Evidence map›Paper›PMID 23989718›Full record

ReviewCirculation research2013

Electromechanical dyssynchrony and resynchronization of the failing heart.

Jonathan A Kirk, David A Kass

Abstract readReview
In one paragraph

Review in Circulation research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed, 2 pooled it
–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

61 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Pooled it
  2. Guidelines for in vivo mouse models of myocardial infarction.American journal of physiology. Heart and circulatory physiology · 2021
    Guideline
  3. Trial
  4. Review
  5. Article
  6. Article
  7. Article
  8. Differential effects of semaglutide and colchicine on atrial remodeling in rats with reduced ejection fraction after myocardial infarction.Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology · 2026
    Article
  9. Article
  10. Article
  11. Implantable Defibrillators: Which Is the Best Device for Each Patient?Journal of cardiovascular electrophysiology · 2025
    Review
  12. Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Article

1 more citing papers are in PubMed but not listed here.

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.

Jonathan A KirkDivision of Cardiology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
David A Kass

Funding

Pathobiology of Cardiac Dyssynchrony &ResynchronizationP01HL077180 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI KASS, DAVID ALAN · 2004 to 2014
$22.8M
PATHOPHYSIOLOGY OF MYOCARDIAL DISEASEST32HL007227 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI Chulan Kwon, WENDY S POST · 1985 to 2026
$21.2M
SCLERODERMA-ASSOCIATED PAHP50HL084946 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI BLUEMKE, DAVID A. · 2007 to 2011
$20.6M
Mechanisms of Right Ventricular Dysfunction in Scleroderma-associated PAHR01HL114910 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI HASSOUN, PAUL M. · 2012 to 2023
$6.2M
A new post-translational modification, citrullination, changes in heart failureR21HL112586 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI VAN EYK, JENNIFER E · 2012 to 2013
$436k
NHLBI NIH HHS HHSN268201000032CNHLBI NIH HHS HL-112586NHLBI NIH HHS HL-114910NHLBI NIH HHS P01 HL077180NHLBI NIH HHS P01-HL077180NHLBI NIH HHS P50 HL084946NHLBI NIH HHS R01 HL114910NHLBI NIH HHS R21 HL112586NHLBI NIH HHS T32 HL007227NHLBI NIH HHS T32-HL07227
6 · The paper itself

Abstract

Patients with heart failure and decreased function frequently develop discoordinate contraction because of electric activation delay. Often termed dyssynchrony, this further decreases systolic function and chamber efficiency and worsens morbidity and mortality. In the mid- 1990s, a pacemaker-based treatment termed cardiac resynchronization therapy (CRT) was developed to restore mechanical synchrony by electrically activating both right and left sides of the heart. It is a major therapeutic advance for the new millennium. Acute chamber effects of CRT include increased cardiac output and mechanical efficiency and reduced mitral regurgitation, whereas reduction in chamber volumes ensues more chronically. Patient candidates for CRT have a prolonged QRS duration and discoordinate wall motion, although other factors may also be important because ≈30% of such selected subjects do not respond to the treatment. In contrast to existing pharmacological inotropes, CRT both acutely and chronically increases cardiac systolic function and work, yet it also reduces long-term mortality. Recent studies reveal unique molecular and cellular changes from CRT that may also contribute to this success. Heart failure with dyssynchrony displays decreased myocyte and myofilament function, calcium handling, β-adrenergic responsiveness, mitochondrial ATP synthase activity, cell survival signaling, and other changes. CRT reverses many of these abnormalities often by triggering entirely new pathways. In this review, we discuss chamber, circulatory, and basic myocardial effects of dyssynchrony and CRT in the failing heart, and we highlight new research aiming to better target and implement CRT, as well as leverage its molecular effects.

Indexed as

Cardiac Resynchronization TherapyHeart FailureHumansVentricular Dysfunctioncardiac resynchronization therapycell physiological phenomenaheart failuremolecular biologymyocyteventricular function

Identifiers

PMID23989718
PMCPMC3874431

What OpenQuestion holds

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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.