportion of the hypertensive population. Similarly, relative risk corresponds to a probability rate that applies to populations rather than individuals. In response to this contradiction, the concept of absolute risk was proposed and corresponds to the prevalence of the disease. The approach to hypertension treatment based on absolute risk has recently been proposed for use in clinical practice. It takes into account lesions of the target organ together with any other risk factors and thus integrates the notion of prevention which remains the principal approach to the problems encountered in the management of hypertension.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.