[Healthcare professionals' perception of advanced nursing practice in Ehpad with regard to the risk of drug iatrogenicity in heart failure patients]. / Perception des professionnels de santé sur la pratique avancée infirmière en Ehpad au regard du risque d'iatrogénie médicamenteuse chez l'insuffisant cardiaque.

Medication iatrogenia is a real public health problem. Elderly people are particularly at risk, due to their multiple pathologies, including heart failure; residents of residential care facilities for the dependent elderly (Ehpad) are no exception. Studies show that this risk is avoidable in 60% of cases, and that advanced practice nurses (APNs) can play a pivotal role in preventive measures. How would the role of the APN be perceived by other healthcare professionals working with these heart failure patients institutionalized in Ehpad?

[Heart failure cooperation protocol: A new way of thinking about the care of heart failure patients]. / Protocole de coopération en insuffisance cardiaque : penser autrement la prise en charge.

To meet the care needs of heart failure patients, a nationwide cooperation protocol has been developed. This heart failure cooperation protocol (PCIC) enables nurses to acquire new skills by delegating medical acts.

[Heart failure treatments]. / Les traitements de l'insuffisance cardiaque.

Heart failure is a frequent pathology in the elderly. In particular, it is responsible for many hospitalizations. A distinction is made between chronic and acute forms of heart failure. The management of these forms of heart failure is well established, with treatment recommendations that are regularly updated on the basis of new studies.

[Two-way teaching of the elderly in the context of heart failure]. / L'enseignement bidirectionnel auprès des personnes âgées dans le contexte de l'insuffisance cardiaque.

In Canada, heart failure (HF) is the second leading cause of hospitalization among the elderly. Heart failure could be improved by the teach-back approach. There are no articles in the French literature describing this educational approach, especially in the context of elderly people living with HF. The aim of this article is to provide French-speaking healthcare professionals, including nurses, with knowledge about this approach, that also includes a specific component on self-care in HF.

The mechanism behind BAF60c in myocardial metabolism in rats with heart failure is through the PGC1α-PPARα-mTOR signaling pathway.

Metabolic remodeling in heart failure (HF) is a type of overload cardiomyopathy caused by insufficient energy supply or an imbalance of glucose and lipid metabolism. Therefore, metabolic pathways may serve as potential targets for HF treatment. BRM-associated factor (BAF) 60c (also known as smarcd3) promotes the transformation of oxidative muscle fibers to glycolytic muscle fibers. Our study aimed to test whether BAF60c and the PGC1α-PPARα-mTOR pathway interact to affect myocardial metabolism in HF rats. Established rat models of HF were injected with BAF60c low or overexpression plasmids to assess cardiac contractile proteins, energy metabolism, oxidative metabolism, glycolysis, high-energy phosphate content, mitochondrial function, and apoptosis. BAF60c overexpression/siRNA plasmid was transfected into H9C2 cells. These results suggest that HF rats present decreased levels of BAF60c, increased glycolysis, and reduced levels of cardiac contractile proteins, PGC1α, PPARα, and oxidative metabolism. Overexpression of BAF60c maintained the balance between oxidative metabolism and glycolysis and activated the PGC1α-PPARα-mTOR pathway. PGC1α interacted with BAF60c, and overexpression of PGC1α decreased BAF60c knockdown, damaging H9C2 cells. Collectively, overexpression of BAF60c activated the PGC1α-PPARα-mTOR pathway, maintained the oxidative metabolism/glycolysis balance, and improved mitochondrial function in HF rats. This study offers novel insights into HF treatment.

Mechanisms of action of SGLT2 inhibitors and their beneficial effects on the cardiorenal axis.

Large clinical studies conducted with sodium-glucose co-transporter 2 inhibitors (SGLT2i) in patients with type 2 diabetes and heart failure with reduced ejection fraction have demonstrated their ability to achieve both cardiac and kidney benefits. Although there is huge evidence on SGLT2i-mediated clinical benefits both in diabetic and non-diabetic patients, the pathophysiological mechanisms underlying their efficacy are still poorly understood. Some favorable mechanisms are likely due to the prompt glycosuric action which is associated with natriuretic effects leading to hemodynamic benefits as well as a reduction in glomerular hyperfiltration and renin-angiotensin-aldosterone system activation. In addition to the renal mechanisms, SGLT2i may play a relevant role in cardiorenal axis protection by improving the cardiomyocyte metabolism, by exerting anti-fibrotic and anti-inflammatory actions, and by increasing cardioprotective adipokine expression. New studies will be needed to better understand the specific molecular mechanisms that mediate the SGLT2i favorable effects in patients suffering diabetes. Our aim is to first discuss about the molecular mechanisms underlying the cardiovascular benefits of SGLT2i in each of the main organs involved in the cardiorenal axis. Furthermore, we update on the most recent clinical trials evaluating the beneficial effects of SGLT2i in treatment of both diabetic and non-diabetic patients suffering heart failure.

Future scope and challenges for congestive heart failure: moving toward development of pharmacotherapy.

Heart failure is invariably associated with cardiac hypertrophy and impaired cardiac performance. Although several drugs have been developed to delay the progression of heart failure, none of the existing interventions have shown beneficial effects in reducing morbidity and mortality. To determine specific targets for future drug development, we have discussed different mechanisms involving both cardiomyocytes and nonmyocyte extracellular matrix (ECM)) alterations for the transition of cardiac hypertrophy to heart failure as well as for the progression of heart failure. We have emphasized the role of oxidative stress, inflammatory cytokines, metabolic alterations, and Ca2+-handling defects in adverse cardiac remodeling and heart dysfunction in hypertrophied myocardium. Alterations in the regulatory process due to several protein kinases, as well as the participation of mitochondrial Ca2+ overload, activation of proteases and phospholipases, and changes in gene expression for subcellular remodeling have also been described for the occurrence of cardiac dysfunction. Association of cardiac arrhythmia with heart failure has been explained as a consequence of catecholamine oxidation products. Since these multifactorial defects in ECM and cardiomyocytes are evident in the failing heart, it is a challenge for experimental cardiologists to develop appropriate combination drug therapy for improving cardiac function in heart failure.

Effect of ivabradine in heart failure: a meta-analysis of heart failure patients with reduced versus preserved ejection fraction.

In clinical trials of heart failure reduced ejection fraction (HFrEF), ivabradine seemed to be an effective heart rate lowering agent associated with lower risk of cardiovascular death. In contrast, ivabradine failed to improve cardiovascular outcomes in heart failure preserved ejection fraction (HFpEF) despite the significant effect on heart rate. This meta-analysis is the first to compare the effects of ivabradine on heart rate and mortality parameters in HFpEF versus HFrEF. We screened three databases: PubMed, Embase, and Cochrane Library. The outcomes of these studies were mortality, reduction in heart rate, and left ventricular function improvement. We compared the efficacy of ivabradine treatment in HFpEF versus HFrEF. Heart rate analysis of pooled data showed decrease in both HFrEF (-17.646 beats/min) and HFpEF (-11.434 beats/min), and a tendency to have stronger bradycardic effect in HFrEF (p = 0.094) in randomized clinical trials. Left ventricular ejection fraction analysis revealed significant improvement in HFrEF (5.936, 95% CI: [4.199-7.672], p < 0.001) when compared with placebo (p < 0.001). We found that ivabradine significantly improves left ventricular performance in HFrEF, at the same time it exerts a tendency to have improved bradycardic effect in HFrEF. These disparate effects of ivabradine and the higher prevalence of non-cardiac comorbidities in HFpEF may explain the observed beneficial effects in HFrEF and the unchanged outcomes in HFpEF patients after ivabradine treatment.

Neuromuscular electrical stimulation but not photobiomodulation therapy improves cardiovascular parameters of rats with heart failure.

The aim of the present study was to analyze the effect of neuromuscular electrical stimulation (NMES) and photobiomodulation (PBMT) on the cardiovascular parameters, hemodynamic function, arterial baroreflex sensitivity (BRS), and autonomic balance (ANS) of rats with heart failure (HF). Male Wistar rats (220-290 g) were organized into five groups: Sham (n = 6), Control-HF (n = 5), NMES-HF (n = 6), PBMT-HF (n = 6), and NMES + PBMT-HF (n = 6). Myocardial infarction (MI) was induced by left coronary artery ligation. Animals were subjected to an eight-week NMES and PBMT protocol. Statistical analysis included the General Linear Model (GLM) followed by a Bonferroni post-hoc test. Rats of the NMES-HF group showed a higher MI area than the Control-HF (P = 0.003), PBMT-HF (P = 0.002), and NMES + PBMT-HF (P = 0.012) groups. NMES-HF and NMES + PBMT-HF showed higher pulmonary congestion (P = 0.004 and P = 0.02) and lower systolic pressure (P = 0.019 and P = 0.002) than the Sham group. NMES + PBMT-HF showed lower mean arterial pressure (P = 0.02) than the Sham group. Control-HF showed a higher heart rate than the NMES-HF and NMES + PBMT-HF (P = 0.017 and P = 0.013) groups. There was no difference in the BRS and ANS variables between groups. In conclusion, eight-week NMES isolated or associated with PBMT protocol reduced basal heart rate, systolic and mean arterial pressure, without influence on baroreflex sensibility and autonomic control, and no effect of PBMT was seen in rats with HF.

Inhibition of angiotensin II-induced hypertrophy and cardiac dysfunction by North American ginseng (Panax quinquefolius).

We determined whether North American ginseng (Panax quinquefolius L.) mitigates the effect of angiotensin II on hypertrophy and heart failure. Angiotensin II (0.3 mg/kg) was administered to rats for 2 or 4 weeks in the presence or absence of ginseng pretreatment. The effect of ginseng (10 µg/mL) on angiotensin II (100 nM) - induced hypertrophy was also determined in neonatal rat ventricular myocytes. We also determined effects of ginseng on fatty acid and glucose oxidation by measuring gene and protein expression levels of key factors. Angiotensin II treatment for 2 and 4 weeks induced cardiac hypertrophy as evidenced by increased heart weights, as well as the upregulation of the hypertrophy-related fetal gene expression levels, with all effects being abolished by ginseng. Ginseng also reduced abnormalities in left ventricular function as well as the angiotensin II-induced increased blood pressure. In myocytes, ginseng abolished the hypertrophic response to angiotensin II as assessed by surface area and gene expression of molecular markers of hypertrophy. Ginseng modulated angiotensin II-induced abnormalities in gene expression and protein levels of CD36, CPT1M, Glut4, and PDK4 in vivo and in vitro. In conclusion, ginseng suppresses angiotensin II-induced cardiac hypertrophy and dysfunction which is related to normalization of fatty acid and glucose oxidation.

Exchange proteins directly activated by cAMP mediate cardiac repolarization and arrhythmogenesis during chronic heart failure.

Most sudden cardiac death in chronic heart failure (CHF) is caused by malignant ventricular arrhythmia (VA); however, the molecular mechanism remains unclear. This study aims to explore the effect of exchange proteins directly activated by cAMP (Epac) on VA in CHF and the potential molecular mechanism. Transaortic constriction was performed to prepare CHF guinea pigs. Epac activation model was obtained with 8-pCPT administration. Programmed electrical stimulation (PES) was performed to detect effective refractory period (ERP) or induce VA. Isolated adult cardiomyocytes were treated with 8-pCPT and (or) the Epac inhibitor. Cellular electrophysiology was examined by whole-cell patch clamp. With Epac activation, corrected QT duration was lengthened by 12.6%. The 8-pCPT increased action potential duration (APD) (APD50: 236.9 ± 18.07 ms vs. 328.8 ± 11.27 ms, p < 0.05; APD90: 264.6 ± 18.22 ms vs. 388.6 ± 6.47 ms, p < 0.05) and decreased rapid delayed rectifier potassium (IKr) current (tail current density: 1.1 ± 0.08 pA/pF vs. 0.7 ± 0.03 pA/pF, p < 0.05). PES induced more malignant arrhythmias in the 8-pCPT group than in the control group (3/4 vs. 0/8, p < 0.05). The selective Epac1 inhibitor CE3F4 rescued the drop in IKr after 8-pCPT stimulation (tail current density: 0.5 ± 0.02 pA/pF vs. 0.6 ± 0.03 pA/pF, p < 0.05). In conclusion, Epac1 regulates IKr, APD, and ERP in guinea pigs, which could contribute to the proarrhythmic effect of Epac1 in CHF.

[Geriatric and social assessment by the heart failure patients' nurse in the FIL-EAS ic]. / Évaluation gériatrique et sociale des patients insuffisants cardiaques par l'infirmière dans la FIL-EAS ic.

The use of geriatric and social assessment grids by dedicated nurses for patients hospitalised for acute heart failure allows for an early and safe return home in home hospitalisation. These grids isolate a sub-group of older patients with a high risk of re-hospitalisation for whom specific actions can be envisaged.

[Therapeutic education and telemonitoring of heart failure patients]. / Éducation thérapeutique et télésuivi des patients insuffisants cardiaques.

At the Jean-Minjoz regional University Hospital Center in Besançon (25), the therapeutic education of patients with heart failure is carried out by a multidisciplinary team. The education nurse conducts the individual interview. The COVID-19 epidemic has changed the organization of care. Tele-monitoring is becoming the norm, the service nurse contacts patients by telephone and registers them on one of the platforms after they have given their agreement.

Taurine and cardiac disease: state of the art and perspectives.

Taurine is a nonessential amino acid that has received much attention. Two organs, the heart and the brain, are known to produce their own taurine, but in very limited quantities. It is for this reason that supplementation with this amino acid is necessary. Today, taurine is present in almost all energy drinks. A very vast literature reported beneficial effects of taurine in hepatic dysfunction, gastrointestinal injury, kidney diseases, diabetes, and cardiovascular diseases. Most of its effects were attributed to its modulation of Ca2+ homeostasis as well as to its antioxidant properties. In this review, we will focus on the current status of taurine modulation of the cardiovascular system and discuss future avenues for its use as a supplement therapy in a specific cardiovascular disease, namely hypertrophy, and heart failure.

miR-142-5p and miR-212-5p cooperatively inhibit the proliferation and collagen formation of cardiac fibroblasts by regulating c-Myc/TP53INP1.

The aim of this study was to investigate the effect and mechanism of miR-142-5p/212-5p on the proliferation and collagen formation of cardiac fibroblasts (CFs) after myocardial infarction (MI). The mouse MI model was established by ligation of the left anterior descending coronary artery. CFs were induced by transforming growth factor-beta 1 (TGF-ß1) or angiotensin (Ang II). The molecule expressions were measured by qRT-PCR and Western blot. CF proliferation was detected by an MTT assay. The effect of miR-142-5p/212-5p on the luciferase activity of c-Myc 3'UTR was assessed by the luciferase reporter assay. miR-142-5p and miR-212-5p were downregulated in cardiac tissues of MI mice and in TGF-ß1- or Ang II-induced CFs, while the protein levels of collagen I and III were upregulated. Moreover, simultaneous overexpression of miR-142-5p/212-5p inhibited the proliferation and collagen formation of TGF-ß1- or Ang II-stimulated CFs to a greater extent than either miR-142-5p or miR-212-5p overexpression alone. MiR-142-5p/212-5p targeted c-Myc and negatively regulated its expression. The effects of miR-142-5p/212-5p overexpression on the TP53INP1 protein level and the proliferation and collagen formation of CFs were reversed by c-Myc overexpression. Moreover, overexpression of miR-142-5p/212-5p improved cardiac function and collagen formation of MI mice. Overexpression of miR-142-5p/212-5p cooperatively suppresses the proliferation and collagen formation after MI by regulating c-Myc/TP53INP1.

Folic acid affects cardiometabolic, oxidative stress, and immunohistochemical parameters in monocrotaline-induced rat heart failure.

Heart failure (HF) is one of the major cardiovascular causes of death worldwide. In this study, we explored the effects of folic acid (FA) on cardiometabolic, oxidative stress biomarker changes, and the activity of proliferation marker Ki67 in monocrotaline-induced HF. The research was conducted during a 4 week period using five experimental groups (eight animals per group): blank solution exposed controls (C1: 1 mL/kg physiological saline, 1 day; C2: 1 mL/kg physiological saline, 28 days), monocrotaline (MCT) induced HF (50 mg/kg MCT), FA (5 mg·kg-1·day-1 FA), and MCT+FA (50 mg/kg MCT, 5 mg·kg-1·day-1 FA). Superoxide dismutase and glutathione peroxidase activities together with total glutathione and parameters of oxidative damage of proteins were determined in cardiac tissue as well as cardiometabolic parameters in plasma or serum. The total glutathionylation was determined by Western blot and proliferation marker Ki67 was assessed by immunohistochemistry. The right ventricular (RV) wall hypertrophy and Ki67 positivity, accompanied by a significant increase of troponin T, has been shown in MCT-induced HF. The antioxidant effect of FA was reflected through superoxide dismutase activity, reduced Ki67 positivity in the RV wall, and a slightly decreased total glutathionylation level.

The influence of subchronic co-application of vitamins B6 and folic acid on cardiac oxidative stress and biochemical markers in monocrotaline-induced heart failure in male Wistar albino rats.

The aim of this study was to test the hypothesis that subchronic co-application of vitamins B6 and folic acid (FA) could affect heart failure (HF) induced by monocrotaline (MCT), with the modulation of oxidative stress parameters and cardiometabolic biomarkers. Biochemical and histomorphometric analyses were assessed in blank solution-exposed controls (C1 physiological saline 1 mL/kg, 1 day, n = 8; C2 physiological saline 1 mL/kg, 28 days, n = 8), MCT-induced HF (MCT 50 mg/kg, n = 8), B6+FA (vitamin B6 7 mg·kg-1·day-1, FA 5 mg·kg-1·day-1; n = 8), and MCT+B6+FA (MCT 50 mg/kg, vitamin B6 7 mg·kg-1·day-1, FA 5 mg·kg-1·day-1; n = 8) in male Wistar albino rats (body mass 160 g at the start). Superoxide dismutase and glutathione peroxidase activities, thiol-, carbonyl groups, and nitrotyrosine were determined in cardiac tissue. Echocardiography was performed to confirm MCT-induced HF. The right ventricular wall hypertrophy, accompanied with significant increase of troponin T and preserved renal and liver function, has been shown in MCT-induced HF. However, these effects were not related to antioxidant effects of vitamin B6 and FA, since several parameters of oxidative stress were more pronounced after treatment. In this study, co-application of vitamins B6 and FA did not attenuate hypertrophy of the right ventricle wall but aggravated oxidative stress, which is involved in HF pathogenesis.

[Elderly heart failure patient, quality or quantity of life?] / Patient âgé insuffisant cardiaque, qualité ou quantité de vie ?

Heart failure is a serious and common disease in the elderly. It causes repeated hospitalizations with a progressive overall decline. It is often difficult at an advanced stage of the disease to "choose" between quality and quantity of life for both patients and their families and caregivers. A reflection conducted at the Centre for Clinical Ethics of the Assistance publique-Hôpitaux de Paris can help to make progress on these difficult choices.

[Early consultation after an acute decompensated heart failure episode]. / La consultation précoce après un épisode de décompensation cardiaque.

Early consultation after acute decompensated heart failure supplements and reinforces the hospital care of patients with severe heart failure. Its aim is to prevent a new episode occurring during the period of increased vulnerability. It requires the active partnership of the patient and the complementary expertise of different professionals, specialised in heart failure and in therapeutic education : cardiologist, nurse and dietician.

[Cardiac failure and remote monitoring: a new management approach?] / Insuffisance cardiaque et télésurveillance.

Heart failure is the leading cause of hospitalization of people aged 60-65 in France, with a rising rate of rehospitalization. This explains the very high healthcare costs in all Western countries and in the United States. Remote monitoring is one of the avenues being studied to reduce this rate of rehospitalisation: it is becoming a reality and should bring about changes in the nursing profession in the years to come.