Enhanced Inflammation is a Marker for Risk of Post-Infarct Ventricular Dysfunction and Heart Failure

Świątkiewicz, Iwona; Magielski, Przemysław; Kubica, Jacek; Zadourian, Adena; DeMaria, Anthony N.; Taub, Pam R.

doi:10.3390/ijms21030807

Cited by 37 publications

(47 citation statements)

References 58 publications

(198 reference statements)

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“…In addition, low-grade inflammation and oxidative stress contribute to the pathophysiology of obesity, atherosclerosis, T2DM, and MetS [ 5 , 63 , 64 , 65 , 66 ]. Elevated C-reactive protein (CRP) levels, which are related to insulin resistance and MetS, are independent predictors of CVD events [ 63 , 67 , 68 , 69 , 70 , 71 ]. Oxidative stress is associated with adiposity, impaired insulin signaling pathways, insulin resistance, and increased risk of cardiometabolic diseases [ 64 , 72 , 73 , 74 ].…”

Section: Impact Of Circadian Rhythms and Circadian Rhythm Disruptimentioning

confidence: 99%

Time-Restricted Eating and Metabolic Syndrome: Current Status and Future Perspectives

2021

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Metabolic syndrome (MetS) occurs in ~30% of adults and is associated with increased risk of cardiovascular disease and diabetes mellitus. MetS reflects the clustering of individual cardiometabolic risk factors including central obesity, elevated fasting plasma glucose, dyslipidemia, and elevated blood pressure. Erratic eating patterns such as eating over a prolonged period per day and irregular meal timing are common in patients with MetS. Misalignment between daily rhythms of food intake and circadian timing system can contribute to circadian rhythm disruption which results in abnormal metabolic regulation and adversely impacts cardiometabolic health. Novel approaches which aim at restoring robust circadian rhythms through modification of timing and duration of daily eating represent a promising strategy for patients with MetS. Restricting eating period during a day (time-restricted eating, TRE) can aid in mitigating circadian disruption and improving cardiometabolic outcomes. Previous pilot TRE study of patients with MetS showed the feasibility of TRE and improvements in body weight and fat, abdominal obesity, atherogenic lipids, and blood pressure, which were observed despite no overt attempt to change diet quantity and quality or physical activity. The present article aims at giving an overview of TRE human studies of individuals with MetS or its components, summarizing current clinical evidence for improving cardiometabolic health through TRE intervention in these populations, and presenting future perspectives for an implementation of TRE to treat and prevent MetS. Previous TRE trials laid the groundwork and indicate a need for further clinical research including large-scale controlled trials to determine TRE efficacy for reducing long-term cardiometabolic risk, providing tools for sustained lifestyle changes and, ultimately, improving overall health in individuals with MetS.

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Section: Impact Of Circadian Rhythms and Circadian Rhythm Disruptimentioning

confidence: 99%

Time-Restricted Eating and Metabolic Syndrome: Current Status and Future Perspectives

2021

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“…Chronic pathological disorders, including cardiovascular diseases (CVDs) [ 1 , 2 ], neurodegenerative diseases [ 3 , 4 ], diabetes [ 5 , 6 ], metabolic syndrome [ 7 , 8 ], and cancer [ 9 , 10 ] share an inflammatory microenvironment as a hallmark [ 11 ]. A Common feature of these complex diseases is the activation of “sterile” inflammatory pathways, in which immune cells represent relevant effectors and drivers for the onset and progression of the disease [ 12 ], due to their extreme capability to reshape their phenotype [ 13 ], to functionally [ 14 ], metabolically [ 15 , 16 ] adapting to the surrounding environment.…”

Section: Introductionmentioning

confidence: 99%

Innate Immunity Effector Cells as Inflammatory Drivers of Cardiac Fibrosis

Baci

Bosi

Parisi

et al. 2020

IJMS

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Despite relevant advances made in therapies for cardiovascular diseases (CVDs), they still represent the first cause of death worldwide. Cardiac fibrosis and excessive extracellular matrix (ECM) remodeling are common end-organ features in diseased hearts, leading to tissue stiffness, impaired myocardial functional, and progression to heart failure. Although fibrosis has been largely recognized to accompany and complicate various CVDs, events and mechanisms driving and governing fibrosis are still not entirely elucidated, and clinical interventions targeting cardiac fibrosis are not yet available. Immune cell types, both from innate and adaptive immunity, are involved not just in the classical response to pathogens, but they take an active part in “sterile” inflammation, in response to ischemia and other forms of injury. In this context, different cell types infiltrate the injured heart and release distinct pro-inflammatory cytokines that initiate the fibrotic response by triggering myofibroblast activation. The complex interplay between immune cells, fibroblasts, and other non-immune/host-derived cells is now considered as the major driving force of cardiac fibrosis. Here, we review and discuss the contribution of inflammatory cells of innate immunity, including neutrophils, macrophages, natural killer cells, eosinophils and mast cells, in modulating the myocardial microenvironment, by orchestrating the fibrogenic process in response to tissue injury. A better understanding of the time frame, sequences of events during immune cells infiltration, and their action in the injured inflammatory heart environment, may provide a rationale to design new and more efficacious therapeutic interventions to reduce cardiac fibrosis.

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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].…”

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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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Enhanced Inflammation is a Marker for Risk of Post-Infarct Ventricular Dysfunction and Heart Failure

Cited by 37 publications

References 58 publications

Time-Restricted Eating and Metabolic Syndrome: Current Status and Future Perspectives

Time-Restricted Eating and Metabolic Syndrome: Current Status and Future Perspectives

Innate Immunity Effector Cells as Inflammatory Drivers of Cardiac Fibrosis

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

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