Evidence map›Paper›PMID 19586943›Full record

ReviewCardiovascular research2009

Vascular endothelial ageing, heartbeat after heartbeat.

Eric Thorin, Nathalie Thorin-Trescases

Open access · bronzeAbstract readReview
In one paragraph

Review in Cardiovascular research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
4.6field-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

35 citing papers in PubMed, 92 citations in OpenAlex.

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  7. Review
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  18. Impact of pulse pressure on cerebrovascular events leading to age-related cognitive decline.American journal of physiology. Heart and circulatory physiology · 2018
    Review
  19. Pulse pressure-dependent cerebrovascular eNOS regulation in mice.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2017
    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

2 authors at 2 institutions in 1 country.

Eric ThorinFaculty of Medicine, Department of Surgery, Montreal Heart Institute, Research Centre, Université de Montréal, 5000 rue Bélanger, Montréal, QC, Canada. eric.thorin@umontreal.ca
Nathalie Thorin-Trescases
Montreal Heart Institute · CAUniversité de Montréal · CA

Funding

CIHR 14496-4
6 · The paper itself

Abstract

The vascular endothelium starts to age at the first heartbeat. There is no longer a need to demonstrate that an increased resting heart rate--above 70 b.p.m.--is associated with the onset of cardiovascular events and reduces lifespan in humans. Each cardiac cycle imposes a mechanical constraint on the arteries, and we would like to propose that this mechanical stress damages the vascular endothelium, its dysfunction being the prerequisite for atherogenesis. Consequently, reducing heart rate could protect the endothelium and slow the onset of atherosclerosis. The potential mechanisms by which reducing heart rate could be beneficial to the endothelium are likely a combination of a reduction in mechanical stress and tissue fatigue and a prolongation of the period of steady laminar flow, and thus sustained shear stress, between each systole. With age, irreparable damage accumulates in endothelial cells and leads to senescence, which is characterized by a pro-atherogenic phenotype. In the body, the highest mechanical stress occurs in the coronary vessels, where blood only flows during diastole and even reverses during systole; thus, coronary arteries are the prime site of atherosclerosis. All classical risk factors for cardiovascular diseases add up, to accelerate atherogenesis, but hypertension, which further raises mechanical stress, is likely the most damaging. By inducing flow through the arteries, the heart rate determines shear stress and its stability: mechanical stress and the associated damage induced by each systole are efficiently counteracted by the repair capacities of a healthy endothelium. The maintenance of a physiological, low heart rate may be key to prolonging the endothelial healthy lifespan and thus, vascular health.

Indexed as

Heart RateAdrenergic beta-AntagonistsAgingAnimalsAtherosclerosisBaroreflexBenzazepinesCardiovascular DiseasesEndothelium, VascularHumansIvabradineNitric OxidePulsatile FlowRisk FactorsShear StrengthStress, MechanicalAdrenergic beta-AntagonistsBenzazepinesIvabradineNitric Oxide

Identifiers

PMID19586943
PMCPMC3700879
OpenAlexW2135797799

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.