Evidence map›Paper›PMID 30762468›Full record

ArticleJournal of the American Heart Association2018

Deleterious Effects of Cold Air Inhalation on Coronary Physiological Indices in Patients With Obstructive Coronary Artery Disease.

Rupert P Williams, Kaleab N Asrress, Matthew Lumley, Satpal Arri, Tiffany Patterson, Howard Ellis, Vasiliki Manou-Stathopoulou, Catherine Macfarlane, Shruthi Chandran, Kostantinos Moschonas and 8 more

Open access · goldAbstract read
In one paragraph

Article in Journal of the American Heart Association, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.3field-weighted citation impact, top 42% 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

4 citing papers in PubMed, 11 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. 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

18 authors at 4 institutions in 1 country.

Rupert P Williams1 Cardiovascular Division Rayne Institute St Thomas' Hospital King's College London London United Kingdom.
Kaleab N Asrress1 Cardiovascular Division Rayne Institute St Thomas' Hospital King's College London London United Kingdom.
Matthew Lumley1 Cardiovascular Division Rayne Institute St Thomas' Hospital King's College London London United Kingdom.
Satpal Arri1 Cardiovascular Division Rayne Institute St Thomas' Hospital King's College London London United Kingdom.
Tiffany Patterson1 Cardiovascular Division Rayne Institute St Thomas' Hospital King's College London London United Kingdom.
Howard Ellis1 Cardiovascular Division Rayne Institute St Thomas' Hospital King's College London London United Kingdom.
Vasiliki Manou-Stathopoulou1 Cardiovascular Division Rayne Institute St Thomas' Hospital King's College London London United Kingdom.
Catherine Macfarlane1 Cardiovascular Division Rayne Institute St Thomas' Hospital King's College London London United Kingdom.
Shruthi Chandran1 Cardiovascular Division Rayne Institute St Thomas' Hospital King's College London London United Kingdom.
Kostantinos Moschonas1 Cardiovascular Division Rayne Institute St Thomas' Hospital King's College London London United Kingdom.
Pippa Oakeshott2 Population Health Research Institute St George's University of London United Kingdom.
Timothy Lockie1 Cardiovascular Division Rayne Institute St Thomas' Hospital King's College London London United Kingdom.
Amedeo Chiribiri1 Cardiovascular Division Rayne Institute St Thomas' Hospital King's College London London United Kingdom.
Brian Clapp1 Cardiovascular Division Rayne Institute St Thomas' Hospital King's College London London United Kingdom.
Divaka Perera1 Cardiovascular Division Rayne Institute St Thomas' Hospital King's College London London United Kingdom.
Sven Plein3 Leeds University Leeds Teaching Hospitals NHS Trust Leeds United Kingdom.
Michael S Marber1 Cardiovascular Division Rayne Institute St Thomas' Hospital King's College London London United Kingdom.
Simon R Redwood1 Cardiovascular Division Rayne Institute St Thomas' Hospital King's College London London United Kingdom.
St Thomas' Hospital · GBKing's College London · GBLeeds Teaching Hospitals NHS Trust · GBSt George's, University of London · GB

Funding

British Heart Foundation CS/16/3/32615British Heart Foundation FS/13/15/30026British Heart Foundation FS/13/75/30432British Heart Foundation FS/14/11/30526British Heart Foundation FS/15/78/31678British Heart Foundation RG/16/1/32092Department of Health 10/57/67Wellcome Trust
6 · The paper itself

Abstract

Background Cold air inhalation during exercise increases cardiac mortality, but the pathophysiology is unclear. During cold and exercise, dual-sensor intracoronary wires measured coronary microvascular resistance ( MVR ) and blood flow velocity ( CBF ), and cardiac magnetic resonance measured subendocardial perfusion. Methods and Results Forty-two patients (62±9 years) undergoing cardiac catheterization, 32 with obstructive coronary stenoses and 10 without, performed either (1) 5 minutes of cold air inhalation (5°F) or (2) two 5-minute supine-cycling periods: 1 at room temperature and 1 during cold air inhalation (5°F) (randomized order). We compared rest and peak stress MVR , CBF , and subendocardial perfusion measurements. In patients with unobstructed coronary arteries (n=10), cold air inhalation at rest decreased MVR by 6% ( P=0.41), increasing CBF by 20% ( P<0.01). However, in patients with obstructive stenoses (n=10), cold air inhalation at rest increased MVR by 17% ( P<0.01), reducing CBF by 3% ( P=0.85). Consequently, in patients with obstructive stenoses undergoing the cardiac magnetic resonance protocol (n=10), cold air inhalation reduced subendocardial perfusion ( P<0.05). Only patients with obstructive stenoses performed this protocol (n=12). Cycling at room temperature decreased MVR by 29% ( P<0.001) and increased CBF by 61% ( P<0.001). However, cold air inhalation during cycling blunted these adaptations in MVR ( P=0.12) and CBF ( P<0.05), an effect attributable to defective early diastolic CBF acceleration ( P<0.05) and associated with greater ST -segment depression ( P<0.05). Conclusions In patients with obstructive coronary stenoses, cold air inhalation causes deleterious changes in MVR and CBF . These diminish or abolish the normal adaptations during exertion that ordinarily match myocardial blood supply to demand.

Indexed as

Cold TemperatureElectrocardiographyBlood Flow VelocityCardiac CatheterizationCoronary AngiographyCoronary CirculationCoronary StenosisCoronary VesselsExercise TestFemaleFollow-Up StudiesHumansMagnetic Resonance Imaging, CineMaleMiddle AgedOxygen Consumptioncoldcoronarycoronary flowcoronary microvascular resistancephysiologywave intensity analysis

Identifiers

PMID30762468
PMCPMC6064824
OpenAlexW2875665452

What Socratic 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 Socratic graph.