The role of diet and nutrition in heart failure: A state-of-the-art narrative review.
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ABSTRACT:
SUBMITTER: Billingsley HE
PROVIDER: S-EPMC7686142 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Heart failure (HF) and type 2 diabetes mellitus (T2DM) are progressive chronic diseases that increase the risk of mortality and have worse outcomes when they coexist. There has been a paucity of data on effective therapeutic measures that reduce the risk of HF in patients with T2DM. However, the issuance of the Food and Drug Administration guidance in 2008 generated data on several antihyperglycemic agents that show cardiovascular (CV) benefits beyond glucose lowering. Among them, sodium-glucose co-transporter 2 (SGLT2) inhibitors have emerged as a class of drug with proven robust benefits in modulating HF and kidney diseases in patients with T2DM. In this article, we reviewed the epidemiology, pathophysiology, prognosis, lifestyle management, and therapeutic options, especially SGLT2 inhibitors, for HF and T2DM.
| S-EPMC9536731 | biostudies-literature
Project description:Sleep-disordered breathing (SDB), either obstructive sleep apnoea (OSA) or central sleep apnoea (CSA)/Cheyne-Stokes respiration (CSR) and often a combination of the two, is highly prevalent in patients with heart failure (HF), is associated with reduced functional capacity and quality of life, and has a negative prognostic impact. European HF guidelines identify that sleep apnoea is of concern in patients with HF. Continuous positive airway pressure is the treatment of choice for OSA, and adaptive servoventilation (ASV) appears to be the most consistently effective therapy for CSA/CSR while also being able to treat concomitant obstructive events. There is a growing body of evidence that treating SDB in patients with HF, particularly using ASV for CSA/CSR, improves functional outcomes such as HF symptoms, cardiac function, cardiac disease markers, exercise tolerance and quality of life. However, conflicting results have been reported on 'hard' outcomes such as mortality and healthcare utilisation, and the influence of effectively treating SDB, including CSA/CSR, remains to be determined in randomised clinical trials. Two such trials (SERVE-HF and ADVENT-HF) in chronic stable HF and another in post-acute decompensated HF (CAT-HF) are currently underway.
| S-EPMC5491026 | biostudies-other
Project description:Morbidity and mortality associated with heart failure (HF) has remained high despite advances in therapy. Furthermore, HF-associated risk in patients with type 2 diabetes mellitus (T2D) is even higher than in patients without T2D owing to the strong reciprocal relationship between conditions. However, until recently, no therapy to treat patients with diabetes also reduced cardiovascular risks related to HF. Recent clinical studies (DAPA-HF, EMPEROR-Reduced and EMPEROR-Preserved, SOLOIST-WHF trial) and meta-analysis have demonstrated that sodium-glucose cotransporter-2 inhibitors (SGLT2i) are among the first antidiabetic drugs capable of reducing cardiovascular risks related to HF and improving the prognosis of patients with and without diabetes. Their pleiotropic mechanisms of action place them at the intersection of hemodynamic, metabolic, and neurohumoral pathways, with clear advantages for treating these patients independent of its glucose-lowering effect. Moreover, the benefits of SGLT2i were consistent across the cardiorenal continuum in different populations and clinical settings, which has led to different guidelines introducing SGLT2i as a first-line treatment for HF.
| S-EPMC9198410 | biostudies-literature
Project description:Background and Objective Heart failure (HF) is a global public health problem with high morbidity, readmission, and mortality rates. The central mediators of cardiomyocyte survival and death are mitochondria. Mitochondria are a key therapeutic target for HF and are closely involved in the pathophysiological process of HF. A recent study proposes that cuproptosis, a novel cell death mechanism, is closely related to mitochondrial respiration. Therefore, this study aims to explore the link between cuproptosis and HF, and to find novel therapeutic targets and treatments for HF. Methods A literature search (up to April 2022) was conducted through PubMed database, and the search range was limited to publications in English. After further literature search and screening, we found that we are currently the first study to explore the association between HF and cuproptosis. Key Content and Findings Research has found that mitochondria are a key therapeutic target in HF and are involved in the pathophysiological processes of energy metabolism, oxidative stress, calcium regulation, and cell death in HF. The micronutrient copper is involved in regulating mitochondrial biological processes, and high serum copper levels are significantly associated with HF. Copper overload affects mitochondrial function and exacerbates the development of HF. And cuproptosis induced by copper overload targeting lipoylated tricarboxylic acid cycle proteins, is closely related to mitochondrial respiration. Copper chelators not only treat HF but also partially rescue copper-mediated cell death. Copper binding to lipoylated components may be the reason for the hyperacetylation of mitochondrial proteins in HF. Ferredoxin 1 (FDX1) may be an upstream regulator of protein lipoylation and is closely related to cuproptosis. Conclusions This study demonstrates the important roles of mitochondria and micronutrient copper in HF. Cuproptosis may be involved in the pathophysiological process of HF and is responsible for the hyperacetylation of mitochondrial proteins in HF. Cuproptosis has the potential to be a novel therapeutic mechanism for HF, and FDX1 may be a key target for cuproptosis-based treatment of HF. This study provides a new research direction for the treatment of HF and new ideas for the development of new drugs.
| S-EPMC9622411 | biostudies-literature
Project description:Heart failure (HF) affects an increasing number of geriatric patients. The condition is classified according to whether the left ventricular ejection fraction (EF) is reduced or preserved. Many patients have heart failure with preserved ejection fraction (HFpEF) and face a shortage of effective therapeutic strategies. However, an emerging mechanical strategy for treatment is gaining momentum. Interatrial septal connection devices, i.e. V-wave device and Interatrial septal device, are new devices for patients with heart failure with preserved ejection fraction. We review the function of these systems and the data from the recent clinical trials. Interatrial septal connection device therapy provided favorable efficacy and safety profile applicable to a wide range of patients with HFpEF. However, the long-term effects of these devices on morbidity.
| S-EPMC8950450 | biostudies-literature
Project description:Background and objectiveImprovement in the affordability and convenience of genetic testing has rapidly expanded the understanding of the mechanistic causes of various pediatric cardiomyopathies. Concurrently, new therapies are being developed to better-target specific pathologies as opposed to classic therapies that treat the maladaptive processes of chronic heart failure. This review will discuss the advances in genetic testing and specific therapies that have been shown to benefit or potentially benefit genetically distinct subsets of the pediatric population with heart failure or at risk of developing heart failure.MethodsWe undertook a comprehensive database search (January 2000-August 2022) of PubMed, utilizing terms 'pediatric', 'cardiomyopathy', 'heart failure', 'genetics', and 'precision medicine'. Additional notable studies were obtained from ClinicalTrials.gov. Studies published in English that examine genetic basis and treatment modalities of pediatric heart failure.Key content and findingsNew and investigational therapies for hypertrophic cardiomyopathies associated with obstruction or Noonan syndrome, Fabry cardiomyopathy, Barth syndrome, Duchenne muscular dystrophy, single ventricle failure, and heart failure in specific demographics are discussed.ConclusionsThe rapid expansion of the genetic understanding of cardiomyopathy and heart failure as well as tailored therapies to specific molecular causes holds great promise for the future of pediatric heart failure treatment. Whereas conventional heart failure therapies target the maladaptive remodeling response that leads to worsening of heart failure, these therapies target the molecular causes of cardiomyopathy and heart failure in certain populations allowing for a potential to more significantly impact the clinical trajectory of pediatric heart failure.
| S-EPMC10080489 | biostudies-literature
Project description:The second most common cause of hospitalization due to adverse drug reactions in the UK is renal dysfunction due to diuretics, particularly in patients with heart failure, where diuretic therapy is a mainstay of treatment regimens. Therefore, the optimal frequency for monitoring renal function in these patients is an important consideration for preventing renal failure and hospitalization. This review looks at the current evidence for optimal monitoring practices of renal function in patients with heart failure according to national and international guidelines on the management of heart failure (AHA/NICE/ESC/SIGN). Current guidance of renal function monitoring is in large part based on expert opinion, with a lack of clinical studies that have specifically evaluated the optimal frequency of renal function monitoring in patients with heart failure. Furthermore, there is variability between guidelines, and recommendations are typically nonspecific. Safer prescribing of diuretics in combination with other antiheart failure treatments requires better evidence for frequency of renal function monitoring. We suggest developing more personalized monitoring rather than from the current medication-based guidance. Such flexible clinical guidelines could be implemented using intelligent clinical decision support systems. Personalized renal function monitoring would be more effective in preventing renal decline, rather than reacting to it.
| S-EPMC5736847 | biostudies-other
Project description:PurposeCardiotoxicity from anti-human epidermal growth factor receptor 2 (HER2) therapy carries a short- and long-term risk of incident heart failure and increased cardiovascular mortality in patients with breast cancer. Interruptions in anti-HER2 therapy due to cardiotoxicity can lead to suboptimal cancer treatment. The purpose of this narrative review is to outline opportunities to optimize cardiovascular care in patients with HER2-positive breast cancer to prevent interruptions in therapy.MethodsThis case-based review presents the current literature on evidence-based strategies for personalized cardiotoxicity risk assessment, risk mitigation interventions, cardiac function surveillance tools, and management of asymptomatic left ventricular dysfunction in breast cancer patients receiving anti-HER2 therapy.ResultsPretreatment cardiac risk assessment incorporates both treatment-related risk factors and patient-related risk factors for the development of cardiac dysfunction. Prevention and monitoring strategies while on treatment utilize risk factor modification, imaging and biomarker surveillance. Management of asymptomatic left ventricular dysfunction due to anti-HER2 therapy is evolving. Permissive cardiotoxicity in asymptomatic patients while starting cardioprotective therapies requires close collaboration between oncology and cardiology, and referral to cardio-oncology if available.ConclusionsPatient-centered, multimodal strategies to prevent, detect, and manage cardiotoxicity from anti-HER2 therapy are necessary to improve outcomes in patients with HER2-positive breast cancer.
| S-EPMC7820093 | biostudies-literature
Project description:BackgroundChronic heart failure (CHF) is the leading cause of all hospitalisations and readmissions in older people, accounting for a large proportion of developed countries' national health care expenditure. CHF can severely affect people's quality of life by reducing their independence and ability to undertake certain activities of daily living, as well as affecting their psychosocial and economic capacity. This paper reports the findings of a systematic narrative review of qualitative studies concerning people's experience of living with CHF, aiming to develop a wide-ranging understanding of what is known about the patient experience.MethodsWe searched eight relevant electronic databases using the terms based on the diagnosis of 'chronic heart failure', 'heart failure' and 'congestive heart failure' and qualitative methods, with restrictions to the years 1990-May 2008. We also used snowballing, hand searching and the expert knowledge of the research team to ensure all relevant papers were included in the review. Of 65 papers collected less than half (n = 30) were found relevant for this review. These papers were subsequently summarised and entered into QSR NVivo7 for data management and analysis.ResultsThe review has identified the most prominent impacts of CHF on a person's everyday life including social isolation, living in fear and losing a sense of control. It has also identified common strategies through which patients with CHF manage their illness such as sharing experiences and burdens with others and being flexible to changing circumstances. Finally, there are multiple factors that commonly impact on patients' self care and self-management in the disease trajectory including knowledge, understanding and health service encounters. These health service encounters encompass access, continuity and quality of care, co-morbid conditions, and personal relationships.ConclusionsThe core and sub-concepts identified within this study provide health professionals, service providers, policy makers and educators with broad insights into common elements of people's experiences of CHF and potential options for improving their health and wellbeing. Future studies should focus on building a comprehensive picture of CHF through examination of differences between genders, and differences within age groups, socioeconomic groups and cultural groups.
| S-EPMC2851714 | biostudies-literature
Project description:Background and objectiveHeart failure is the end-stage of various cardiovascular diseases. Recent progress in molecular biology has facilitated the understanding of the mechanisms of heart failure development at the molecular level. N6-adenosine methylation (m6A) is a post-transcriptional modification of RNA. Recent research work reported that m6A regulates gene expression and subsequently affects the activation of cell signaling pathways related to heart failure. Moreover, m6A regulators like methyltransferase-like 3 (METTL3) were reported to participate in myocardium hypertrophy. However, the current research work related to the role of m6A participating in the occurrence of heart failure is rare in some aspects like immune cell infiltration and diabetic heart diseases. Thus, it is reasonable to review the current achievements and provide further study orientation.MethodsWe searched related literature using the keywords: m6A AND heart failure in PubMed, Web of Science and Medline. The language was confined to English. The published year of searched literature ranged from 2012 to 2022. The searched results were put into Endnote software for management. Two authors investigated the searching terms and reviewed the full text of selected terms.Key content and findingsm6A and its regulators are involved in the metabolism of various types of RNAs. m6A modification can regulate various types of cell signaling pathways related to the heart failure via interaction with m6A regulators. m6A and its regulators broadly participate in the myocardium fibrosis, myocardium hypertrophy, myocardial cell apoptosis, and ischemic reperfusion injury. Specifically, m6A participates in the cell apoptosis via regulation of autophagy flux. However, the current research work does not have enough evidence to prove that m6A regulator played its specific effect on the target transcript via regulating the m6A level.Conclusionsm6A and its regulators participates in the progression of heart failure via modifying the RNA level. Future investigation of m6A should focus on the interaction between the m6A regulators and targeted transcript. Besides, the regulation role of m6A in immune cell infiltration and diabetic heart diseases should also be focused.
| S-EPMC9808110 | biostudies-literature