Evidence map›Paper›PMID 24743925›Full record

ReviewBasic research in cardiology2014

The role of capillary transit time heterogeneity in myocardial oxygenation and ischemic heart disease.

Leif Ostergaard, Steen Buus Kristiansen, Hugo Angleys, Jørgen Frøkiær, J Michael Hasenkam, Sune Nørhøj Jespersen, Hans Erik Bøtker

Open access · hybridAbstract readReview
In one paragraph

Review in Basic research in cardiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
5.1field-weighted citation impact, top 5% 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

40 citing papers in PubMed, 70 citations in OpenAlex.

  1. Article
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  3. Review
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  7. Vascular (dys)function in the failing heart.Nature reviews. Cardiology · 2025
    Review
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  9. Review
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  11. Article
  12. Article
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  15. Article
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  18. Can EAT be an INOCA goalkeeper.Frontiers in endocrinology · 2022
    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

7 authors at 2 institutions in 1 country.

Leif OstergaardDepartment of Neuroradiology, Aarhus University Hospital, Building 10G, Nørrebrogade 44, 8000, Aarhus C, Denmark, leif@cfin.dk.
Steen Buus Kristiansen
Hugo Angleys
Jørgen Frøkiær
J Michael Hasenkam
Sune Nørhøj Jespersen
Hans Erik Bøtker
Aarhus University Hospital · DKAarhus University · DK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ischemic heart disease (IHD) is characterized by an imbalance between oxygen supply and demand, most frequently caused by coronary artery disease (CAD) that reduces myocardial perfusion. In some patients, IHD is ascribed to microvascular dysfunction (MVD): microcirculatory disturbances that reduce myocardial perfusion at the level of myocardial pre-arterioles and arterioles. In a minority of cases, chest pain and reductions in myocardial flow reserve may even occur in patients without any other demonstrable systemic or cardiac disease. In this topical review, we address whether these findings might be caused by impaired myocardial oxygen extraction, caused by capillary flow disturbances further downstream. Myocardial blood flow (MBF) increases approximately linearly with oxygen utilization, but efficient oxygen extraction at high MBF values is known to depend on the parallel reduction of capillary transit time heterogeneity (CTH). Consequently, changes in capillary wall morphology or blood viscosity may impair myocardial oxygen extraction by preventing capillary flow homogenization. Indeed, a recent re-analysis of oxygen transport in tissue shows that elevated CTH can reduce tissue oxygenation by causing a functional shunt of oxygenated blood through the tissue. We review the combined effects of MBF, CTH, and tissue oxygen tension on myocardial oxygen supply. We show that as CTH increases, normal vasodilator responses must be attenuated in order to reduce the degree of functional shunting and improve blood-tissue oxygen concentration gradients to allow sufficient myocardial oxygenation. Theoretically, CTH can reach levels such that increased metabolic demands cannot be met, resulting in tissue hypoxia and angina in the absence of flow-limiting CAD or MVD. We discuss these predictions in the context of MVD, myocardial infarction, and reperfusion injury.

Indexed as

Coronary CirculationMicrocirculationOxygen ConsumptionAnimalsBlood Flow VelocityCapillariesHemodynamicsHumansModels, CardiovascularMyocardial IschemiaMyocardiumOxygenTime FactorsOxygen

Identifiers

PMID24743925
PMCPMC4013440
OpenAlexW2150460525

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.