Evidence map›Paper›PMID 22676942›Full record

ArticleJournal of the American College of Cardiology2012

Autonomic and hemodynamic origins of pre-hypertension: central role of heredity.

Jason T Davis, Fangwen Rao, Dalal Naqshbandi, Maple M Fung, Kuixing Zhang, Andrew J Schork, Caroline M Nievergelt, Michael G Ziegler, Daniel T O'Connor

Abstract read
In one paragraph

Article in Journal of the American College of Cardiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
3.2field-weighted citation impact, top 7% 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

17 citing papers in PubMed, 40 citations in OpenAlex.

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  7. Elevated resting blood pressure augments autonomic imbalance in posttraumatic stress disorder.American journal of physiology. Regulatory, integrative and comparative physiology · 2018
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  8. Article
  9. Prehypertension is a comorbid state with autonomic and metabolic dysfunction.Journal of clinical hypertension (Greenwich, Conn.) · 2018
    Article
  10. Polyphenols: a Promising Nutritional Approach to Prevent or Reduce the Progression of Prehypertension.High blood pressure & cardiovascular prevention : the official journal of the Italian Society of Hypertension · 2016
    Review
  11. Prehypertension: Defining the Transitional Phenotype.Current hypertension reports · 2016
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  12. Observational
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 1 institution in 1 country.

Jason T DavisDepartment of Medicine, University of California-San Diego, and V.A. San Diego Healthcare System, 9500 Gilman Drive, La Jolla, CA 92093, USA.
Fangwen Rao
Dalal Naqshbandi
Maple M Fung
Kuixing Zhang
Andrew J Schork
Caroline M Nievergelt
Michael G Ziegler
Daniel T O'Connor
University of California San Diego · US

Funding

Trafficking of catecholamine storage vesicle proteinsP01HL058120 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI TAUPENOT, LAURENT · 1999 to 2009
$18.5M
SAN DIEGO CLINICAL AND TRANSLATIONAL RESEARCH INSTITUTEUL1RR031980 · NCRR · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI FIRESTEIN, GARY S · 2010 to 2011
$14.0M
Phenotyping--vasoactive post synaptic agonist pharmacogU01HL069758 · NHLBI · UNIVERSITY OF CALIFORNIA SAN DIEGO · PI O'CONNOR, DANIEL T · 2001 to 2004
$12.1M
San Diego EXPORT Comprehensive NCMHD Research CenterP60MD000220 · NIMHD · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI VILLARREAL, FRANCISCO · 2002 to 2011
$11.0M
Hypertensive kidney disease: Novel pathogenic and therapeutic pathwayR01DK094894 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI VAINGANKAR, SUCHETA M · 2012 to 2015
$1.4M
San Diego Export: An University Community Partnership E*P60MD000263 · NIMHD · SAN DIEGO STATE UNIVERSITY · PI BRODINE, STEPHANIE · 2002 to 2006
$1.1M
San Diego Clinical and Translational Research InstituteKL2RR031978 · NCRR · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI FIRESTEIN, GARY S · 2010 to 2011
$615k
NCRR NIH HHS 1UL1RR031980NCRR NIH HHS KL2 RR031978NCRR NIH HHS UL1 RR031980NHLBI NIH HHS HL58120NHLBI NIH HHS P01 HL058120NHLBI NIH HHS U01 HL069758NIDDK NIH HHS R01 DK094894NIMHD NIH HHS P60 MD000220NIMHD NIH HHS P60 MD000263
6 · The paper itself

Abstract

objectivesThe purpose of this study is to better understand the origins and progression of pre-hypertension.

backgroundPre-hypertension is a risk factor for progression to hypertension, cardiovascular disease, and increased mortality. We used a cross-sectional twin study design to examine the role of heredity in likely pathophysiological events (autonomic or hemodynamic) in pre-hypertension.

methodsEight hundred twelve individuals (337 normotensive, 340 pre-hypertensive, 135 hypertensive) were evaluated in a sample of twin pairs, their siblings, and other family members. They underwent noninvasive hemodynamic, autonomic, and biochemical testing, as well as estimates of trait heritability (the percentage of trait variance accounted for by heredity) and pleiotropy (the genetic covariance or shared genetic determination of traits) by variance components.

resultsIn the hemodynamic realm, an elevation of cardiac contractility prompted increased stroke volume, in turn increasing cardiac output, which elevated blood pressure into the pre-hypertension range. Autonomic monitoring detected an elevation of norepinephrine secretion plus a decline in cardiac parasympathetic tone. Twin pair variance components documented substantial heritability as well as joint genetic determination for blood pressure and the contributory autonomic and hemodynamic traits. Genetic variation at a pathway locus also indicated pleiotropic effects on contractility and blood pressure.

conclusionsElevated blood pressure in pre-hypertension results from increased cardiac output, driven by contractility as well as heart rate, which may reflect both diminished parasympathetic and increased sympathetic tone. In the face of increased cardiac output, systemic vascular resistance fails to decline homeostatically. Such traits display substantial heritability and shared genetic determination, although by loci not yet elucidated. These findings clarify the role of heredity in the origin of pre-hypertension and its autonomic and hemodynamic pathogenesis. The results also establish pathways that suggest new therapeutic targets for pre-hypertension, or approaches to its prevention.

Indexed as

AdultBlood PressureCalcium Channels, L-TypeCardiac OutputCross-Sectional StudiesDisease ProgressionFemaleHemodynamicsHumansMaleMyocardial ContractionNorepinephrinePrehypertensionStroke VolumeVascular ResistanceCACNA1C protein, humanCalcium Channels, L-TypeNorepinephrine

Identifiers

PMID22676942
PMCPMC3374873
OpenAlexW1602715635

What OpenQuestion holds

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Registered trials

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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.