Evidence map›Paper›PMID 27278135›Full record

ArticleWiener klinische Wochenschrift2016

Hypertension and coronary artery disease: epidemiology, physiology, effects of treatment, and recommendations : A joint scientific statement from the Austrian Society of Cardiology and the Austrian Society of Hypertension.

Thomas Weber, Irene Lang, Robert Zweiker, Sabine Horn, Rene R Wenzel, Bruno Watschinger, Jörg Slany, Bernd Eber, Franz Xaver Roithinger, Bernhard Metzler

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In one paragraph

Article in Wiener klinische Wochenschrift, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed, 1 pooled it
0.9field-weighted citation impact, top 22% of its field
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

31 citing papers in PubMed, 1 synthesis or guideline pooled it, 81 citations in OpenAlex.

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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

10 authors at 6 institutions in 1 country.

Thomas WeberCardiology Department, Klinikum Wels-Grieskirchen, Grieskirchnerstraße 42, 4600, Wels, Austria. thomas.weber@klinikum-wegr.at.
Irene LangDivision of Cardiology, Department of Internal Medicine II, Medical University of Vienna, Vienna, Austria.
Robert ZweikerDivision of Cardiology, Department of Internal Medicine, Medical University Graz, Graz, Austria.
Sabine HornDivision of Nephrology, Department of Internal Medicine, Medical University Graz, Graz, Austria.
Rene R WenzelDepartment of Internal Medicine, Krankenhaus Tauernkliniken, Zell am See, Austria.
Bruno WatschingerDivision of Nephrology, Department of Internal Medicine III, Medical University Vienna, Vienna, Austria.
Jörg Slany, Vienna, Austria.
Bernd EberCardiology Department, Klinikum Wels-Grieskirchen, Grieskirchnerstraße 42, 4600, Wels, Austria.
Franz Xaver RoithingerSecond Department of Internal Medicine, Landesklinikum Wiener Neustadt, Vienna, Austria.
Bernhard MetzlerDepartment of Internal Medicine III, Medical University Innsbruck, Innsbruck, Austria.
Klinikum Wels-Grieskirchen · ATMedical University of Graz · ATMedical University of Vienna · ATFachhochschule Wiener Neustadt · ATInnsbruck Medical University · ATTauern Hospital Zell am See · AT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

High blood pressure is a major modifiable risk factor for all clinical manifestations of coronary artery disease (CAD). In people without known cardiovascular disease, the lowest systolic (down to 90-114 mmHg) and the lowest diastolic (down to 60-74 mmHg) pressures are associated with the lowest risk for developing CAD. Although diastolic blood pressure is the strongest predictor of CAD in younger and middle-aged people, this relationship becomes inverted and pulse pressure shows the strongest direct relationship with CAD in people above 60 years of age.Pathophysiological mechanisms of blood pressure as a risk factor for CAD are complex and include the influence of blood pressure as a physical force on the development of the atherosclerotic plaque, and the relationship between pulsatile hemodynamics/arterial stiffness and coronary perfusion. Treatment of arterial hypertension has been proven to prevent coronary events in patients without clinical CAD. In patients with established CAD, the effect of blood pressure lowering per se is beneficial, probably more than specific drugs or drug classes. The important exceptions are beta blockers (BBs), which are superior to all other drug classes for use after a recent myocardial infarction. Blood pressure targets in patients with established CAD have created controversy in the light of the so-called J-curve phenomenon, which describes an increase in coronary events at lower diastolic blood pressures. One explanation for this observation is that perfusion of the left ventricle occurs predominantly during diastole, and that coronary autoregulation may be exhausted with low diastolic blood pressure in the setting of left ventricular hypertrophy and atherosclerotic narrowing of the epicardial coronaries. The worst situation is a high systolic blood pressure in the presence of a low diastolic blood pressure, both a hallmark of increased aortic stiffness. However, the lowering of systolic blood pressure is clearly beneficial in this setting, even at the price of further lowering diastolic pressure. Primary blood pressure goal in patients with established CAD is below 140/90 mmHg. Recent studies suggest that a lower systolic blood pressure may be appropriate, whereas caution is advised with diastolic blood pressure below 60 mmHg.

Indexed as

Practice Guidelines as TopicAntihypertensive AgentsAustriaCardiologyCausalityCoronary Artery DiseaseEvidence-Based MedicineHumansHypertensionPrevalenceRisk FactorsTreatment OutcomeAntihypertensive AgentsArterial hypertensionArterial stiffnessBlood pressure goalsCoronary artery diseaseJ‑curve

Identifiers

PMID27278135
OpenAlexW2412620151

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.