Evidence map›Paper›PMID 32638076›Full record

ArticleHeart and vessels2021

Impact of pericoronary adipose tissue inflammation on left ventricular hypertrophy and regional physiological indices in stable coronary artery disease patients with preserved systolic function.

Hidenori Hirano, Yoshihisa Kanaji, Tomoyo Sugiyama, Masahiro Hoshino, Tomoki Horie, Toru Misawa, Kai Nogami, Hiroki Ueno, Masahiro Hada, Masao Yamaguchi and 7 more

Abstract read
PubMed Publisher
In one paragraph

Article in Heart and vessels, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.9field-weighted citation impact, top 23% 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

5 citing papers in PubMed, 6 citations in OpenAlex.

  1. Article
  2. Article
  3. Evaluation of pericoronary adipose tissue attenuation on CT.The British journal of radiology · 2023
    Review
  4. Article
  5. 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

17 authors at 2 institutions in 1 country.

Hidenori HiranoDepartment of Cardiology, Tsuchiura Kyodo General Hospital, 4-1-1 Otsuno, Tsuchiura, Ibaraki, 300-0028, Japan.
Yoshihisa KanajiDepartment of Cardiology, Tsuchiura Kyodo General Hospital, 4-1-1 Otsuno, Tsuchiura, Ibaraki, 300-0028, Japan.
Tomoyo SugiyamaDepartment of Cardiology, Tsuchiura Kyodo General Hospital, 4-1-1 Otsuno, Tsuchiura, Ibaraki, 300-0028, Japan.
Masahiro HoshinoDepartment of Cardiology, Tsuchiura Kyodo General Hospital, 4-1-1 Otsuno, Tsuchiura, Ibaraki, 300-0028, Japan.
Tomoki HorieDepartment of Cardiology, Tsuchiura Kyodo General Hospital, 4-1-1 Otsuno, Tsuchiura, Ibaraki, 300-0028, Japan.
Toru MisawaDepartment of Cardiology, Tsuchiura Kyodo General Hospital, 4-1-1 Otsuno, Tsuchiura, Ibaraki, 300-0028, Japan.
Kai NogamiDepartment of Cardiology, Tsuchiura Kyodo General Hospital, 4-1-1 Otsuno, Tsuchiura, Ibaraki, 300-0028, Japan.
Hiroki UenoDepartment of Cardiology, Tsuchiura Kyodo General Hospital, 4-1-1 Otsuno, Tsuchiura, Ibaraki, 300-0028, Japan.
Masahiro HadaDepartment of Cardiology, Tsuchiura Kyodo General Hospital, 4-1-1 Otsuno, Tsuchiura, Ibaraki, 300-0028, Japan.
Masao YamaguchiDepartment of Cardiology, Tsuchiura Kyodo General Hospital, 4-1-1 Otsuno, Tsuchiura, Ibaraki, 300-0028, Japan.
Yohei SuminoDepartment of Cardiology, Tsuchiura Kyodo General Hospital, 4-1-1 Otsuno, Tsuchiura, Ibaraki, 300-0028, Japan.
Rikuta HamayaDepartment of Cardiology, Tsuchiura Kyodo General Hospital, 4-1-1 Otsuno, Tsuchiura, Ibaraki, 300-0028, Japan.
Eisuke UsuiDepartment of Cardiology, Tsuchiura Kyodo General Hospital, 4-1-1 Otsuno, Tsuchiura, Ibaraki, 300-0028, Japan.
Tadashi MuraiDepartment of Cardiology, Tsuchiura Kyodo General Hospital, 4-1-1 Otsuno, Tsuchiura, Ibaraki, 300-0028, Japan.
Tetsumin LeeDepartment of Cardiovascular Medicine, Tokyo Medical and Dental University, Tokyo, Japan.
Taishi YonetsuDepartment of Cardiovascular Medicine, Tokyo Medical and Dental University, Tokyo, Japan.
Tsunekazu KakutaDepartment of Cardiology, Tsuchiura Kyodo General Hospital, 4-1-1 Otsuno, Tsuchiura, Ibaraki, 300-0028, Japan. kaz@joy.email.ne.jp.
Tsuchiura Kyodo General Hospital · JPTokyo Medical and Dental University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Systemic low-grade inflammation has been shown to be associated with left ventricular hypertrophy (LVH). However, the relationship between pericoronary adipose tissue attenuation (PCATA) and both LVH and regional physiological indices remains unknown. This study aimed to evaluate the association of PCATA with LVH and regional physiological indices in stable coronary artery disease (CAD) patients with preserved systolic function. A total of 114 CAD patients who underwent coronary CT angiography (CTA) and invasive physiological tests showing ischemia due to a single de novo lesion were included in the study. On proximal 40-mm segments of all three major coronary vessels on CTA, PCATA was assessed by the crude analysis of the mean CT attenuation value [- 190 to - 30 Hounsfield units [HU)] and the culprit vessel PCATA was used for the analysis. Regional physiological indices were invasively obtained by pressure-temperature sensor-tipped wire. The patients were divided into three groups by culprit vessel PCATA tertiles, and clinical, CTA-derived, and physiological indices were compared. Univariable and multivariable analyses were further performed to determine the predictors of LVH. Angiographic stenosis severity, culprit lesion locations, culprit vessel fractional flow reserve, coronary flow reserve, index of microcirculatory resistance, total and target vessel coronary calcium score, and biomarkers including high-sensitivity C-reactive protein were not different among the groups. The left ventricular (LV) mass, LV mass index (LVMI), and LV mass at risk were all significantly different in the three groups with the greatest values in the highest tertile group (all, P < 0.05). On multivariable analysis, male gender, NT-proBNP, and PCATA were independent predictors of LVMI. Culprit vessel PCATA was significantly associated with LVMI, but not with regional physiology in CAD patients with functionally significant lesions and preserved systolic function. Our results may offer insight into the pathophysiological mechanisms linking pericoronary inflammation and LVH to worse prognosis.

Indexed as

Adipose TissueAgedComputed Tomography AngiographyCoronary AngiographyCoronary Artery DiseaseCoronary VesselsFemaleFollow-Up StudiesFractional Flow Reserve, MyocardialHumansHypertrophy, Left VentricularInflammationMaleMicrocirculationMiddle AgedProspective StudiesCoronary artery diseaseInflammationLeft ventricular hypertrophy

Identifiers

PMID32638076
OpenAlexW3041596615

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.