Evidence map›Paper›PMID 27411403›Full record

ReviewNature reviews. Cardiology2016

Myocardial energy depletion and dynamic systolic dysfunction in hypertrophic cardiomyopathy.

Julian O M Ormerod, Michael P Frenneaux, Mark V Sherrid

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Cardiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 1 pooled it
1.8field-weighted citation impact, top 14% 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

24 citing papers in PubMed, 1 synthesis or guideline pooled it, 41 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Observational
  5. Why the septum thickens in hypertrophic cardiomyopathy.Journal of molecular and cellular cardiology plus · 2026
    Review
  6. Review
  7. Article
  8. Cardiac myosin inhibitors in hypertrophic cardiomyopathy.Journal of cardiovascular imaging · 2025
    Review
  9. Article
  10. Review
  11. Article
  12. AnBioMed research international · 2024
    Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Article
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

3 authors at 3 institutions in 2 countries.

Julian O M OrmerodOxford Heart Centre, Oxford University Hospitals, Headley Way, Oxford, OX3 9DU, UK.
Michael P FrenneauxNorwich Medical School, University of East Anglia, James Watson Road, Norwich, NR4 7UQ, UK.
Mark V SherridNew York University School of Medicine, Skirball 9N, 530 First Avenue, New York City, New York 10543, USA.
New York University · USOxford University Hospitals NHS Trust · GBUniversity of East Anglia · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Evidence indicates that anatomical and physiological phenotypes of hypertrophic cardiomyopathy (HCM) stem from genetically mediated, inefficient cardiomyocyte energy utilization, and subsequent cellular energy depletion. However, HCM often presents clinically with normal left ventricular (LV) systolic function or hyperkinesia. If energy inefficiency is a feature of HCM, why is it not manifest as resting LV systolic dysfunction? In this Perspectives article, we focus on an idiosyncratic form of reversible systolic dysfunction provoked by LV obstruction that we have previously termed the 'lobster claw abnormality' - a mid-systolic drop in LV Doppler ejection velocities. In obstructive HCM, this drop explains the mid-systolic closure of the aortic valve, the bifid aortic pressure trace, and why patients cannot increase stroke volume with exercise. This phenomenon is characteristic of a broader phenomenon in HCM that we have termed dynamic systolic dysfunction. It underlies the development of apical aneurysms, and rare occurrence of cardiogenic shock after obstruction. We posit that dynamic systolic dysfunction is a manifestation of inefficient cardiomyocyte energy utilization. Systolic dysfunction is clinically inapparent at rest; however, it becomes overt through the mechanism of afterload mismatch when LV outflow obstruction is imposed. Energetic insufficiency is also present in nonobstructive HCM. This paradigm might suggest novel therapies. Other pathways that might be central to HCM, such as myofilament Ca

Indexed as

Energy MetabolismCardiomyopathy, HypertrophicDiastoleHumansMyocytes, CardiacStroke VolumeSystoleTachycardiaVentricular Dysfunction, Left

Identifiers

PMID27411403
OpenAlexW2466279388

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.