scholarly journals Cardiorenal syndrome: Decongestion in heart failure across wide spectrum of kidney pathophysiology

2022 ◽  
Vol 31 (4) ◽  
pp. 0-0
Author(s):  
Aneta Kosiorek ◽  
Jan Biegus ◽  
Piotr Rozentryt ◽  
Magdalena Hurkacz ◽  
Robert Zymliński
Keyword(s):  
Heart Failure ◽  
Wide Spectrum ◽  
Cardiorenal Syndrome

scholarly journals Effects of levosimendan in patients with acute heart failure and cardiorenal syndrome

2021 ◽  
Vol 10 (Supplement_1) ◽  
Author(s):  
M Ribeiro Da Silva ◽  
G Santos Silva ◽  
D Caeiro ◽  
M Passos Silva ◽  
C Guerreiro ◽  
...  
Keyword(s):  
Heart Failure ◽  
Acute Heart Failure ◽  
Natriuretic Peptides ◽  
Angiotensin Receptor Blockers ◽  
Cardiorenal Syndrome ◽  
Baseline Serum ◽  
Beneficial Effects ◽  
Funding Sources ◽  
Tertiary Center ◽  
Short Term Mortality

Abstract Funding Acknowledgements Type of funding sources: None. Introduction Cardiorenal syndrome (CRS) is common in patients with acute heart failure (AHF) and is associated with poor prognosis. Levosimendan (LVS) is an inodilator used in AHF and has beneficial effects on renal function (RF). However, its effects on RF in CRS patients are not established. Purpose To evaluate whether LVS could improve RF in AHF patients with or without CRS. Methods Retrospective study that included patients with AHF treated with LVS in a cardiac intensive care unit of a tertiary center, between January 2015 and June 2018. Baseline serum creatinine (SCr) was recorded and SCr and glomerular filtration rate (GFR) were accessed before and within 5 days after LSV use. CRS was defined as an increase in SCr > 0,3 mg/dL over baseline (before LVS use). RF improvement was defined as a decrease in SCr after LVS use. We evaluate outcomes at 1-year. Results 61 patients were included, 84% males, mean age 65 years, ejection fraction ≤40% in 87%. INTERMACS 4 and hemodynamic profile C were the most frequent presentation. LSV was administered in 24h, without bolus, in most patients. CRS was present in 44,3% of patients. Basal characteristics were similar between CRS and no-CRS patients, including prevalence of chronic kidney disease, baseline SCr or natriuretic peptides (p> 0,05 for all). CRS patients had a significant improvement in RF after LVS use (SCr 2,08 to 1,65 mg/dL, p< 0,001 and GFR 40,4 to 54,6 mL/min/m2, p< 0,001), while no-CRS patients had no significant improvement in RF (SCr 1,33 to 1,32 mg/dL and GFR 64,1 to 64,5 mL/min/m2, p> 0,05 for all). Also, there was a significant decrease in natriuretic peptides after LVS in CRS patients (NT-proBNP 13527,5 to 10708,8 pg/mL, p= 0,006), without significant differences in no-CRS patients. It is noteworthy that at discharge, CRS patients were more likely to titrate HF optimal medical therapy (OMT) compared with no-CRS patients (p= 0,039). There was a lower tendency to suspend angiotensin-converting enzyme (ACE-I) and angiotensin receptor blockers (ARB) in CRS patients (p= 0,05). At discharge CRS patients received more furosemide than at admission (77,2 mg/day to 97,1 mg/day, p= 0,019) compared with no-CRS patients (89,6 mg/day to 97,0 mg/day, p= 0,469), receiving similar doses at discharge. In CRS patients, RF improvement was associated with a decrease in intra-hospital mortality (p= 0,043) and a tendency to decrease 30-day mortality (p= 0,060), but without differences in one-year mortality. Conclusion In CRS patients, LVS improved RF and NT-proBNP, allowed to titrate OMT and decreased the need to suspend ACE-I or ARB and was associated to a decrease in short-term mortality.

Management of the cardiorenal syndrome in heart failure

2006 ◽  
Vol 8 (3) ◽  
pp. 211-216 ◽  
Author(s):  
Jigar Patel ◽  
J. Thomas Heywood
Keyword(s):  
Heart Failure ◽  
Cardiorenal Syndrome

Abstract 8: Effectiveness of Combination Allogeneic Stem Cells in a Novel Large Animal Model of Chronic Kidney Disease-induced Heart Failure With Preserved Ejection Fraction (HFpEF)

2017 ◽  
Vol 121 (suppl_1) ◽  
Author(s):  
Angela Castellanos Rieger ◽  
Bryon A Tompkins ◽  
Makoto Natsumeda ◽  
Victoria Florea ◽  
Kevin Collon ◽  
...  
Keyword(s):  
Heart Failure ◽  
Chronic Kidney Disease ◽  
Animal Model ◽  
Cell Therapy ◽  
Renal Artery ◽  
Cardiorenal Syndrome ◽  
Large Animal Model ◽  
Large Animal ◽  
Preserved Ejection Fraction ◽  
Lv Mass

Background: Chronic Kidney Disease (CKD) is an independent risk factor for cardiovascular morbidity and mortality. Left ventricular (LV) hypertrophy and heart failure with preserved ejection fraction (HFpEF) are the primary manifestations of the cardiorenal syndrome in 60 to 80% of CKD patients. Therapies that improve morbidity and mortality in HFpEF are lacking. Stem cell therapy reduces fibrosis, increases neovascularization, and promotes cardiac repair in ischemic and non-ischemic cardiomyopathies. We hypothesized that stem cell treatment ameliorates HFpEF in a CKD model. Methods: Yorkshires pigs (n=27) underwent 5/6 nephrectomy via renal artery embolization and 4-weeks later received either: allogeneic (allo-) MSC (10х10 6 ), allo-kidney c-kit + cells (c-kit; 10х10 6 ), combination (MSC+c-kit; 1:1 ratio [5х10 6 each]), or placebo (each n=5). Cell therapy was delivered via the patent renal artery. Kidney function, renal and cardiac MRI, and PV loops were measured at baseline, and at 4- and 12-weeks (euthanasia) post-embolization. Results: The CKD model was confirmed by increased creatinine and BUN and decreased GFR. Mean arterial pressure (MAP) was not different between groups from baseline to 4 weeks (p=0.7). HFpEF was demonstrated at 4 weeks by increased LV mass (20.3%; p= 0.0001), wall thickening (p<0.008), EDP (p=0.01), EDPVR (p=0.005), and arterial elastance (p=0.03), with no change in EF. Diffuse intramyocardial fibrosis was evident in histological analysis and delayed enhancement MRI imaging. After 12 weeks, there was a significant difference in MAP between groups (p=0.04), with an increase in the placebo group (19.97± 8.65 mmHg, p=0.08). GFR significantly improved in the combination group (p=0.033). EDV increased in the placebo (p=0.009) and c-kit (p=0.004) groups. ESV increased most in the placebo group (7.14±1.62ml; p=0.022). EF, wall thickness, and LV mass did not differ between groups at 12 weeks. Conclusion: A CKD large animal model manifests the characteristics of HFpEF. Intra-renal artery allogeneic cell therapy was safe. A beneficial effect of cell therapy was observed in the combination and MSC groups. These findings have important implications on the use of cell therapy for HFpEF and cardiorenal syndrome.

Abstract 15523: Dynamic Protein S-palmitoylation Contributes to Cardiac Remodeling During Aging With Chronic Hypertension

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Madeleine R Miles ◽  
John Seo ◽  
Zachary Wilson ◽  
Min Jiang ◽  
Gea-ny Tseng
Keyword(s):  
Heart Failure ◽  
Protein Function ◽  
Ventricular Myocytes ◽  
Wide Spectrum ◽  
Enrichment Analysis ◽  
Protein S ◽  
Ventricular Myocardium ◽  
Chronic Hypertension ◽  
Post Translational Modification ◽  
Α Subunit

Introduction: More that 10% of human proteins can be S-palmitoylated, a post-translational modification (PTM) whereby palmitoyl chains are covalently linked to cysteine thiol groups. S-palmitoylation influences protein trafficking, distribution and function. There is no information on the scope of protein S-palmitoylation in the heart, or how this enzyme-mediated reversible PTM is regulated. Hypothesis: S-palmitoylation occurs to a wide spectrum of proteins in cardiomyocytes, and is coordinated by membrane-embedded palmitoylating (DHHC) enzymes. DHHC enzymes are subject to remodeling during chronic hypertension. Methods: We used resin-assisted capture to purify S-palmitoylated proteins from ventricular myocardium of 3 species: human, dog, and rat. We used global unbiased proteomic search to identify S-palmitoylated proteins. We validated DHHC antibodies and used them to monitor protein level and subcellular distribution of native DHHC enzymes in ventricular myocytes. Results: We built a 'composite' cardiac palmitome composed of 462 S-palmitoylatable proteins identified in ≥ 2 species-specific cardiac palmitomes. Enrichment analysis based on GO term 'cellular component' indicated that they are mainly involved in cell-cell and cell-substrate associations, sarcolemma and sarcomere organization, vesicular trafficking, G-protein function, ATP-dependent transmembrane transport, and mitochondria inner and outer membrane organization. Among the 23 DHHC enzymes, we detected ten in hearts across species. In ventricular myocytes with well-defined subcellular compartments, DHHC enzymes exhibited distinct distribution patterns: peripheral sarcolemma (DHHC1), M-lines (DHHC2), Z-lines (DHHC5), vesicles (DHHC7) and intercalated disc (DHHC9). In aging spontaneously hypertensive rats (a model of chronic hypertension, some in heart failure), seven DHHC enzymes were upregulated in the heart, accompanied by a higher degree of S-palmitoylation of CaMK II, caveolin3, Na/Ca exchanger, and Na/K pump α-subunit. Conclusion: S-palmitoylation is involved in most, if not all, aspects of cardiomyocyte function. Palmitoylation dysregulation may contribute to pathological progression in hypertrophy leading to heart failure.

Shift of conventional paradigm of heart failure treatment: from angiotensin receptor neprilysin inhibitor to sodium–glucose co-transporter 2 inhibitors?

2021 ◽  
Vol 17 (3) ◽  
pp. 497-506
Author(s):  
Alexander E Berezin ◽  
Alexander A Berezin
Keyword(s):  
Heart Failure ◽  
Wide Spectrum ◽  
Large Body ◽  
Renin Angiotensin System ◽  
Angiotensin Receptor ◽  
Heart Failure Treatment ◽  
Angiotensin System ◽  
Reduced Ejection Fraction ◽  
Neprilysin Inhibitor ◽  
Angiotensin Receptor Neprilysin Inhibitor

Current clinical guidelines for heart failure (HF) contain a brand new therapeutic strategy for HF with reduced ejection fraction (HFrEF), which is based on neurohumoral modulation through the use of angiotensin receptor neprilysin inhibitors. There is a large body of evidence for the fact that sodium-glucose co-transporter 2 inhibitors may significantly improve all-cause mortality, cardiovascular mortality and hospitalization for HF in patients with HFrEF who received renin–angiotensin system blockers including angiotensin receptor neprilysin inhibitors, β-blockers and mineralocorticoid receptor antagonists. The review discusses that sodium-glucose co-transporter 2 inhibitors have a wide spectrum of favorable molecular effects and contribute to tissue protection, improving survival in HFrEF patients.

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