Evidence map›Paper›PMID 34551866›Full record

ReviewJournal of cardiology2022

Human genetics and its impact on cardiovascular disease.

Hayato Tada, Noboru Fujino, Kenshi Hayashi, Masa-Aki Kawashiri, Masayuki Takamura

Abstract readReview
PubMed Publisher
In one paragraph

Review in Journal of cardiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 2 pooled it
–field-weighted citation impact
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

26 citing papers in PubMed, 2 syntheses or guidelines pooled it.

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  9. Different Polymorphisms of the Renin-Angiotensin-Aldosterone System Genes are Associated with Poorer Blood Pressure Control in Hypertensive Older Adults.High blood pressure & cardiovascular prevention : the official journal of the Italian Society of Hypertension · 2025
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors.

Hayato TadaDepartment of Cardiovascular Medicine, Kanazawa University Graduate School of Medical Sciences, Kanazawa, Japan. Electronic address: ht240z@med.kanazawa-u.ac.jp.
Noboru FujinoDepartment of Cardiovascular Medicine, Kanazawa University Graduate School of Medical Sciences, Kanazawa, Japan.
Kenshi HayashiDepartment of Cardiovascular Medicine, Kanazawa University Graduate School of Medical Sciences, Kanazawa, Japan.
Masa-Aki KawashiriDepartment of Cardiovascular Medicine, Kanazawa University Graduate School of Medical Sciences, Kanazawa, Japan.
Masayuki TakamuraDepartment of Cardiovascular Medicine, Kanazawa University Graduate School of Medical Sciences, Kanazawa, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cardiovascular disease (CVD) is a major cause of death worldwide. Given that CVD is a highly heritable trait, researchers have attempted to fully understand the genetic basis of CVD for a long time. The human genome comprises 3,100 Mbp per haploid genome and 6,200 Mbp in total (diploid genome). However, there is a tendency for rare genetic variations to exhibit a large effect size, whereas common genetic variations have a small effect on diseases, because of natural selection. In this sense, dividing genetic variations into two groups based on allele frequency (and effect sizes on diseases) is a good idea. We know there are several important genes (especially lipid-related genes) in which rare genetic variations are apparently associated with CVD risk, while a polygenic risk score comprising common genetic variations appears to work quite well among general populations. That information can be used not only for risk stratification but also for discoveries for novel pharmacologic targets. In this review article, we provide the important and simple idea that human genetics is important for CVD because it is a highly heritable trait, and we believe that it will lead to precision medicine in this field.

Indexed as

Cardiovascular DiseasesGenetic Predisposition to DiseaseHuman GeneticsHumansCardiovascular diseaseGeneticsRisk factorRisk stratification

Identifiers

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.