Evidence map›Paper›PMID 21376836›Full record

ArticleHeart rhythm2011

Increased left ventricular mass and decreased left ventricular systolic function have independent pathways to ventricular arrhythmogenesis in coronary artery disease.

Kyndaron Reinier, Celia Dervan, Tejwant Singh, Audrey Uy-Evanado, Shenghan Lai, Karen Gunson, Jonathan Jui, Sumeet S Chugh

Abstract read
In one paragraph

Article in Heart rhythm, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
3.9field-weighted citation impact, top 6% 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

44 citing papers in PubMed, 82 citations in OpenAlex.

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  13. Impact of obstructive sleep apnea on left ventricular mass index in men with coronary artery disease.Journal of clinical sleep medicine : JCSM : official publication of the American Academy of Sleep Medicine · 2020
    Article
  14. Review
  15. Article
  16. Myocardial Microvascular Dysfunction in Rheumatoid ArthritisCirculation. Cardiovascular imaging · 2019
    Article
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  18. Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 3 institutions in 1 country.

Kyndaron ReinierHeart Institute, Cedars-Sinai Medical Center, Los Angeles California, USA.
Celia Dervan
Tejwant Singh
Audrey Uy-Evanado
Shenghan Lai
Karen Gunson
Jonathan Jui
Sumeet S Chugh
Cedars-Sinai Medical Center · USOregon Health & Science University · USJohns Hopkins University · US

Funding

Determinants of Sudden Death Risk with Left Ventricular HypertrophyR01HL088416 · NHLBI · OREGON HEALTH & SCIENCE UNIVERSITY · PI CHUGH, SUMEET S. · 2007 to 2011
$2.4M
Prolonged Ventricular Depolarization and Sudden Death in the CommunityR01HL105170 · NHLBI · CEDARS-SINAI MEDICAL CENTER · PI CHUGH, SUMEET S. · 2010 to 2013
$1.6M
NHLBI NIH HHS 3R01HL088416-03SNHLBI NIH HHS R01 HL088416NHLBI NIH HHS R01HL088416NHLBI NIH HHS R01 HL105170
6 · The paper itself

Abstract

backgroundFollowing myocardial infarction, individual patients can have wide variations in the extent of left ventricular systolic dysfunction (LVSD) and increased left ventricular (LV) mass. Both affect the risk for sudden cardiac death, but only LV ejection fraction is used for risk prediction.

objectiveThe purpose of this study was to evaluate the independent as well as the additive contributions of increased LV mass and decreased LV ejection fraction to sudden cardiac death in the general population.

methodsIn the ongoing Oregon Sudden Unexpected Death Study, we studied consecutive SCD cases (n = 191) and coronary artery disease controls (n = 203) from the Portland, Oregon, metropolitan area (population approximately 1,000,000; 2002-2008). Comparisons of echocardiographic LV mass obtained prior and unrelated to sudden cardiac death (SCD) were conducted, and a logistic regression model was used to evaluate the relationship between SCD, severe LVSD, LV mass, and other relevant clinical variables.

resultsIn a multivariate model, both severe LVSD and left ventricular hypertrophy (LVH) were associated with increased SCD risk (odds ratio [OR] 1.9, 95% confidence interval [CI] 1.1-3.2 for severe LVSD; OR 1.8, 95% CI 1.1-2.9 for LVH). In patients with coexisting severe LVSD and LVH, risk of SCD was additive (OR 3.5, 95% CI 1.7-7.2). In the same model, increased age, atrial fibrillation/flutter, elevated creatinine, and diabetes independently increased risk, and use of angiotensin receptor blockers attenuated risk.

conclusionReduced LV ejection fraction and increased LV mass had independent and additive effects on risk of sudden death. Despite the significant overlap between the two conditions, these findings point toward the existence of independent mechanistic pathways for ventricular arrhythmias that occur due to LVSD and LVH.

Indexed as

Death, Sudden, CardiacAgedCase-Control StudiesCoronary Artery DiseaseFemaleHumansHypertrophy, Left VentricularLogistic ModelsMaleRisk AssessmentRisk FactorsStroke VolumeSystoleUltrasonographyVentricular Dysfunction, Left

Identifiers

PMID21376836
PMCPMC3123721
OpenAlexW2003746240

What OpenQuestion holds

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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.