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1.
Race, Ancestry, and Risk: Targeting Prevention to Address Heart Failure Disparities.
Youmans, QR, Lloyd-Jones, DM, Khan, SS
Circulation. Heart failure. 2022;(1):e008741
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2.
The Efficacy and Safety of Sacubitril/Valsartan in Heart Failure Patients: A Review.
Zhang, R, Sun, X, Li, Y, He, W, Zhu, H, Liu, B, Zhang, A
Journal of cardiovascular pharmacology and therapeutics. 2022;:10742484211058681
Abstract
Heart failure (HF) is one of the leading causes of morbidity and mortality worldwide. Sacubitril/valsartan, an angiotensin receptor-neprilysin inhibitor, has been approved for the treatment of HF. At present, there have been few systematic and detailed reviews discussing the efficacy and safety of sacubitril/valsartan in HF. In this review, we first introduced the pharmacological mechanisms of sacubitril/valsartan, including the reduction in the degradation of natriuretic peptides in the natriuretic peptide system and inhibition of the renin-angiotensin system. Then, we summarized the efficacy of sacubitril/valsartan in HF patients with reduced ejection fraction (HFrEF) or preserved ejection fraction (HFpEF) including the reduction in risks of mortality and hospitalization, reversal of cardiac remodeling, regulation of biomarkers of HF, improvement of the quality of life, antiarrhythmia, improving renal dysfunction and regulation of metabolism. Finally, we discussed the safety and tolerability of sacubitril/valsartan in the treatment of HFrEF or HFpEF. Compared with ACEIs/ARBs or placebo, sacubitril/valsartan showed good safety and tolerability, although the risk of hypotension might be high. In conclusion, the overwhelming majority of studies show that sacubitril/valsartan is effective and safe in the treatment of HFrEF patients but that it has little benefit in HFpEF patients. Sacubitril/valsartan will probably be a promising anti-HF drug in the near future.
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3.
Dietary Management of Heart Failure: DASH Diet and Precision Nutrition Perspectives.
Wickman, BE, Enkhmaa, B, Ridberg, R, Romero, E, Cadeiras, M, Meyers, F, Steinberg, F
Nutrients. 2021;(12)
Abstract
Heart failure (HF) is a major health care burden increasing in prevalence over time. Effective, evidence-based interventions for HF prevention and management are needed to improve patient longevity, symptom control, and quality of life. Dietary Approaches to Stop Hypertension (DASH) diet interventions can have a positive impact for HF patients. However, the absence of a consensus for comprehensive dietary guidelines and for pragmatic evidence limits the ability of health care providers to implement clinical recommendations. The refinement of medical nutrition therapy through precision nutrition approaches has the potential to reduce the burden of HF, improve clinical care, and meet the needs of diverse patients. The aim of this review is to summarize current evidence related to HF dietary recommendations including DASH diet nutritional interventions and to develop initial recommendations for DASH diet implementation in outpatient HF management. Articles involving human studies were obtained using the following search terms: Dietary Approaches to Stop Hypertension (DASH diet), diet pattern, diet, metabolism, and heart failure. Only full-text articles written in English were included in this review. As DASH nutritional interventions have been proposed, limitations of these studies are the small sample size and non-randomization of interventions, leading to less reliable evidence. Randomized controlled interventions are needed to offer definitive evidence related to the use of the DASH diet in HF management.
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4.
Mitochondrial Homeostasis Mediates Lipotoxicity in the Failing Myocardium.
Kretzschmar, T, Wu, JMF, Schulze, PC
International journal of molecular sciences. 2021;(3)
Abstract
Heart failure remains the most common cause of death in the industrialized world. In spite of new therapeutic interventions that are constantly being developed, it is still not possible to completely protect against heart failure development and progression. This shows how much more research is necessary to understand the underlying mechanisms of this process. In this review, we give a detailed overview of the contribution of impaired mitochondrial dynamics and energy homeostasis during heart failure progression. In particular, we focus on the regulation of fatty acid metabolism and the effects of fatty acid accumulation on mitochondrial structural and functional homeostasis.
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5.
Delineating phenotypes of Kawasaki disease and SARS-CoV-2-related inflammatory multisystem syndrome: a French study and literature review.
Cherqaoui, B, Koné-Paut, I, Yager, H, Bourgeois, FL, Piram, M
Rheumatology (Oxford, England). 2021;(10):4530-4537
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Abstract
OBJECTIVE To better define the clinical distinctions between the new severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)-related paediatric inflammatory multisystem syndrome (PIMS) and Kawasaki disease (KD). METHODS We compared three groups of patients: group 1, cases from our national historic KD database (KD-HIS), before the SARS-CoV-2 pandemic; group 2, patients with KD admitted to an intensive care unit (KD-ICU) from both our original cohort and the literature, before the SARS-CoV-2 pandemic; and group 3, patients with PIMS from the literature. RESULTS KD-HIS included 425 patients [male:female ratio 1.3, mean age 2.8 years (s.d. 2.4)], KD-ICU 176 patients [male:female ratio 1.3, mean age 3.5 years (s.d. 3.1)] and PIMS 404 patients [male:female ratio 1.4, mean age 8.8 years (s.d. 3.7)]. As compared with KD-HIS patients, KD-ICU and PIMS patients had a higher proportion of cardiac failure, digestive and neurological signs. KD-ICU and PIMS patients also had a lower frequency of typical KD-mucocutaneous signs, lower platelet count, higher CRP and lower sodium level. As compared with KD-HIS and KD-ICU patients, PIMS patients were older and more frequently had myocarditis; they also had fewer coronary abnormalities and lower sodium levels. Unresponsiveness to IVIG was more frequent in KD-ICU than KD-HIS and PIMS patients. CONCLUSION On clinical grounds, KD-HIS, KD-ICU and PIMS might belong to a common spectrum of non-specific pathogen-triggered hyperinflammatory states. The causes of increasing inflammation severity within the three entities and the different effects on the heart remain to be determined.
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Timely and individualized heart failure management: need for implementation into the new guidelines.
Abdin, A, Bauersachs, J, Frey, N, Kindermann, I, Link, A, Marx, N, Lainscak, M, Slawik, J, Werner, C, Wintrich, J, et al
Clinical research in cardiology : official journal of the German Cardiac Society. 2021;(8):1150-1158
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Abstract
Due to remarkable improvements in heart failure (HF) management over the last 30 years, a significant reduction in mortality and hospitalization rates in HF patients with reduced ejection fraction (HFrEF) has been observed. Currently, the optimization of guideline-directed chronic HF therapy remains the mainstay to further improve outcomes for patients with HFrEF to reduce mortality and HF hospitalization. This includes established device therapies, such as implantable defibrillators and cardiac resynchronization therapies, which improved patients' symptoms and prognosis. Over the last 10 years, new HF drugs have merged targeting various pathways, such as those that simultaneously suppress the renin-angiotensin-aldosterone system and the breakdown of endogenous natriuretic peptides (e.g., sacubitril/valsartan), and those that inhibit the If channel and, thus, reduce heart rate (e.g., ivabradine). Furthermore, the treatment of patient comorbidities (e.g., iron deficiency) has shown to improve functional capacity and to reduce hospitalization rates, when added to standard therapy. More recently, other potential treatment mechanisms have been explored, such as the sodium/glucose co-transporter inhibitors, the guanylate cyclase stimulators and the cardiac myosin activators. In this review, we summarize the novel developments in HFrEF pharmacological and device therapy and discuss their implementation strategies into practice to further improve outcomes.
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Physical activity and the risk of heart failure: a systematic review and dose-response meta-analysis of prospective studies.
Aune, D, Schlesinger, S, Leitzmann, MF, Tonstad, S, Norat, T, Riboli, E, Vatten, LJ
European journal of epidemiology. 2021;(4):367-381
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Abstract
Although physical activity is an established protective factor for cardiovascular diseases such as ischemic heart disease and stroke, less is known with regard to the association between specific domains of physical activity and heart failure, as well as the association between cardiorespiratory fitness and heart failure. We conducted a systematic review and meta-analysis of prospective observational studies to clarify the relations of total physical activity, domains of physical activity and cardiorespiratory fitness to risk of heart failure. PubMed and Embase databases were searched up to January 14th, 2020. Summary relative risks (RRs) were calculated using random effects models. Twenty-nine prospective studies (36 publications) were included in the review. The summary RRs for high versus low levels were 0.77 (95% CI 0.70-0.85, I2 = 49%, n = 7) for total physical activity, 0.74 (95% CI 0.68-0.81, I2 = 88.1%, n = 16) for leisure-time activity, 0.66 (95% CI 0.59-0.74, I2 = 0%, n = 2) for vigorous activity, 0.81 (95% CI 0.69-0.94, I2 = 86%, n = 3) for walking and bicycling combined, 0.90 (95% CI 0.86-0.95, I2 = 0%, n = 3) for occupational activity, and 0.31 (95% CI 0.19-0.49, I2 = 96%, n = 6) for cardiorespiratory fitness. In dose-response analyses, the summary RRs were 0.89 (95% CI 0.83-0.95, I2 = 67%, n = 4) per 20 MET-hours per day of total activity and 0.71 (95% CI 0.65-0.78, I2 = 85%, n = 11) per 20 MET-hours per week of leisure-time activity. Nonlinear associations were observed in both analyses with a flattening of the dose-response curve at 15-20 MET-hours/week for leisure-time activity. These findings suggest that high levels of total physical activity, leisure-time activity, vigorous activity, occupational activity, walking and bicycling combined and cardiorespiratory fitness are associated with reduced risk of developing heart failure.
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Muscle Wasting and Sarcopenia in Heart Failure-The Current State of Science.
Lena, A, Anker, MS, Springer, J
International journal of molecular sciences. 2020;(18)
Abstract
Sarcopenia is primarily characterized by skeletal muscle disturbances such as loss of muscle mass, quality, strength, and physical performance. It is commonly seen in elderly patients with chronic diseases. The prevalence of sarcopenia in chronic heart failure (HF) patients amounts to up to 20% and may progress into cardiac cachexia. Muscle wasting is a strong predictor of frailty and reduced survival in HF patients. Despite many different techniques and clinical tests, there is still no broadly available gold standard for the diagnosis of sarcopenia. Resistance exercise and nutritional supplementation represent the currently most used strategies against wasting disorders. Ongoing research is investigating skeletal muscle mitochondrial dysfunction as a new possible target for pharmacological compounds. Novel agents such as synthetic ghrelin and selective androgen receptor modulators (SARMs) seem promising in counteracting muscle abnormalities but their effectiveness in HF patients has not been assessed yet. In the last decades, many advances have been accomplished but sarcopenia remains an underdiagnosed pathology and more efforts are needed to find an efficacious therapeutic plan. The purpose of this review is to illustrate the current knowledge in terms of pathogenesis, diagnosis, and treatment of sarcopenia in order to provide a better understanding of wasting disorders occurring in chronic heart failure.
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Cardiac Cachexia: A Well-Known but Challenging Complication of Heart Failure.
Krysztofiak, H, Wleklik, M, Migaj, J, Dudek, M, Uchmanowicz, I, Lisiak, M, Kubielas, G, Straburzyńska-Migaj, E, Lesiak, M, Kałużna-Oleksy, M
Clinical interventions in aging. 2020;:2041-2051
Abstract
Heart failure (HF) is a common complication of various cardiac diseases, and its incidence constantly increases. This is caused mainly by aging of populations and improvement in the treatment of coronary artery disease. As HF patients age, they tend to develop comorbidities, creating new problems for health-care professionals. Sarcopenia, defined as the loss of muscle mass and function, and cachexia, defined as weight loss due to an underlying illness, are muscle wasting disorders of particular relevance in the heart failure population, but they go mostly unrecognized. The coexistence of chronic HF and metabolic disorders facilitates the development of cachexia. Cachexia, in turn, significantly worsens a patient's prognosis and quality of life. The mechanisms underlying cachexia have not been explained yet and require further research. Understanding its background is crucial in the development of treatment strategies to prevent and treat tissue wasting. There are currently no specific European guidelines or recommended therapy for cachexia treatment in HF ("cardiac cachexia").
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10.
Strategies of Unloading the Failing Heart from Metabolic Stress.
Koutroumpakis, E, Jozwik, B, Aguilar, D, Taegtmeyer, H
The American journal of medicine. 2020;(3):290-296
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Abstract
We propose a unifying perspective of heart failure in patients with type 2 diabetes mellitus. The reasoning is as follows: cellular responses to fuel overload include dysregulated insulin signaling, impaired mitochondrial respiration, reactive oxygen species formation, and the accumulation of certain metabolites, collectively termed glucolipotoxicity. As a consequence, cardiac function is impaired, with intracellular calcium cycling and diastolic dysfunction as an early manifestation. In this setting, increasing glucose uptake by insulin or insulin sensitizing agents only worsens the disrupted fuel homeostasis of the heart. Conversely, restricting fuel supply by means of caloric restriction, surgical intervention, or certain pharmacologic agents will improve cardiac function by restoring metabolic homeostasis. The concept is borne out by clinical interventions, all of which unload the heart from metabolic stress.