Evidence map›Paper›PMID 33654238›Full record

ArticleJournal of human hypertension2022

Characterisation of hypertensive heart disease: pathological insights from a sudden cardiac death cohort to inform clinical practice.

J D Westaby, C Miles, I Chis Ster, S T E Cooper, T F Antonios, D Meijles, E R Behr, M N Sheppard

Abstract read
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In one paragraph

Article in Journal of human hypertension, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.4field-weighted citation impact, top 10% 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

16 citing papers in PubMed, 29 citations in OpenAlex.

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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

8 authors at 1 institution in 1 country.

J D WestabyCardiology Clinical Academic Group, Molecular and Clinical Sciences Research Institute, St George's University of London, London, SW17 0RE, UK. jwestaby@sgul.ac.uk.ORCID 0000-0002-1903-2390
C MilesCardiology Clinical Academic Group, Molecular and Clinical Sciences Research Institute, St George's University of London, London, SW17 0RE, UK.
I Chis SterInfection and Immunity Research Institute, St George's University of London, London, SW17 0RE, UK.ORCID 0000-0003-2637-1259
S T E CooperCardiology Clinical Academic Group, Molecular and Clinical Sciences Research Institute, St George's University of London, London, SW17 0RE, UK.ORCID 0000-0002-2960-6140
T F AntoniosCardiology Clinical Academic Group, Molecular and Clinical Sciences Research Institute, St George's University of London, London, SW17 0RE, UK.
D MeijlesCardiology Clinical Academic Group, Molecular and Clinical Sciences Research Institute, St George's University of London, London, SW17 0RE, UK.
E R BehrCardiology Clinical Academic Group, Molecular and Clinical Sciences Research Institute, St George's University of London, London, SW17 0RE, UK.
M N SheppardCardiology Clinical Academic Group, Molecular and Clinical Sciences Research Institute, St George's University of London, London, SW17 0RE, UK.
St George's, University of London · GB

Funding

British Heart Foundation FS/18/28/33549British Heart Foundation FS/19/24/34262Department of Health
6 · The paper itself

Abstract

Hypertensive heart disease refers to changes in the myocardium that result from hypertension. The relationship between hypertensive heart disease and sudden cardiac death is well established, but there are few pathological studies. We examined the clinical and pathological features of hypertensive heart disease in sudden cardiac death victims from a national cardiovascular pathology registry. We investigated 5239 cases of sudden cardiac death between 1994 and 2018. Hearts were examined by two expert cardiac pathologists. Diagnostic criteria included history of hypertension, increased heart weight and left ventricular wall thickness in the absence of other causes. Collagen was quantified using picrosirius red staining and imaging software. Of 75 sudden cardiac death cases due to hypertensive heart disease (age at death: 54 ± 16 years; 56% males), 56 (75%) reported no prior cardiac symptoms. Thirty-four (45%) recorded a BMI ≥ 30. Only two (2.7%) had hypertensive heart disease diagnosed antemortem. Four (5%) were diagnosed clinically with hypertrophic cardiomyopathy, but lacked myocyte disarray at autopsy. All hearts showed concentric left ventricular hypertrophy and myocyte hypertrophy. Fibrosis was identified microscopically in 59 cases (81%). The posterior left ventricular wall showed the greatest increase in the percentage of collagen in hypertensive diseased hearts compared to controls (25.2% vs 17.9%, p = 0.034). Most sudden deaths due to hypertensive heart disease occur without prior cardiac symptoms; thus, clinical risk stratification is challenging. Hypertensive heart disease can be misdiagnosed in life as hypertrophic cardiomyopathy which has major implications for relatives. Pathologists require a history of hypertension and histology for a definitive diagnosis of hypertensive heart disease.

Indexed as

Cardiomyopathy, HypertrophicHeart DiseasesHypertensionAdultAgedCollagenDeath, Sudden, CardiacFemaleHumansMaleMiddle AgedMyocardiumCollagen

Identifiers

PMID33654238
OpenAlexW3133904002

What OpenQuestion holds

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Read underepoch 390

Registered trials

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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.