Evidence map›Paper›PMID 22210280›Full record

ReviewJournal of molecular and cellular cardiology2012

Coronary collateral growth--back to the future.

William M Chilian, Marc S Penn, Yuh Fen Pung, Feng Dong, Maritza Mayorga, Vahagn Ohanyan, Suzanna Logan, Liya Yin

Abstract readReview
In one paragraph

Review in Journal of molecular and cellular cardiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

30 citing papers in PubMed, 61 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Coronary remodeling and biomechanics: Are we going with the flow in 2020?American journal of physiology. Heart and circulatory physiology · 2021
    Review
  8. Article
  9. Article
  10. Review
  11. Cardioprotection during ischemia by coronary collateral growth.American journal of physiology. Heart and circulatory physiology · 2019
    Review
  12. Article
  13. Review
  14. Regulation of Coronary Blood Flow.Comprehensive Physiology · 2017
    Review
  15. Article
  16. Article
  17. Article
  18. Article
  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

8 authors at 1 institution in 1 country.

William M ChilianDepartment of Integrative Medical Sciences, Northeast Ohio Medical University, Rootstown, Ohio 44272, USA. wchilian@neomed.edu
Marc S Penn
Yuh Fen Pung
Feng Dong
Maritza Mayorga
Vahagn Ohanyan
Suzanna Logan
Liya Yin
Northeast Ohio Medical University · US

Funding

MICROCIRCULATORY DYNAMICS IN THE CORONARY CIRCULATIONR01HL032788 · NHLBI · UNIVERSITY OF IOWA · PI CHILIAN, WILLIAM M · 1986 to 2008
$3.3M
Reactive Oxygen Species in Coronary Collateral GrowthR01HL083366 · NHLBI · NORTHEAST OHIO MEDICAL UNIVERSITY · PI CHILIAN, WILLIAM M · 2009 to 2013
$2.3M
Stem Cell Induction of Coronary ArteriogenesisRC1HL100828 · NHLBI · NORTHEAST OHIO MEDICAL UNIVERSITY · PI CHILIAN, WILLIAM M · 2009 to 2010
$998k
MECHANISM OF PLASMINOGEN ACTIVATION BY STREPTOKINASEF32HL010082 · NHLBI · VANDERBILT UNIVERSITY · PI BOXRUD, PAUL D · 1998 to 2000
$39k
NHLBI NIH HHS HL100828ZNHLBI NIH HHS HL32788NHLBI NIH HHS HL83366NHLBI NIH HHS R01 HL032788NHLBI NIH HHS R01 HL083366NHLBI NIH HHS RC1 HL100828
6 · The paper itself

Abstract

The coronary collateral circulation is critically important as an adaptation of the heart to prevent the damage from ischemic insults. In their native state, collaterals in the heart would be classified as part of the microcirculation, existing as arterial-arterial anastomotic connections in the range of 30 to 100 μM in diameter. However, these vessels also show a propensity to remodel into components of the macrocirculation and can become arteries larger than 1000 μM in diameter. This process of outward remodeling is critically important in the adaptation of the heart to ischemia because the resistance to blood flow is inversely related to the fourth power of the diameter of the vessel. Thus, an expansion of a vessel from 100 to 1000 μM would reduce resistance (in this part of the circuit) to a negligible amount and enable delivery of flow to the region at risk. Our goal in this review is to highlight the voids in understanding this adaptation to ischemia-the growth of the coronary collateral circulation. In doing so we discuss the controversies and unknown aspects of the causal factors that stimulate growth of the collateral circulation, the role of genetics, and the role of endogenous stem and progenitor cells in the context of the normal, physiological situation and under more pathological conditions of ischemic heart disease or with some of the underlying risk factors, e.g., diabetes. The major conclusion of this review is that there are many gaps in our knowledge of coronary collateral growth and this knowledge is critical before the potential of stimulating collateralization in the hearts of patients can be realized. This article is part of a Special Issue entitled "Coronary Blood Flow".

Indexed as

Collateral CirculationCoronary Artery DiseaseCoronary CirculationHumansMyocardial IschemiaNeovascularization, Physiologic

Identifiers

PMID22210280
PMCPMC3939792
OpenAlexW2132220702

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.