Evidence map›Paper›PMID 22999493›Full record

ReviewJournal of electrocardiology

Hypertrophic reprogramming of the left ventricle: translation to the ECG.

Joseph A Hill

Open access · greenAbstract readReview
In one paragraph

Review in Journal of electrocardiology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.5field-weighted citation impact, top 16% 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

6 citing papers in PubMed, 30 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

1 author at 1 institution in 1 country.

Joseph A HillDepartment of Internal Medicine, Cardiology, University of Texas Southwestern Medical Center, Dallas, TX 75390-8573, USA. joseph.hill@utsouthwestern.edu
The University of Texas Southwestern Medical Center · US

Funding

HDAC Inhibition in Cardiac Hypertrophy and FailureR01HL080144 · NHLBI · UT SOUTHWESTERN MEDICAL CENTER · PI HILL, JOSEPH A · 2007 to 2011
$2.0M
Calcineurin-Mediated Regulation of Cardiac Ca2+ ChannelR01HL075173 · NHLBI · UT SOUTHWESTERN MEDICAL CENTER · PI HILL, JOSEPH A · 2005 to 2009
$1.7M
Foxo: Negative Regulator of Cardiac HypertrophyR01HL090842 · NHLBI · UT SOUTHWESTERN MEDICAL CENTER · PI HILL, JOSEPH A · 2009 to 2012
$1.6M
Functional Genomics of Complex Vascular DiseaseP30HL101254 · NHLBI · UT SOUTHWESTERN MEDICAL CENTER · PI HILL, JOSEPH A · 2009 to 2010
$1.3M
NHLBI NIH HHS HL-075173NHLBI NIH HHS HL-080144NHLBI NIH HHS HL-090842NHLBI NIH HHS P30 HL101254NHLBI NIH HHS R01 HL075173NHLBI NIH HHS R01 HL080144NHLBI NIH HHS R01 HL090842
6 · The paper itself

Abstract

Hypertrophic growth of the heart occurs in many clinical scenarios, and it confers substantially increased risk of untoward sequelae. Among them, transition to ventricular dilation, wall thinning, contractile dysfunction, and a clinical syndrome of heart failure are paramount. Left ventricular hypertrophy (LVH) is typically diagnosed by either electrocardiography or echocardiography. However, these two means of assessing hypertrophic transformation of the left ventricle can sometimes disagree. At one level, this may not be surprising as the two methodologies are based on entirely divergent signals: electrical potential between two places on the surface of the skin and ultrasound energy reflected from the ventricle itself. Echocardiography is an effective means of assessing ventricular mass, which is a cardinal feature of LVH. Importantly, however, LVH is characterized by a wide range of remodeling events beyond simple increases in muscle mass. Electrocardiographic changes in LVH are reflective of the electrophysiological aspects of hypertrophic transformation. Here, I present an overview of the complex biology of left ventricular hypertrophy with an eye toward enhancing our understanding of its ECG manifestations.

Indexed as

Models, CardiovascularElectrocardiographyHeart Conduction SystemHumansHypertrophy, Left VentricularVentricular Dysfunction, Left

Identifiers

PMID22999493
PMCPMC3483360
OpenAlexW2077471038

What OpenQuestion holds

Textmetadata
LicenceTDM
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.