Evidence map›Paper›PMID 42949836›Full record

ReviewEchocardiography (Mount Kisco, N.Y.)2026

Global Longitudinal Strain in Type 1 and Type 2 Diabetes: Why Similar Abnormalities May Not Mean the Same Thing.

Zuhal Fazli, Vivetha Pooranachandran

Abstract readReview
In one paragraph

Review in Echocardiography (Mount Kisco, N.Y.), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

Zuhal FazliThe Royal Wolverhampton Hospital, Wolverhampton, UK.
Vivetha PooranachandranDepartment of Natural Sciences, Middlesex University, London, UK.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Global longitudinal strain (GLS) is increasingly used to detect subclinical myocardial dysfunction in diabetes, but similar abnormalities may not carry the same biological meaning in type 1 diabetes (T1D) and type 2 diabetes (T2D). In T1D, chronic hyperglycemia, oxidative stress, microvascular dysfunction, and progressive interstitial remodeling may contribute prominently to impaired myocardial deformation. In T2D, insulin resistance, adiposity, lipotoxicity, mitochondrial dysfunction, and altered myocardial energetics may have greater influence, although substantial mechanistic overlap exists. This review examines how these differing pathophysiological contexts influence the interpretation of GLS, the evolution of myocardial dysfunction, and reported responses to contemporary cardiometabolic therapies. Complementary deformation parameters are also considered where they provide additional insight into ventricular mechanics. Importantly, GLS is a sensitive marker of myocardial dysfunction but is not mechanism-specific and may be influenced by metabolic, hemodynamic, and loading conditions. Interpretation should therefore incorporate diabetes subtype, disease duration, glycemic burden, comorbidity, and complementary imaging findings. A mechanistically informed approach may improve the clinical and research interpretation of myocardial deformation in diabetes.

Indexed as

Diabetes Mellitus, Type 1Diabetes Mellitus, Type 2Diabetic CardiomyopathiesGlobal Longitudinal StrainHumansdiabetic cardiomyopathyglobal longitudinal strainspeckle‐tracking echocardiographytype 1 diabetestype 2 diabetes

Identifiers

PMID42949836
PMCPMC13715998

What OpenQuestion holds

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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.