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A wide range of comorbidities play a pivotal role in worsening outcomes and increasing mortality risk in patients with heart failure (HF). Among them, renal dysfunction has been recognized as a highly prevalent prognostic variable, with a strong impact on prognosis, length of hospital stay and need for intensive care. In this context, recent evidence has pointed out the relevance of both systemic hypoperfusion and venous congestion on the imbalance of renal function as well as on the conditioning the pathophysiological crosstalk between heart and kidneys through a wide range of haemodynamic and biochemical pathways. This narrative review aims to investigate the intricate interplay between impaired systemic perfusion and venous congestion in cardiorenal syndrome, as well as their haemodynamic and biochemical implications for renal damage in HF., Competing Interests: The authors declare no conflict of interest., (© 2022 The Author(s). Published by IMR Press.)

Aims: The role of the implantable cardioverter defibrillator (ICD) in primary prevention real-world population is debated. We sought to evaluate the incidence, predictors and prognostic impact of ICD shocks in consecutive heart failure patients implanted for primary prevention at our tertiary institution., Methods and Results: We retrospectively selected a sample of 497 patients (mean age 64.8 years, 82.1% men, average left ventricular ejection fraction, LVEF, 27.1%). At long-term follow-up (median time 70.4 months), total mortality was 40.8%, and 16.5% of patients had received at least one appropriate shock (3.12%/year). Inappropriate shock [odds ratio (OR) 1.93, 95% confidence interval (95% CI) 1.08-3.47; P = 0.027] and length of follow-up (1 year, OR 1.01, 95% CI 1.00-1.01; P = 0.0031) were associated with the occurrence of appropriate shock, whereas atrial fibrillation (OR 2.65, 95% CI 1.55-4.51, P < 0.001), length of follow-up (1-year OR 1.01, 95% CI 1.00-1.01, P < 0.001) and appropriate shock (OR 1.93, 95% CI 1.08-3.47, P = 0.027) were associated with the occurrence of inappropriate shock. Neither appropriate nor inappropriate shock independently increased mortality risk, whereas older age (hazard ratio 1.05; 95% CI 1.04-1.07; P < 0.001), atrial fibrillation (hazard ratio 2.25; 95% CI 1.67-3.02; P < 0.001) and lower LVEF (hazard ratio 0.97; 95% CI 0.94-0.99; P = 0.004) did., Conclusion: Incidence of shocks in real-world primary prevention ICD recipients might be lower than expected, and the association between ICD shocks and prolongation of survival is not as clear-cut as might be perceived. Further investigations from larger real-world samples are warranted., (Copyright © 2020 Italian Federation of Cardiology - I.F.C. All rights reserved.)

Guidelines recommend angiotensin-converting enzyme inhibitors (ACEi) and angiotensin II receptor blockers (ARB) for treatment of heart failure with reduced ejection fraction (HFrEF), but these medications are underprescribed in clinical practice. We reviewed the records of HF patients receiving a first visit in a tertiary outpatient clinic from January 1st 2004 to May 31st 2015, and selected those with a serum creatinine concentration (sCr) available at both the first and last visit and < 3.5 mg/dL at baseline, and a left ventricular ejection fraction (LVEF) < 50% at the first visit. Of 570 eligible patients, 92 (16.1%) never received ACEi/ARB. Compared to ACEi/ARB users, never-users were older, more often women, had higher sCr and lower systolic blood pressure, were less commonly on beta-blocker, and had more frequently anemia. Current or prior cancer also tended to be more common in ACEi/ARB never-users. ACEi/ARB users displayed an improvement in LVEF by ≥ 10% of the baseline value more often than ACEi/ARB never-users (33.7% vs. 20.7%, respectively, P = 0.01), whereas no difference in percent variation of sCr levels was found between the two groups (8.2% vs. 3.1%, respectively; P = 0.13). Over a median follow-up of 56 months (range 1-137 months), 215 (37.7%) patients died. After multiple adjustments, ACEi/ARB never-use was associated with an almost twofold increased risk of all-cause mortality (HR 1.97, 95%CI 1.39-2.80). ACEi/ARB underuse in HFrEF is a standing issue with dramatic prognostic consequences. Efforts are needed to eliminate perceived contraindications to these drugs and ensure their implementation in real-life cardiology.

Background: Heart failure (HF) is a major public health problem and represents the only cardiac disease continuing to increase in prevalence, in particular among elderly patients. The frequent rehospitalizations have a negative impact on quality of life of patients with HF, constituting a substantial cost for patients and the health system. The aim of this review was to look into biochemical, echocardiographic and socioeconomical parameters as predictors of clinical outcomes and rehospitalizations., Methods: This narrative review is based on the material searched for and obtained via PubMed from January 2000 up to March 2018. The search terms we used were as follows: "elderly, heart failure, cardiovascular" in combination with "biomarker, echocardiography and hospitalization.", Results: This review analyses the potential predictive role of biochemical and echocardiographic and socioeconomical parameters on clinical outcomes (particularly cardiovascular) and hospital readmissions in patients with chronic HF. We focused on risk stratification of elderly patients with HF, who constitute a category of frail subjects at higher risk for readmission to hospital., Conclusions: In elderly subjects with chronic HF, the risk stratification could benefit of a multiparametric approach combining biochemical, echocardiographic, demographic and socioeconomical parameters, thus ensuring a better quality of life and at the same time a better allocation of financial resources., (© 2018 Stichting European Society for Clinical Investigation Journal Foundation.)

Introduction: Atrial fibrillation (AF) and heart failure (HF) often coexist. When AF and HF are both present, they are associated with negative outcomes, increased hospitalizations and mortality. As β-blockade is effective inF and may be useful in presence of AF, bucindolol, a non-selective β-blocker with α-1 vasodilatory effect, may be used. Area covered: This review evaluates the efficacy and safety of bucindolol in HF patients with AF. The largest amount of data comes from BEST trial which evaluated the efficacy of bucindolol in HF patients. Since bucindolol's effects are genetically modulated by β1 and α2c-adrenergic receptor polymorphisms BEST genetic substudy arose. Expert opinion: In the BEST Trial, bucindolol demonstrated efficacy in HF patients showing a 74% reduction in new-onset atrial fibrillation events particularly in β1 389 Arg/Arg homozygous. GENETIC-AF study was designed to determine whether bucindolol therapy is superior to metoprolol in preventing recurrent AF in a genetically targeted population of HF patients. Furthermore, this drug is safe, but presents the same side effects as all β-blockers and has showed no clear benefits in African-Americans and in class IV NYHA patients. Further studies are needed to confirm and validate the role of bucindolol and its economic implications.

Introduction: Ivabradine is a new heart-rate-lowering drug; the aim of this review was to analyze its role in heart failure (HF)., Areas Covered: This systematic review on the role of ivabradine in HF is based on material searched and obtained through Pubmed and Medline up to September 2013., Expert Opinion: Heart rate (HR) is a risk factor in patients with HF, and its reduction is considered an important goal of therapy. The BEAUTIFUL trial demonstrated the benefits of ivabradine on prognosis (only on ischemic endpoints) in patients with coronary artery disease (CAD) and left ventricular systolic dysfunction (LVSD) and HR ≥ 60 bpm. In the SHIFT trial, which enrolled patients with LVSD, HF and HR ≥ 70 bpm, ivabradine administration (on top of guideline-based therapy, including β-blockers [BB]) was associated with a reduction of cardiovascular death and hospitalizations for HF, but BB were underutilized. Further studies are needed to test the efficacy of ivabradine in CAD patients with high HR and to shed light on the comparison between ivabradine and a more aggressive therapy with higher doses of BB in HF patients.

Aims: Cardiac resynchronization therapy is currently used in selected patients with end-stage heart failure. However, 30% of patients do not respond to CRT. The aim of our study was to find echocardiographic (TDI), electrocardiographic (QRS interval and electric distance between right and left catheter), clinical (6MW test) or autonomical (HRV) parameters able to predict responsiveness to CRT., Materials and Methods: 47 patients (mean age 74+/-10 years) with end-stage heart failure, symptomatic, with left ventricular (LV) ejection fraction less than 35% and QRS 120 ms, underwent CRT., Results: At thirteen months follow up, all clinical and echocardiographic parameters significantly improves (EF p<0.001; LVED volume p<0.001; 6MWT p<0.001; max delay TDI p<0.001; HRV p<0.05; Right-left distance p<0.05). A positive response was documented in 31/47 (67.4%) patients who presented an increase in LVEF > or = 5 units. There was a significant difference of LVED diameter (p<0.05) and HRV (p<0.05) between responders and non responders. Receiver-operating curve analysis showed that a positive response to CRT may be predicted in patients with LVED diameter <67 mm (with a sensitivity of 77% and a specificity of 88%)., Conclusions: Our results confirm the clinical improvement obtained by CRT in end-stage heart failure patients as well as the limited value of QRS duration and intraventricular dyssynchrony as predictor of clinical recovery after CRT. While a most-advanced clinical stage of disease (HRV) without an advance left ventricular remodeling (LVED diameter) demonstrated to predict response to CRT, with sensitivity of 77% and specificity of 88%.

Our aim was to define the distribution of monocyte subsets in a cohort of congestive heart failure (CHF) patients, to verify whether increased severity of CHF is linked to the expansion of specific monocyte subsets, and finally to investigate the relationship between monocyte subset relative frequencies, laboratory parameters of inflammation, and monocyte ACE expression. Thirty consecutive CHF patients and 26 healthy control subjects were evaluated for peripheral blood monocyte expression of CD14, CD16 and CD143 (ACE) by flow-cytometry, and for endothelial-derived soluble CD146 levels by ELISA. CD14++ CD16+ frequency was significantly higher in CHF patients than in Controls (%, median value and IQ) (12.3, 8.7-14.8 vs 5.9, 4.7-6.9, p< 0.05, CHF vs Controls), and it increased depending on how high NYHA class was, on worsening LV ejection fraction and on circulating pro-BNP values. Furthermore, it was associated with increasing creatinine and with decreasing GFR and albumin levels. Monocyte CD143 expression was significantly elevated in CHF patients as compared to Controls, and positively associated with CD14++ CD16+ levels. Frequencies of CD14+ CD16+ monocytes were significantly lower in CHF patients as compared to Controls, and negatively correlated with levels of soluble CD146 (r=-0.529; p 0.048). In conclusion, monocytic CD14++ CD16+ frequency and CD143 levels are increased and reflect disease status and progressive cardiac deterioration in CHF patients. The CD14+ CD16+ subset is depleted in CHF and is linked to endothelial damage in this group of patients. Although the question of whether differences in monocyte CD14CD16 expansion are causal or whether they represent a marker of HF progression which is potentially relevant for risk prediction remains unanswered, we believe that our data represent an important tool for exploring the role of selective inflammatory pathways in CHF progression.

Aims: Congestive heart failure (CHF) can be thought of as a state of chronic immune activation. Polymorphonuclear neutrophil (PMN) apoptosis is one of the mechanisms responsible for the resolution of inflammation. A reduced PMN apoptotic rate in CHF patients may generate a persistent inflammatory response and hence mediate tissue damage in this group of patients. We aimed to measure levels of spontaneous apoptosis of circulating PMNs in CHF patients and in controls, and to examine whether NYHA class, left ventricular ejection fraction (LV-EF), and laboratory parameters of inflammation, endothelial damage, and of liver and renal function, could predict the rate of PMN apoptosis in CHF patients., Methods and Results: A total of 29 CHF patients and 26 controls were studied. Propidium iodide and flow cytometry were used to assess PMN apoptosis. Delay in PMN apoptosis was expressed as percentage (expressed as median, first and third quartiles) of surviving PMNs in the study subjects. We found an increased percentage of surviving PMNs [38(27.1-47.1)] in CHF patients compared with controls [19.4 (15.8-25.2)] (P < 0.05). The PMN survival rate in the CHF group was correlated to NYHA class, and plasma levels of C-reactive protein and alkaline phosphatase, while it was inversely correlated to LV-EF and protein levels. A positive relationship between PMN survival and increased ex vivo endothelial apoptosis was found., Conclusion: Increased PMN lifespan in patients with worsening CHF could be used as a novel measurement of tissue and endothelial damage in this group of patients.

We have examined the effects of 6 months of treatment with growth hormone (GH) (0.02 U/kg/day) in 10 patients with chronic postischemic cardiac failure. Ten patients matched for age, body mass index, functional class, and ejection fraction served as a control group. In the GH group, 1 patient died and 2 were withdrawn from the study because of arrhythmia or worsening of heart failure. In the control group, 1 patient died and 1 patient was withdrawn from the study because of progressive heart failure. Among GH patients, those with an unfavorable outcome had a greater left ventricular end-diastolic diameter (79, 82, and 88 mm) on entry to the study than patients without adverse events (range 62 to 72 mm). At the end of the study, the seven GH patients reported a feeling of well-being and had a significant increase in their exercise test duration (462 +/- 121 vs 591 +/- 105 seconds, p <0.05). Low baseline insulin-like growth factor-I values were increased with GH treatment (189 +/- 52 vs 100 +/- 22 ng/ml, p <0.01). GH did not change left ventricular diameters or wall thickness. A trend toward decreased serum triglyceride levels and adipose body tissue associated with an increase in high-density lipoproteins was observed in the GH group. In conclusion, our present data support previous suggestions that GH treatment exerts some beneficial effects in patients with chronic, stabilized, moderately severe heart failure, but may have deleterious effects in patients with more severe heart failure.

It is clearly settled that the management of overt heart failure offers poor prognostic impact due to the advanced setting of the disease. Relief of symptoms, objective benefits, as testified by short-term hemodynamic improvements, are as a matter of fact not reliable prognostic markers. Myocardial dysfunction starts early in the natural history of many cardiac diseases, and runs through the steps of progressive wall remodeling, witnessed by quantitative and qualitative changes in cells, interstitium and connective tissue. Experimental studies offered keys to interventions modulated to oppose the pathophysiological changes present in early myocardial dysfunction. At present, medical therapy has made great strides in testing early myocardial dysfunction. Angiotensin-converting enzyme inhibitors, which retard ventricular dilatation and thus may lower myocardial oxygen consumption requirements seem to offer a unique prognostic profile. Preliminary pilot studies on them and some of many large-scale multicentre trials still in progress reached evidence that this class of drugs is by this time a cornerstone of medical therapy, useful to lower cardiac events-rate in patients with heart failure.

Congestive heart failure is a syndrome with multiple causes and manifestations. While rheumatic heart disease and hypertension are in decline, coronary artery disease is the leading cause in patients referred for evaluation of heart failure. Decrease in cardiac contractility and general neurohormonal activation, which trigger alterations in mechanical and biochemical factors in cardiac muscle and bring derangements of haemodynamics, are now considered as excessively early compensatory mechanisms which can be regarded as deleterious in patients with heart failure. Therapeutic principles illustrated in this article emphasize the importance of basic research and clinical observations derived from trials set the stage for therapeutic interventions. The approach to the patient with silent myocardial dysfunction must be treated so as to have the greatest beneficial impact on the prognosis of this disease.

Abstract Background Progression of heart failure is associated with interstitial changes in the heart and in areas distant from the heart. Enhanced expression of metalloproteinases 2 and 9 and of metalloproteinases tissue inhibitors 1 and 2 have been found in ventricular tissue of patients with heart failure. Our aim was to determine whether increased activity of metalloproteinase-2, metalloproteinase-9 and of metalloproteinases tissue inhibitor-1 and metalloproteinases tissue inhibitor-2 were also present in plasma of patients with heart failure. Design Levels of metalloproteinase-2, metalloproteinase-9 and of metalloproteinase tissue inhibitor-1 and metalloproteinases tissue inhibitor-2 were measured in venous blood of 51 patients with heart failure, and were compared with levels of 52 control subjects. Samples collected from patients and control subjects were assayed for gelatinolytic activity (zymography) and for protein levels. Results Compared with the control subjects, the patients with heart failure had a significant increase in activity levels (mean ± SE, ng mL-1 ) of prometalloproteinase-9 (95·1 ± 11·2 and 38·9 ± 4·5* ), activ. metalloproteinase-9 (18·4 ± 2·5 and 10·9 ± 1·3* ), and of prometalloproteinase-2 (571·4 ± 26·1 and 456·8 ± 21·1* ) (respectively: patients and control sub jects; * P < 0·05). Metalloproteinases tissue inhibitor-1, but not metalloproteinases tissue inhibitor-2 protein values were higher in the patients. Among the patients, clinical status and New York Heart Association (NYHA) class did not correlate with the metalloproteinase concentrations. Positive correlations with left ventricular volumes, and negative correlations with lipid values were obtained for prometalloproteinase-2; positive correlations with total number of white cells and neutrophils were obtained for... [ABSTRACT FROM AUTHOR]