Evidence map›Paper›PMID 19343394›Full record

ReviewDer Internist2009

[Cardiac sequelae of hypertension].

M Steinmetz, G Nickenig

Abstract readEnglish AbstractReview
PubMed Publisher
In one paragraph

Review in Der Internist, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors.

M SteinmetzMed. Klinik und Poliklinik II/Kardiologie, Pneumologie und Angiologie, Universitätsklinikum Bonn, Sigmund-Freud-Strasse 25, Bonn, Germany. martin.steinmetz@ukb.uni-bonn.de
G Nickenig

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Arterial hypertension leads to cardiac restructuring and damage. This "hypertensive heart disease" includes left ventricular hypertrophy. In addition, it is also considered responsible for diastolic and systolic dysfunction, vascular manifestations of microangiopathy and in a broader sense also coronary heart disease as well as cardiac dysrhythmias and sudden cardiac death. The pathophysiological mechanisms depend on a complex neurohumoral regulation and the ensuing change in cardiac structure and output. The initial compensation for increased cardiac demand is followed by permanent heart damage and successive decompensation. At this point the typical complaints involved in cardiac insufficiency or ischemia become evident. Determining the diagnosis is particularly important early on since the prognosis with regard to morbidity and mortality deteriorates if the hypertensive condition persists and the heart develops lasting damage.

Indexed as

Models, CardiovascularHumansHypertensionMyocardial IschemiaVentricular Dysfunction, Left

Identifiers

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.