Global longitudinal strain by feature tracking for optimized prediction of adverse remodeling after ST-elevation myocardial infarction

Reindl, Martin; Tiller, Christina; Holzknecht, Magdalena; Lechner, Ivan; Eisner, Dorothea; Riepl, Laura; Pamminger, Mathias; Henninger, Benjamin; Mayr, Agnes; Schwaiger, Johannes; Klug, Gert; Bauer, Axel; Metzler, Bernhard; Reinstadler, Sebastian Johannes

doi:10.1007/s00392-020-01649-2

Cited by 28 publications

(38 citation statements)

References 45 publications

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“…In Iran, 24/7 primary percutaneous coronary intervention (PCI) as the standard treatment strategy for patients with ST-elevation myocardial infarction (STEMI) [3][4][5][6][7] was launched in September 2015 to achieve a fair distribution of healthcare resources. Currently, 49 general and heart hospitals provide these services, with 48 915 patients having undergone primary PCI thus far.…”

Section: Sirsmentioning

confidence: 99%

COVID-19 sends STEMI to quarantine!?

et al. 2020

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Section: Sirsmentioning

confidence: 99%

COVID-19 sends STEMI to quarantine!?

et al. 2020

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“…For the definition of adverse LV remodeling, we considered LVEDV and/or an LVESV delta change of 12%, which is lower than most reports, and 6 months for follow-up, longer if compared to other studies, mostly around 3/4 months. Thus, this issue may have induced a larger rate of adverse remodeling in our population (49%), as compared to other cohorts (17–24.4%) ( 11 , 12 , 22 , 23 ). In the majority of studies, baseline GLS was the best predictor of adverse remodeling among all strain values ( 11 , 22 – 24 ).…”

Section: Discussionmentioning

confidence: 65%

“…Regarding FT-CMR strain analysis, the adverse remodeling group showed worse GCS and GLS values at baseline and FU-CMR ( Figure 5 ), if compared to reverse and null remodeling categories as one. Various studies investigated the value of FT-CMR features in predicting adverse remodeling ( 11 , 12 , 22 ), using different cut-off values and follow-up periods. For the definition of adverse LV remodeling, we considered LVEDV and/or an LVESV delta change of 12%, which is lower than most reports, and 6 months for follow-up, longer if compared to other studies, mostly around 3/4 months.…”

Section: Discussionmentioning

confidence: 99%

Protective Value of Aspirin Loading Dose on Left Ventricular Remodeling After ST-Elevation Myocardial Infarction

Calvieri

Galea

Cilia

et al. 2022

Front. Cardiovasc. Med.

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AimsLeft ventricular (LV) remodeling after ST-elevation myocardial infarction (STEMI) is a complex process, defined as changes of LV volumes over time. CMR feature tracking analysis (CMR-FT) offers an accurate quantitative assessment of LV wall deformation and myocardial contractile function. This study aimed to evaluate the role of myocardial strain parameters in predicting LV remodeling and to investigate the effect of Aspirin (ASA) dose before primary coronary angioplasty (pPCI) on myocardial injury and early LV remodeling.Methods and ResultsSeventy-eight patients undergoing CMR, within 9 days from symptom onset and after 6 months, were enrolled in this cohort retrospective study. We divided the study population into three groups based on a revised Bullock's classification and we evaluated the role of baseline CMR features in predicting early LV remodeling. Regarding CMR strain analysis, worse global circumferential and longitudinal strain (GCS and GLS) values were associated with adverse LV remodeling. Patients were also divided based on pre-pPCI ASA dosage. Significant differences were detected in patients receiving ASA 500 mg dose before pPCI, which showed lower infarct size extent and better strain values compared to those treated with ASA 250 mg. The stepwise multivariate logistic regression analysis, adjusted for covariates, indicated that a 500 mg ASA dose remained an inverse independent predictor of early adverse LV remodeling.ConclusionGCS and GLS have high specificity to detect early LV adverse remodeling. We first reported a protective effect of ASA loading dose of 500 mg before pPCI on LV myocardial damage and in reducing early LV adverse remodeling.

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“…GLS has been shown to be an independent predictor of adverse remodeling after ST-elevated MI in humans and can be a more sensitive functional output than the traditionally used EF. 40 We further explored changes to tissue architecture which led to an improvement in cardiac function and alterations in scar formation. A heavier collagen burden increases passive tissue stiffness, heightening afterload and hindering systolic function.…”

Section: Discussionmentioning

confidence: 99%

Targeting 5-HT _2B Receptor Signaling Prevents Border Zone Expansion and Improves Microstructural Remodeling After Myocardial Infarction

et al. 2021

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Background: Myocardial infarction (MI) induces an intense injury response which ultimately generates a collagen-dominated scar. While required to prevent ventricular rupture, the fibrotic process is often sustained in a manner detrimental to optimal recovery. Cardiac myofibroblasts are the cells tasked with depositing and remodeling collagen and are a prime target to limit the fibrotic process post-MI. Serotonin 2B receptor (5-HT 2B ) signaling has been shown to be harmful in a variety of cardiopulmonary pathologies and could play an important role in mediating scar formation after MI. Methods: We employed two pharmacologic antagonists to explore the effect of 5-HT 2B inhibition on outcomes post-MI and characterized the histological and microstructural changes involved in tissue remodeling. Inducible, 5-HT 2B ablation driven by Tcf21 MCM and Postn MCM were used to evaluate resident cardiac fibroblast- and myofibroblast-specific contributions of 5-HT 2B , respectively. RNA sequencing was used to motivate subsequent in vitro analyses to explore cardiac fibroblast phenotype. Results: 5-HT 2B antagonism preserved cardiac structure and function by facilitating a less fibrotic scar, indicated by decreased scar thickness and decreased border zone area. 5-HT 2B antagonism resulted in collagen fiber redistribution to thinner collagen fibers which were more anisotropic, enhancing left ventricular contractility, while fibrotic tissue stiffness was decreased, limiting the hypertrophic response of uninjured cardiomyocytes. Using a tamoxifen-inducible Cre, we ablated 5-HT 2B from Tcf21 -lineage resident cardiac fibroblasts and saw similar improvements to the pharmacologic approach. Tamoxifen-inducible Cre-mediated ablation of 5-HT 2B after onset of injury in Postn -lineage myofibroblasts also improved cardiac outcomes. RNA sequencing and subsequent in vitro analyses corroborate a decrease in fibroblast proliferation, migration, and remodeling capabilities through alterations in Dnajb4 expression and Src phosphorylation. Conclusions: Together, our findings illustrate that 5-HT 2B expression in either cardiac fibroblasts or activated myofibroblasts directly contributes to excessive scar formation, resulting in adverse remodeling and impaired cardiac function after MI.

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Global longitudinal strain by feature tracking for optimized prediction of adverse remodeling after ST-elevation myocardial infarction

Cited by 28 publications

References 45 publications

COVID-19 sends STEMI to quarantine!?

COVID-19 sends STEMI to quarantine!?

Protective Value of Aspirin Loading Dose on Left Ventricular Remodeling After ST-Elevation Myocardial Infarction

Targeting 5-HT _2B Receptor Signaling Prevents Border Zone Expansion and Improves Microstructural Remodeling After Myocardial Infarction

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Global longitudinal strain by feature tracking for optimized prediction of adverse remodeling after ST-elevation myocardial infarction

Cited by 28 publications

References 45 publications

COVID-19 sends STEMI to quarantine!?

COVID-19 sends STEMI to quarantine!?

Protective Value of Aspirin Loading Dose on Left Ventricular Remodeling After ST-Elevation Myocardial Infarction

Targeting 5-HT 2B Receptor Signaling Prevents Border Zone Expansion and Improves Microstructural Remodeling After Myocardial Infarction

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Targeting 5-HT _2B Receptor Signaling Prevents Border Zone Expansion and Improves Microstructural Remodeling After Myocardial Infarction