Acute regional changes in myocardial strain may predict ventricular remodelling after myocardial infarction in a large animal model

Mansell, Doyin S.; Bruno, Vito Domenico; Sammut, Eva; Chiribiri, Amedeo; Johnson, Tom; Khaliulin, Igor; López, Daymir; Gill, Harinderjit; Fraser, Katharine; Murphy, Michele; Krieg, Thomas; Suleiman, M‐Saadeh; George, Sarah J.; Ascione, Raimondo; Cookson, Andrew

doi:10.1038/s41598-021-97834-y

Cited by 9 publications

(14 citation statements)

References 36 publications

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“…The novel method for calculating strains proposed by Mansell et al (Mansell et al, 2020; Mansell et al, 2021) was used here. Endocardial circumferential strains,

ε_{n}

, were calculated from the perimeter length data extracted from the segmentations produced by CVI42, using the definition in Equation :

ε_{n} goodbreak= \frac{L_{n} - L_{0}}{L_{0}}

where

L_{0}

is the endocardial perimeter reference length at end diastole (ED), and

L_{n}

the endocardial perimeter length at time

n

throughout the cardiac cycle for a given cine slice.…”

Section: Methodsmentioning

confidence: 99%

“…The novel method for calculating strains proposed by Mansell et al (Mansell et al, 2020;Mansell et al, 2021) was used here. Endocardial circumferential strains, n , were calculated from the perimeter length data extracted from the segmentations produced by CVI42, using the definition in Equation 1:…”

Section: Deformation Analysismentioning

confidence: 99%

“…In Mansell et al (2021), strain metrics were shown to be sensitive to MI location in the acute and early-chronic phases post-MI.…”

Section: Links Between MI and Strainsmentioning

confidence: 99%

“…Its ability to characterise acute changes to LV function post MI was similar to volume metrics such as ejection fraction. However, in that study it was found that these changes in strain also persisted to the chronic period more strongly than changes in ejection fraction, suggesting that strains may provide additional information on ventricular remodelling and function (Mansell et al, 2021).…”

Section: Introductionmentioning

confidence: 95%

“…In previous works (Mansell et al, 2020;Mansell et al, 2021) a localised, layer-specific, circumferential LV strain metric was developed, using porcine imaging data. The reproducibility of this strain metric was demonstrated across different users and software packages and compared favourably to that of standard clinical metrics such as global strains and ejection fraction (Mansell et al, 2020).…”

Section: Introductionmentioning

confidence: 99%

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MRI‐based strain measurements reflect morphological changes following myocardial infarction: A study on the UK Biobank cohort

et al. 2022

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In a porcine experimental model of myocardial infarction, a localised, layer‐specific, circumferential left ventricular strain metric has been shown to indicate chronic changes in ventricular function post‐infarction more strongly than ejection fraction. This novel strain metric might therefore provide useful prognostic information clinically. In this study, existing clinical volume indices, global strains, and the novel, layer‐specific strain were calculated for a large human cohort to assess variations in ventricular function and morphology with age, sex, and health status. Imaging and health data from the UK Biobank were obtained, including healthy volunteers and those with a history of cardiovascular illness. In total, 710 individuals were analysed and stratified by age, sex and health. Significant differences in all strain metrics were found between healthy and unhealthy populations, as well as between males and females. Significant differences in basal circumferential strain and global circumferential strain were found between healthy males and females, with males having smaller absolute values for both (all p≤ 0.001). There were significant differences in the functional variables left ventricular ejection fraction, end‐systolic volume, end‐systolic volume index and mid‐ventricular circumferential strain between healthy and unhealthy male cohorts aged 65–74 (all p≤ 0.001). These results suggest that whilst regional circumferential strains may be useful clinically for assessing cardiovascular health, care must be taken to ensure critical values are indexed correctly to age and sex, due to the differences in these values observed here.

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“…The novel method for calculating strains proposed by Mansell et al (Mansell et al, 2020; Mansell et al, 2021) was used here. Endocardial circumferential strains,

ε_{n}

, were calculated from the perimeter length data extracted from the segmentations produced by CVI42, using the definition in Equation :

ε_{n} goodbreak= \frac{L_{n} - L_{0}}{L_{0}}

where

L_{0}

is the endocardial perimeter reference length at end diastole (ED), and

L_{n}

the endocardial perimeter length at time

n

throughout the cardiac cycle for a given cine slice.…”

Section: Methodsmentioning

confidence: 99%

Section: Deformation Analysismentioning

confidence: 99%

“…In Mansell et al (2021), strain metrics were shown to be sensitive to MI location in the acute and early-chronic phases post-MI.…”

Section: Links Between MI and Strainsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 95%

Section: Introductionmentioning

confidence: 99%

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MRI‐based strain measurements reflect morphological changes following myocardial infarction: A study on the UK Biobank cohort

et al. 2022

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Defining cardiac fibrosis complexity and regulation towards therapeutic development

Claridge

Drack

Pinto

et al. 2023

Clinical and Translational Dis

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Cardiac fibrosis is insidious, accelerating cardiovascular diseases, heart failure, and death. With a notable lack of effective therapies, advances in both understanding and targeted treatment of fibrosis are urgently needed. Remodelling of the extracellular matrix alters the biomechanical and biochemical cardiac structure and function, disrupting cell-matrix interactions and exacerbating pathogenesis to ultimately impair cardiac function. Attempts at clinical fibrotic reduction have been fruitless, constrained by an understanding which severely underestimates its dynamic complexity and regulation. Integration of single-cell sequencing and quantitative proteomics has provided new insights into cardiac fibrosis, including reparative or maladaptive processes, spatiotemporal changes and fibroblast heterogeneity. Further studies have revealed microenvironmental and intercellular signalling mechanisms (including soluble mediators and extracellular vesicles), and intracellular regulators including posttranslational/epigenetic modifications, RNA binding proteins, and non-coding RNAs. This understanding of novel disease processes and molecular targets has supported the development of innovative therapeutic strategies. Indeed, targeted modulation of cellular heterogeneity, microenvironmental signalling, and intracellular regulation offer promising pre-clinical therapeutic leads. Clinical development will require further advances in our mechanistic understanding of cardiac fibrosis and dissection of the molecular basis for fibrotic remodelling.This review provides an overview of the complexities of cardiac fibrosis, emerging regulatory mechanisms and therapeutic strategies, and highlights knowledge gaps and opportunities for further investigation towards therapeutic/clinical translation.

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Development and translation of thiometallate sulfide donors using a porcine model of coronary occlusion and reperfusion

Johnson,

Holt,

Kleyman

et al. 2024

Redox Biology

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Acute regional changes in myocardial strain may predict ventricular remodelling after myocardial infarction in a large animal model

Cited by 9 publications

References 36 publications

MRI‐based strain measurements reflect morphological changes following myocardial infarction: A study on the UK Biobank cohort

MRI‐based strain measurements reflect morphological changes following myocardial infarction: A study on the UK Biobank cohort

Defining cardiac fibrosis complexity and regulation towards therapeutic development

Development and translation of thiometallate sulfide donors using a porcine model of coronary occlusion and reperfusion

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