Left Ventricular Post-Infarct Remodeling

Bijl, Pieter van der; Abou, Rachid; Goedemans, Laurien; Gersh, Bernard J.; Holmes, David R.; Marsan, Nina Ajmone; Delgado, Victoria; Bax, Jeroen J.

doi:10.1016/j.jchf.2019.08.014

Cited by 95 publications

(40 citation statements)

References 29 publications

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“…Later on, it became more general term. Nowadays, heart remodeling means the complex process of disturbances in myocardial structure and function in response to the damaging myocardial overload and loss of the functioning myocardium ( 4 ).…”

Section: Introductionmentioning

confidence: 99%

Cells of the Immune System in Cardiac Remodeling: Main Players in Resolution of Inflammation and Repair After Myocardial Infarction

et al. 2021

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The burden of heart failure (HF), developing after myocardial infarction MI, still represents a major issue in clinical practice. Failure of appropriate resolution of inflammation during post-myocardial injury is associated with unsuccessful left ventricular remodeling and underlies HF pathogenesis. Cells of the immune system have been shown to mediate both protective and damaging effects in heart remodeling. This ambiguity of the role of the immune system and inconsistent results of the recent clinical trials question the benefits of anti-inflammatory therapies during acute MI. The present review will summarize knowledge of the roles that different cells of the immune system play in the process of post-infarct cardiac healing. Data on the phenotype, active molecules and functions of the immune cells, based on the results of both experimental and clinical studies, will be provided. For some cellular subsets, such as macrophages, neutrophils, dendritic cells and lymphocytes, an anti-inflammatory activity has been attributed to the specific subpopulations. Activity of other cells, such as eosinophils, mast cells, natural killer (NK) cells and NKT cells has been shown to be highly dependent of the signals created by micro-environment. Also, new approaches for classification of cellular phenotypes based on the single-cell RNA sequencing allow better understanding of the phenotype of the cells involved in resolution of inflammation. Possible perspectives of immune-mediated therapy for AMI patients are discussed in the conclusion. We also outline unresolved questions that need to be solved in order to implement the current knowledge on the role of the immune cells in post-MI tissue repair into practice.

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Section: Introductionmentioning

confidence: 99%

Cells of the Immune System in Cardiac Remodeling: Main Players in Resolution of Inflammation and Repair After Myocardial Infarction

et al. 2021

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“…The pathophysiology of post-infarct LVSD is complex and poor understood [5]. Much evidence has revealed that processes such as myocardial injury associated with infarct size, left ventricular remodelling, myocardial stress, oxidative stress, and local and systemic inflammatory responses are all involved in the pathophysiology of post-infarct LVSD [5,[7][8][9]. Recent studies further indicated that stress-induced hyperglycaemia (SIH) and concomitant metabolic perturbations also play an extremely important role in the initiation and progression of post-infarct LVSD [10][11][12].…”

mentioning

confidence: 99%

Augmented glycaemic gap is a marker for an increased risk of post-infarct left ventricular systolic dysfunction

Zhu

Liu

Meng

et al. 2020

Cardiovasc Diabetol

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Background: Left ventricular systolic dysfunction (LVSD) occurs frequently after acute ST-segment elevation myocardial infarction (STEMI). The predisposing factors and underlying mechanism of post-infarct LVSD are not fully understood. The present study mainly investigated the correlation between glycaemic gap, a novel index of stressinduced hyperglycaemia (SIH), and post-infarct LVSD. Methods: A total of 274 first STEMI patients were enrolled in this cross-sectional study. Transthoracic echocardiography was performed within 48 h after admission and at 6 months after discharge to obtain left ventricular ejection fraction (LVEF). The change in LVEF was calculated as LVEF at 6 months after discharge minus baseline LVEF. Additionally, post-infarct LVSD was defined as LVEF ≤ 50%. Most importantly, glycaemic gap was calculated as admission blood glucose (ABG) minus the estimated average glucose over the previous 3 months. Results: In patients without diabetes mellitus (DM), multivariate linear regression analysis revealed that both glycaemic gap (Beta = − 1.214, 95% CI − 1.886 to − 0.541, p < 0.001) and ABG (Beta = − 1.124, 95% CI − 1.795 to − 0.453, p = 0.001) were associated with change in LVEF. In DM patients, only glycaemic gap was still associated with change in LVEF, although this association was not observed in univariate linear regression analysis. Regarding the association between SIH and post-infarct LVSD, multivariate logistic regression analysis revealed that both glycaemic gap (OR = 1.490, 95% CI 1.043 to 2.129, p = 0.028) and ABG (OR = 1.600, 95% CI 1.148 to 2.229, p = 0.005) were associated with an increased risk of having post-infarct LVSD in non-DM patients. However, after multivariate adjustment in DM patients, only glycaemic gap (OR = 1.399, 95% CI 1.021 to 1.919, p = 0.037) remained associated with an increased risk of having post-infarct LVSD. Furthermore, the predictive value of glycaemic gap for postinfarct LVSD was not inferior to ABG in non-DM patients (p = 0.499), and only glycaemic gap, instead of ABG, could significantly predict post-infarct LVSD in DM patients (AUC = 0.688, 95% CI 0.591 to 0.774, p = 0.002). Conclusions: Glycaemic gap was strongly associated with a change in LVEF and an increased risk of having postinfarct LVSD in patients following STEMI. In STEMI patients with DM, glycaemic gap could provide more valuable information than ABG in identifying patients at high risk of developing post-infarct LVSD.

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“…However, mortality and LVR remain substantial in these patients. Interestingly, LV remodelers are more likely to be admitted to hospital for HF than non-remodelers [6,7]. As such, novel therapeutic interventions are required to reduce IS, preserve LV systolic function, and improve survival in reperfused-STEMI patients.…”

Section: Clinical Perspectives For Nep Inhibition In Miri Preventionmentioning

confidence: 99%

“…The improvement of strategies for the protection of myocardium following acute ischemic insult represents, nowadays, the real challenge of the clinical research in cardiology. In fact, despite the widespread use of the best available therapies (i.e., timely revascularization, antiplatelet and anti-remodeling drugs, vascular devices), up to 30% of patients with ST-elevated myocardial infarction (STEMI) still develop left ventricular remodeling (LVR) [1][2][3][4][5] and heart failure (HF) [6,7].…”

Section: Introductionmentioning

confidence: 99%

The Rationale of Neprilysin Inhibition in Prevention of Myocardial Ischemia-Reperfusion Injury during ST-Elevation Myocardial Infarction

Bellis¹,

Mauro

Barbato³

et al. 2020

Cells

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During the last three decades, timely myocardial reperfusion using either thrombolytic therapy or primary percutaneous intervention (pPCI) has allowed amazing improvements in outcomes with a more than halving in 1-year ST-elevation myocardial infarction (STEMI) mortality. However, mortality and left ventricle (LV) remodeling remain substantial in these patients. As such, novel therapeutic interventions are required to reduce myocardial infarction size, preserve LV systolic function, and improve survival in reperfused-STEMI patients. Myocardial ischemia-reperfusion injury (MIRI) prevention represents the main goal to reach in order to reduce STEMI mortality. There is currently no effective therapy for MIRI prevention in STEMI patients. A significant reason for the weak and inconsistent results obtained in this field may be the presence of multiple, partially redundant, mechanisms of cell death during ischemia-reperfusion, whose relative importance may depend on the conditions. Therefore, it is always more recognized that it is important to consider a “multi-targeted cardioprotective therapy”, defined as an additive or synergistic cardioprotective agents or interventions directed to distinct targets with different timing of application (before, during, or after pPCI). Given that some neprilysin (NEP) substrates (natriuretic peptides, angiotensin II, bradykinin, apelins, substance P, and adrenomedullin) exert a cardioprotective effect against ischemia-reperfusion injury, it is conceivable that antagonism of proteolytic activity by this enzyme may be considered in a multi-targeted strategy for MIRI prevention. In this review, by starting from main pathophysiological mechanisms promoting MIRI, we discuss cardioprotective effects of NEP substrates and the potential benefit of NEP pharmacological inhibition in MIRI prevention.

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Left Ventricular Post-Infarct Remodeling

Cited by 95 publications

References 29 publications

Cells of the Immune System in Cardiac Remodeling: Main Players in Resolution of Inflammation and Repair After Myocardial Infarction

Cells of the Immune System in Cardiac Remodeling: Main Players in Resolution of Inflammation and Repair After Myocardial Infarction

Augmented glycaemic gap is a marker for an increased risk of post-infarct left ventricular systolic dysfunction

The Rationale of Neprilysin Inhibition in Prevention of Myocardial Ischemia-Reperfusion Injury during ST-Elevation Myocardial Infarction

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