Current Cardiovascular Imaging Reports, Год журнала: 2024, Номер 18(1)
Опубликована: Дек. 1, 2024
Язык: Английский
ESC Heart Failure, Год журнала: 2024, Номер 11(2), С. 1051 - 1060
Опубликована: Янв. 19, 2024
Abstract Aims The combination of haemoglobin, albumin, lymphocytes, and platelets (HALP) is a new metric used to assess patient prognosis in many diseases. This study aimed the relationship between HALP short‐ long‐term mortality patients with heart failure. Methods results retrospective cohort included adult failure who were hospitalized 2019 2021. primary outcomes 1‐month 1‐year mortality. multivariable logistic regression analysis was evaluate association risk Stratified analyses conducted based on New York Heart Association functional classification (NYHA) stage (II/III, IV) left ventricular ejection fraction (LVEF, <50%, ≥50%). area under receiver operating characteristic curve (AUC) ability HALP, prognostic nutritional index (PNI), C‐reactive protein (CRP), Meta‐Analysis Global Group Chronic Failure (MAGGIC‐HF) score predicting A total 730 included, whom 61 (8.36%) died within 1 month 77 (10.55%) year. High scores associated reduced (odds ratio (OR) = 0.978, 95% confidence interval (CI): 0.963–0.992, P 0.003) (OR 0.987, CI: 0.977–0.997, 0.009) In different NYHA stages or LVEF levels, high correlated II/III 0.957–1.000, 0.045) ≥50% 0.970, 0.945–0.996, 0.024). AUC for PNI, CRP, MAGGIC‐HF predict 0.677 (95% 0.619–0.735), 0.666 0.608–0.723), 0.638 0.572–0.704), 0.654 0.591–0.717), respectively. Conclusions may be potential marker Further exploration yield better clinical predictors
Язык: Английский
Процитировано
15
European Journal of Heart Failure, Год журнала: 2024, Номер 26(10), С. 2282 - 2292
Опубликована: Авг. 30, 2024
Язык: Английский
Процитировано
10
ESC Heart Failure, Год журнала: 2024, Номер unknown
Опубликована: Июль 22, 2024
Abstract Systemic aging influences various physiological processes and contributes to structural functional decline in cardiac tissue. These alterations include an increased incidence of left ventricular hypertrophy, a diastolic function, atrial dilation, fibrillation, myocardial fibrosis amyloidosis, elevating susceptibility chronic heart failure (HF) the elderly. Age‐related dysfunction stems from prolonged exposure genomic, epigenetic, oxidative, autophagic, inflammatory regenerative stresses, along with accumulation senescent cells. Concurrently, age‐related changes vascular system, attributed endothelial dysfunction, arterial stiffness, impaired angiogenesis, oxidative stress inflammation, impose additional strain on heart. Dysregulated mechanosignalling nitric oxide signalling play critical roles associated HF. Metabolic drives intricate shifts glucose lipid metabolism, leading insulin resistance, mitochondrial within cardiomyocytes. contribute contractility, ultimately propelling low‐grade conjunction senescence‐associated secretory phenotype, aggravates age by promoting immune cell infiltration into myocardium, fostering This is further exacerbated comorbidities like coronary artery disease (CAD), atherosclerosis, hypertension, obesity, diabetes kidney (CKD). CAD atherosclerosis induce ischaemia adverse remodelling, while hypertension hypertrophy fibrosis. Obesity‐associated inflammation dyslipidaemia create profibrotic environment, whereas diabetes‐related metabolic disturbances impair function. CKD‐related fluid overload, electrolyte imbalances uraemic toxins exacerbate HF through systemic neurohormonal renin‐angiotensin‐aldosterone system (RAAS) activation. Recognizing as modifiable process has opened avenues target both lifestyle interventions therapeutics. Exercise, known for its antioxidant effects, can partly reverse pathological remodelling elderly countering linked HF, such senescence declining cardiomyocyte regeneration. Dietary plant‐based ketogenic diets, caloric restriction macronutrient supplementation are instrumental maintaining energy balance, reducing adiposity addressing micronutrient Therapeutic advancements targeting underway. Key approaches senomorphics senolytics limit senescence, antioxidants stress, anti‐inflammatory drugs interleukin (IL)‐1β inhibitors, rejuvenators nicotinamide riboside, resveratrol sirtuin (SIRT) activators autophagy enhancers metformin sodium‐glucose cotransporter 2 (SGLT2) all which offer potential preserving function alleviating burden.
Язык: Английский
Процитировано
9
Journal of Cardiac Failure, Год журнала: 2025, Номер unknown
Опубликована: Фев. 1, 2025
During the last century characteristics of patients with heart failure (HF) and acute HF (AHF) have shifted from severe pump due to rheumatic, hypertensive ischemic disease older more obese multiple comorbidities. The pathophysiology AHF has in parallel that advanced, end-stage, caused by left ventricular dysfunction age, obesity comorbidity-related cardiovascular combined neurohormonal inflammatory dysregulation or "inflammaging". With advent blockers leading improved outcomes chronic HF, focus therapy also changed care directed at early symptom improvement therapies towards longer-term improvements quality life outcomes. Studies conducted 5 years suggest beneficial effects seen 4 pillars guideline-directed medical for mostly comprising blockade, can be extended when these are initiated rapidly uptitrated during admission after discharge. A recent pilot study (CORTAHF) suggested benefits treating markers activation anti-inflammatory therapies. Future studies should further examine whether blockade lead reversal disrupted underlying remission AHF.
Язык: Английский
Процитировано
1
Frontiers in Cardiovascular Medicine, Год журнала: 2023, Номер 10
Опубликована: Ноя. 17, 2023
Acute heart failure (AHF) represents a common clinical scenario that requires prompt evaluation and therapy is characterized by high risk of mortality or subsequent rehospitalizations. The pathophysiology leading to AHF decompensation still not fully understood. Significant activation inflammatory pathways has been identified in patients with AHF, particularly its most severe forms, it hypothesized systemic inflammation role pathogenesis. Several mediators cytokines, such as sensitivity C-reactive protein, tumor necrosis factor-α, interleukin-6, interleukin-1, soluble suppression tumorigenicity 2 galectin-3, have shown play the pathogenesis, development worsening this condition an independent prediction adverse outcomes. This manuscript reviews prevalence prognostic value well potential anti-inflammatory therapies, focusing on available evidence from trials ongoing studies.
Язык: Английский
Процитировано
20
Matrix Biology, Год журнала: 2024, Номер 134, С. 1 - 22
Опубликована: Авг. 29, 2024
Язык: Английский
Процитировано
7
ESC Heart Failure, Год журнала: 2024, Номер 11(6), С. 3530 - 3538
Опубликована: Июль 19, 2024
Abstract Aims Heart failure (HF) is recognized as an inflammatory disease in which cytokines play important role. In animal HF models, interleukin‐17A (IL‐17) has been linked to deterioration of cardiac function and fibrosis, whereas knock‐out IL‐17 showed beneficial effects. However, there limited evidence involvement patients with HF. This study aims investigate the clinical characteristics, outcomes, pathophysiological processes associated circulating concentrations Methods results was measured by ELISA 2082 diagnosed along 363 proteins using proximity extension assay technology for differential expression pathway analysis. Data were validated independent cohort 1737 Patients elevated had more severe HF, reflected frequent current or previous hospitalizations higher New York Association functional class (NYHA) levels N‐terminal pro‐B‐type natriuretic peptide (NT‐proBNP). High independently increased risk hospitalization mortality. both cohorts, most strongly up‐regulated high fibroblast growth factor 21 (FGF‐21), interleukin‐6 (IL‐6), C‐X‐C motif chemokine ligand 13 (CXCL13), tumour necrosis receptor superfamily member 6B (TNFRSF6B) interleukin‐1 antagonist (IL‐1RA). Pathway over‐representation analysis activity pathways related lymphocyte‐mediated immunity, leukocyte activation regulation immune response. Conclusions indicate known be involved pathophysiology might hold potential identifying targeting inflammation
Язык: Английский
Процитировано
5
European Heart Journal, Год журнала: 2024, Номер 45(9), С. 685 - 687
Опубликована: Янв. 25, 2024
Journal Article 'Training' of innate immunity following myocardial infarction exacerbates atherosclerosis Get access Niranjana Natarajan, Natarajan Department Medicine, University Pittsburgh School 200 Lothrop Street, Pittsburgh, PA 15213, USA https://orcid.org/0000-0003-4967-3524 Search for other works by this author on: Oxford Academic PubMed Google Scholar Partha Dutta Corresponding author. Tel: +1 412 383 7277, Email: [email protected] https://orcid.org/0000-0001-7456-1757 European Heart Journal, Volume 45, Issue 9, 1 March 2024, Pages 685–687, https://doi.org/10.1093/eurheartj/ehae024 Published: 25 January 2024
Язык: Английский
Процитировано
4
Nature Reviews Rheumatology, Год журнала: 2024, Номер 20(10), С. 614 - 634
Опубликована: Сен. 2, 2024
Язык: Английский
Процитировано
4
Journal of Cardiac Failure, Год журнала: 2024, Номер unknown
Опубликована: Сен. 1, 2024
Язык: Английский
Процитировано
4