Epidemiology, pathophysiology, diagnosis and management of chronic right-sided heart failure and tricuspid regurgitation. A clinical consensus statement of the Heart Failure Association (HFA) and the European Association of Percutaneous Cardiovascular Interventions (EAPCI) of the ESC.

Right-sided heart failure and tricuspid regurgitation are common and strongly associated with poor quality of life and an increased risk of heart failure hospitalizations and death. While medical therapy for right-sided heart failure is limited, treatment options for tricuspid regurgitation include surgery and, based on recent developments, several transcatheter interventions. However, the patients who might benefit from tricuspid valve interventions are yet unknown, as is the ideal time for these treatments given the paucity of clinical evidence. In this context, it is crucial to elucidate aetiology and pathophysiological mechanisms leading to right-sided heart failure and tricuspid regurgitation in order to recognize when tricuspid regurgitation is a mere bystander and when it can cause or contribute to heart failure progression. Notably, early identification of right heart failure and tricuspid regurgitation may be crucial and optimal management requires knowledge about the different mechanisms and causes, clinical course and presentation, as well as possible treatment options. The aim of this clinical consensus statement is to summarize current knowledge about epidemiology, pathophysiology and treatment of tricuspid regurgitation in right-sided heart failure providing practical suggestions for patient identification and management.

Acute heart failure and valvular heart disease: A scientific statement of the Heart Failure Association, the Association for Acute CardioVascular Care and the European Association of Percutaneous Cardiovascular Interventions of the European Society of Cardiology.

Acute heart failure (AHF) represents a broad spectrum of disease states, resulting from the interaction between an acute precipitant and a patient's underlying cardiac substrate and comorbidities. Valvular heart disease (VHD) is frequently associated with AHF. AHF may result from several precipitants that add an acute haemodynamic stress superimposed on a chronic valvular lesion or may occur as a consequence of a new significant valvular lesion. Regardless of the mechanism, clinical presentation may vary from acute decompensated heart failure to cardiogenic shock. Assessing the severity of VHD as well as the correlation between VHD severity and symptoms may be difficult in patients with AHF because of the rapid variation in loading conditions, concomitant destabilization of the associated comorbidities and the presence of combined valvular lesions. Evidence-based interventions targeting VHD in settings of AHF have yet to be identified, as patients with severe VHD are often excluded from randomized trials in AHF, so results from these trials do not generalize to those with VHD. Furthermore, there are not rigorously conducted randomized controlled trials in the setting of VHD and AHF, most of the data coming from observational studies. Thus, distinct to chronic settings, current guidelines are very elusive when patients with severe VHD present with AHF, and a clear-cut strategy could not be yet defined. Given the paucity of evidence in this subset of AHF patients, the aim of this scientific statement is to describe the epidemiology, pathophysiology, and overall treatment approach for patients with VHD who present with AHF.

Rationale and design of the Biventricular Evaluation of Gliflozins effects In chroNic Heart Failure: BEGIN-HF study.

AIMS: Sodium-glucose cotransporter type 2 inhibitors (SGLT-2i) represent a unique class of anti-hyperglycaemic agents for type 2 diabetes mellitus that selectively inhibit renal glucose reabsorption, thereby increasing urinary excretion of glucose. Several studies have demonstrated the cardioprotective effects of SGLT-2i in patients with heart failure (HF), unrelated to its glucosuric effect. It is unclear whether the benefits of SGLT-2i therapy also rely on the improvement of left ventricular (LV) and/or right ventricular (RV) function in patients with HF. This study aimed to evaluate the effect of SGLT-2i on LV and RV function through conventional and advanced echocardiographic parameters with a special focus on RV function in patients with HF. METHODS AND RESULTS: The Biventricular Evaluation of Gliflozins effects In chroNic Heart Failure (BEGIN-HF) study is an international multicentre, prospective study that will evaluate the effect of SGLT-2i on echocardiographic parameters of myocardial function in patients with chronic stable HF across the left ventricular ejection fraction (LVEF) spectrum. Patients with New York Heart Association Class II/III symptoms, estimated glomerular filtration rate > 25 mL/min/1.73 m2 , age > 18 years, and those who were not previously treated with SGLT-2i will be included. All patients will undergo conventional, tissue-derived imaging (TDI), and strain echocardiography in an ambulatory setting, at time of enrolment and after 6 months of SGLT-2i therapy. The primary endpoint is the change in LV function as assessed by conventional, TDI, and myocardial deformation speckle tracking parameters. Secondary outcomes include changes in RV and left atrial function as assessed by conventional and deformation speckle tracking echocardiography. Univariate and multivariate analyses will be performed to identify predictors associated with primary and secondary endpoints. CONCLUSIONS: The BEGIN-HF will determine whether SGLT-2i therapy improves LV and/or RV function by conventional and advanced echocardiography in patients with HF irrespective of LVEF.

Left Ventricular Pseudoaneurysms Discovered Early After Acute Myocardial Infarction: The Surgical Timing Dilemma.

Left ventricular pseudoaneurysm is a rare disease; it is defined as a ventricular rupture contained by epicardium, pericardial adhesions, or both. It most frequently occurs as a complication of acute myocardial infarction. Surgical treatment is recommended for pseudoaneurysms that are large or symptomatic and for those discovered less than 3 months after myocardial infarction. We report our experience with 2 patients who had left ventricular pseudoaneurysms discovered less than a week after inferior myocardial infarction. Both patients were middle-aged men with right coronary occlusion in whom the diagnoses were established by echocardiography during the first week after infarction. Because both patients were clinically stable, we opted to defer surgery until scarring could facilitate correction; this decision was based on a review of the literature showing that in-hospital mortality is higher with early surgery. The patients were monitored closely in the intensive care unit and were prescribed ß-blockers and vasodilators. Both patients underwent left ventricular patch reconstruction with exclusion of the pseudoaneurysm and posterior septum; both received moderate inotropic support and prophylactic intra-aortic balloon pump assistance. Their postoperative courses were uneventful. In 5 prior reports describing 45 patients (13 with acute pseudoaneurysm [≤2 wk after infarction] and 32 with nonacute pseudoaneurysm), in-hospital mortality was 61.5% for patients in the acute group and 15.6% for the nonacute group (P = .0066). We recommend that clinicians consider deferring surgery for patients with stable acute left ventricular pseudoaneurysm to reduce the risks associated with early repair.

Ventricular and Atrial Ejection Fractions are Associated with Mean Compartmental Cavity Volume in Cardiac Disease.

Ejection fraction (EF) is considered to provide clinically useful information. Despite its enormous popularity, with more than 75,000 citations in PubMed, only few studies have traced the origin(s) of its foundation. This fact is surprising, as there are perhaps more papers published that criticize EF, than the number of publications that actually provide a solid (mathematical) basis for its alleged applicability. EF depends on two volume determinations, namely end-systolic volume (ESV) and end-diastolic volume (EDV). EF is defined as 1-ESV/EDV, yielding a metric without physical units. Previously we formulated a robust analytical expression for the nonlinear connection between EF and ESV. Here we extend that approach by providing a formula to illustrate that EF is strongly associated with half the sum (HS) of ESV and EDV. HS is not new, but forms a major component in the recently introduced Global Function Index. For 420 heart failure (HF) patients we found for left ventricular angio data: R(ESV, eDv) = 0.92, R(EF, ESV) = -0.90, and R(EF, HS) = -0.65. For echo (33 HF patients stages A, B, C and D): R(EF, HS) = -0.82. For the right atrium (CMRI in 21 acute myocardial infarction patients): R(EF, HS)=-0.65. For the left atrium (N=86) R (EF, hS)=-0.46. ESV indicates the level to which the ventricle is able to squeeze blood out of the cavity via pressure build-up. In contrast, EF refers to relative volume changes, not to the mechanism of pumping action. We conclude that for each cardiac compartment EF borrows its acclaimed attractiveness from the fact that for a wide patient spectrum the ESVand EDV correlate in a fairly linear manner. Attractiveness of EF features a straightforward mathematical derivation, rather than reflecting underlying physiology. Clinical Relevance - Ejection fraction (EF) is found to reflect (mean) ventricular / atrial size, and is primarily associated with end-systolic volume, which variable in turn highly correlates with diastolic volume. As a mathematical construct, EF has little affinity with "function", which is a central concept in physiology.

Triple-valve replacement for Rhizobium radiobacter endocarditis with septic shock in an adult with ventricular septal defect. A case report.

INTRODUCTION AND IMPORTANCE: Triple-valve replacement in active infective endocarditis has rarely been reported. This paper is the first report of a triple-valve replacement performed in endocarditis with septic shock and the first presentation of multivalvular endocarditis due to Rhizobium radiobacter. CASE PRESENTATION: A 26-year-old patient with a neglected ventricular septal defect referred to us in septic shock, with multiple organ failure, severe biventricular dysfunction, and pulmonary hypertension, due to Rhizobium radiobacter infective endocarditis affecting the aortic, tricuspid and pulmonary valves. Initially, he was deemed unfit for surgery. However, after clinical stabilization, triple-valve replacement, aortic annular abscess repair, membranous septum aneurysm resection, and ventricular septal defect patch closure were performed. The postoperative evolution was good; both ventricles showed functional recovery after six months. CLINICAL DISCUSSION: Although surgery provides the best chances of survival in endocarditis with septic shock, reportedly, most cases are considered inoperable. Clinical stabilization under intensive care using specific therapies to manage septic shock, myocardial dysfunction, and pulmonary hypertension was crucial for surgery success. Custodiol® cardioplegia, and replacement of the right-sided valves using a beating-heart technique were used to reduce the myocardial ischemic time. CONCLUSION: Rhizobium radiobacter, an opportunistic gram-negative bacterium, potentially may cause multiple valve endocarditis. Patients with endocarditis and septic shock initially considered inoperable can still benefit from surgery after tenacious intensive care (cytokine hemoadsorption and levosimendan are helpful in this process). In complex multivalvular procedures, a beating heart technique to replace the right-sided valves should be considered to minimize the duration of myocardial ischemia.

Paradigm shift in heart failure treatment: are cardiologists ready to use gliflozins?

Despite recent advances in chronic heart failure (HF) therapy, the prognosis of HF patients remains poor, with high rates of HF rehospitalizations and death in the early months after discharge. This emphasizes the need for incorporating novel HF drugs, beyond the current approach (that of modulating the neurohumoral response). Recently, new antidiabetic oral medications (sodium-glucose cotransporter 2 inhibitors (SGLT2i)) have been shown to improve prognosis in diabetic patients with previous cardiovascular (CV) events or high CV risk profile. Data from DAPA-HF study showed that dapaglifozin is associated with a significant reduction in mortality and HF hospitalization as compared with placebo regardless of diabetes status. Recently, results from EMPEROR-Reduced HF trial were consistent with DAPA-HF trial findings, showing significant beneficial effect associated with empagliflozin use in a high-risk HF population with markedly reduced ejection fraction. Results from the HF with preserved ejection fraction trials using these same agents are eagerly awaited. This review summarizes the evidence for the use of gliflozins in HF treatment.

Antithrombotic and anticoagulation therapies in cardiogenic shock: a critical review of the published literature.

Cardiogenic shock (CS) is a complex multifactorial clinical syndrome, developing as a continuum, and progressing from the initial insult (underlying cause) to the subsequent occurrence of organ failure and death. There is a large phenotypic variability in CS, as a result of the diverse aetiologies, pathogenetic mechanisms, haemodynamics, and stages of severity. Although early revascularization remains the most important intervention for CS in settings of acute myocardial infarction, the administration of timely and effective antithrombotic therapy is critical to improving outcomes in these patients. In addition, other clinical settings or non-acute myocardial infarction aetiologies, associated with high thrombotic risk, may require specific regimens of short-term or long-term antithrombotic therapy. In CS, altered tissue perfusion, inflammation, and multi-organ dysfunction induce unpredictable alterations to antithrombotic drugs' pharmacokinetics and pharmacodynamics. Other interventions used in the management of CS, such as mechanical circulatory support, renal replacement therapies, or targeted temperature management, influence both thrombotic and bleeding risks and may require specific antithrombotic strategies. In order to optimize safety and efficacy of these therapies in CS, antithrombotic management should be more adapted to CS clinical scenario or specific device, with individualized antithrombotic regimens in terms of type of treatment, dose, and duration. In addition, patients with CS require a close and appropriate monitoring of antithrombotic therapies to safely balance the increased risk of bleeding and thrombosis.

Overcoming the Limits of Ejection Fraction and Ventricular-Arterial Coupling in Heart Failure.

Left ventricular ejection fraction (LVEF) and ventricular-arterial coupling (VAC) [VAC = Ea/Ees; Ea: effective arterial elastance; Ees: left ventricle (LV) elastance] are both dimensionless ratios with important limitations, especially in heart failure setting. The LVEF to VAC relationship is a divergent non-linear function, having a point of intersection at the specific value of 0.62, where V0 = 0 ml (V0: the theoretical extrapolated value of the volume-axis intercept at end-systolic pressure 0 mmHg). For the dilated LV, both LVEF and VAC are highly dependent on V0 which is inconclusive when derived from single-beat Ees formulas. VAC simplification should be avoided. Revisiting the relationship between systolic time intervals (STI), pressure, and volumes could provide simple-to-use guiding formulas, affordable for daily clinical practice. We have analyzed by echocardiography the hemodynamics of 21 patients with severe symptomatic heart failure with reduced ejection (HFrEF) compared to 12 asymptomatic patients (at risk of heart failure with mild structural disease). The groups were unequivocally separated by 'classic' measures (LVEF, LV end-systolic volume (ESV), LV mass, STI). Chen's Ees formula was weakly correlated with LVEF and indexed ESV (ESVi) but better correlated to the pre-ejection period (PEP); PEP/total ejection time (PEP/TET); systolic blood pressure/PEP (SBP/PEP) (P < 0.001). Combining the predictability of the LVEF to the determinant role of SBP/PEP on the Ees variations, we obtained: (SBP*LVEF)/PEP mm Hg/ms, with an improved R 2 value (R 2 = 0.848; P < 0.001). The strongest correlations to VAC were for LVEF (R = -0.849; R 2 = 0.722) and PEP/TET (R = 0.925; R 2 = 0.857). By multiple regression, the VAC was strongly predicted (N = 33): (R = 0.975; R 2 = 0.95): VAC = 0.553-0.009*LVEF + 3.463*PEP/TET, and natural logarithm: Ln (VAC) = 0.147-1.4563*DBP/SBP*0.9-0.010*LVEF + 4.207*PEP/TET (R = 0.987; R 2 = 0.975; P = 0) demonstrating its exclusive determinants: LVEF, PEP/TET, and DBP/SBP. Considering Ea as a known value, the VAC-derived Ees formula: Ees_d ≈ Ea/(0.553-0.009*LVEF+3.463*PEP/TET) was strongly correlated to Chen's Ees formula (R = 0.973; R 2 = 0.947) being based on SBP, ESV, LVEF, and PEP/TET and no exponential power. Thus, the new index supports our hypothesis, in the limited sample of patients with HFrEF. Indices like SBP/PEP, (SBP*LVEF)/PEP, PEP/TET, and DBP/SBP deserve further experiments, underlining the major role of the forgotten STI.

Revisiting the relationship between left ventricular ejection fraction and ventricular-arterial coupling.

The aim of this article was to analyse in-depth the relationship between left ventricular (LV) ejection fraction (EF) (LVEF) and the most commonly used formulas for the calculation of LV elastance (Ees), volume intercept at 0 mmHg pressure (V0), effective arterial elastance (Ea), and ventricular-arterial coupling (VAC) as are validated today. We analyse the mathematical resulting consequences, raising the question on the physiological validity. To our knowledge, some of the following mathematical consequences have never been published. On the basis of studies demonstrating that normal LV dimensions and LVEF have a Gaussian unimodal distribution, we considered that the normal modal LVEF is 62% or very close to it. Expressed as a fraction, it is 0.62, that is, the reciprocal of the Phi number (namely, 1/Φ ~ 0.618). Applying Euclid's mathematical law on the extreme and mean ratio (the golden ratio), we studied the LVEF-VAC relationship in normal hearts. The simplification of the VAC formula (with V0 = 0) leads to false physiological results; V0 extraction from single-beat Chen's formula leads to high negative results in normal subjects; based on the Euclid law, LVEF and Ea/Ees will be equal for a ratio value of 0.618 (62%) where V0 cannot be different from 0 mL; LVEF and VAC inverse relationship formula (Ea/Ees = 1/LVEF - 1) is reducible to a fundamental property of Phi: 1/Φ = (Φ - 1), being valid only if LVEF = VAC at a 0.618 value; according to this restriction, Vo can only be 0 mL, thus describing a very limited range. The Ea/Ees ratio, owing to its mathematical more dynamic behaviour, can be more sensitive than LVEF, being a valuable clinical tool in patients with heart failure (HF) with reduced EF, acute unstable haemodynamic situations, where Ees and Ea variations are disproportionate. However, the application is doubtful in HF with preserved EF where Ees and Ea may have same-direction augmentation. The modified VAC formula suffers from oversimplification, reducing it to a dimensionless ratio, which is supposed to approximate non-linear time-varying functions. Thus, we advocate for caution and in-depth understanding when using simplified formulas in clinical practice.

Epidemiology, pathophysiology and contemporary management of cardiogenic shock - a position statement from the Heart Failure Association of the European Society of Cardiology.

Cardiogenic shock (CS) is a complex multifactorial clinical syndrome with extremely high mortality, developing as a continuum, and progressing from the initial insult (underlying cause) to the subsequent occurrence of organ failure and death. There is a large spectrum of CS presentations resulting from the interaction between an acute cardiac insult and a patient's underlying cardiac and overall medical condition. Phenotyping patients with CS may have clinical impact on management because classification would support initiation of appropriate therapies. CS management should consider appropriate organization of the health care services, and therapies must be given to the appropriately selected patients, in a timely manner, whilst avoiding iatrogenic harm. Although several consensus-driven algorithms have been proposed, CS management remains challenging and substantial investments in research and development have not yielded proof of efficacy and safety for most of the therapies tested, and outcome in this condition remains poor. Future studies should consider the identification of the new pathophysiological targets, and high-quality translational research should facilitate incorporation of more targeted interventions in clinical research protocols, aimed to improve individual patient outcomes. Designing outcome clinical trials in CS remains particularly challenging in this critical and very costly scenario in cardiology, but information from these trials is imperiously needed to better inform the guidelines and clinical practice. The goal of this review is to summarize the current knowledge concerning the definition, epidemiology, underlying causes, pathophysiology and management of CS based on important lessons from clinical trials and registries, with a focus on improving in-hospital management.

Therapeutic Advances in the Management of Acute Decompensated Heart Failure.

BACKGROUND: Acute decompensated heart failure (ADHF) is the most common presenting phenotype of acute heart failure (AHF). The main goal of this article was to review the contemporary management strategies in these patients and to describe how future clinical trials may address unmet clinical needs. AREAS OF UNCERTAINTY: The current pathophysiologic understanding of AHF is incomplete. The guideline recommendations for the management of ADHF are based only on algorithms provided by expert consensus guided by blood pressure and/or clinical signs of congestion or hypoperfusion. The lack of adequately conducted trials to address the unmet need for evidence therapy in AHF has not yet been surpassed, and at this time, there is no evidence-based strategy for targeted decongestive therapy to improve outcomes. The precise time point for initiation of guideline-directed medical therapies (GDMTs), as respect to moment of decompensation, is also unknown. DATA SOURCES: The available data informing current management of patients with ADHF are based on randomized controlled trials, observational studies, and administrative databases. THERAPEUTIC ADVANCES: A major step-forward in the management of ADHF patients is recognizing congestion, either clinical or hemodynamic, as a major trigger for heart failure (HF) hospitalization and most important target for therapy. However, a strategy based exclusively on congestion is not sufficient, and at present, comprehensive assessment during hospitalization of cardiac and noncardiovascular substrate with identification of potential therapeutic targets represents "the corner-stone" of ADHF management. In the last years, substantial data have emerged to support the continuation of GDMTs during hospitalization for HF decompensation. Recently, several clinical trials raised hypothesis of "moving to the left" concept that argues for very early implementation of GDMTs as potential strategy to improve outcomes. CONCLUSIONS: The management of ADHF is still based on expert consensus documents. Further research is required to identify novel therapeutic targets, to establish the precise time point to initiate GDMTs, and to identify patients at risk of recurrent hospitalization.

Therapeutic Advances in the Management of Cardiogenic Shock.

BACKGROUND: Cardiogenic shock (CS) is a life-threatening state of tissue hypoperfusion, associated with a very high risk of mortality, despite intensive monitoring and modern treatment modalities. The present review aimed at describing the therapeutic advances in the management of CS. AREAS OF UNCERTAINTY: Many uncertainties about CS management remain in clinical practice, and these relate to the intensity of invasive monitoring, the type and timing of vasoactive therapies, the risk-benefit ratio of mechanical circulatory support (MCS) therapy, and optimal ventilation mode. Furthermore, most of the data are obtained from CS in the setting of acute myocardial infarction (AMI), although for non-AMI-CS patients, there are very few evidences for etiological or MCS therapies. DATA SOURCES: The prospective multicentric acute heart failure registries that specifically presented characteristics of patients with CS, distinct to other phenotypes, were included in the present review. Relevant clinical trials investigating therapeutic strategies in post-AMI-CS patients were added as source information. Several trials investigating vasoactive medications and meta-analysis providing information about benefits and risks of MCS devices were reviewed in this study. THERAPEUTIC ADVANCES: Early revascularization remains the most important intervention for CS in settings of AMI, and in patients with multivessel disease, recent trial data recommend revascularization on a "culprit-lesion-only" strategy. Although diverse types of MCS devices improve hemodynamics and organ perfusion in patients with CS, results from almost all randomized trials incorporating clinical end points were inconclusive. However, development of new algorithms for utilization of MCS devices and progresses in technology showed benefit in selected patients. A major advance in the management of CS is development of concept of regional CS centers based on the level of facilities and expertise. The modern systems of care with CS centers used as hubs integrated with emergency medical systems and other referee hospitals have the potential to improve patient outcomes. CONCLUSIONS: Additional research is needed to establish new triage algorithms and to clarify intensity and timing of pharmacological and mechanical therapies.

A new educational program in heart failure drug development: the Brescia international master program.

: Despite recent advances in chronic heart failure treatment, prognosis of acute heart failure patients remains poor with a heart failure rehospitalization rate or death reaching approximately 25% during the first 6 months after discharge. In addition, about half of these patients have preserved ejection fraction for which there are no evidence-based therapies. Disappointing results from heart failure clinical trials over the past 20 years emphasize the need for developing novel approaches and pathways for testing new heart failure drugs and devices. Indeed, many trials are being conducted without matching the mechanism and action of the drug with the clinical event. The implementation of these novel approaches should be coupled with the training of a new generation of heart failure physicians and scientists in the art and science of clinical trials. Currently, drug development is led by opinion leaders and experts who, despite their huge personal experience, were never trained systematically on drug development. The aim of this article is to propose a training program of 'drug development in Heart Failure'. A physician attending this course would have to be trained with a major emphasis on heart failure pathophysiology to better match mechanisms of death and rehospitalization with mechanism of action of the drug. Applicants will have to prove their qualifications and special interest in heart failure drug development before enrollment. This article should serve as a roadmap on how to apply emerging general principles in an innovative drug-development-in-heart-failure-process as well as the introduction of a new educational and mentorship program focusing on younger generations of researchers.

Anticoagulation in heart failure without atrial fibrillation: gaps and dilemmas in current clinical practice.

Data from observational and post-hoc analyses suggest that heart failure (HF) itself may be associated with higher risk of thromboembolic events compared to populations without HF. Although oral anticoagulants (OACs) might be a therapeutic option in individual cases, anticoagulation therapy in HF patients in sinus rhythm is not generally recommended, as the implementation of OACs in clinical practice in this HF population is not supported by large randomized clinical trials to date. Indeed, the available data suggest that the risk of major bleeding overshadows the potential anti-thromboembolic benefit of OACs in HF patients in sinus rhythm with no net beneficial effect on mortality rates. In this review we explore the current available evidence for the clinical outcomes of anticoagulation therapy in patients with HF in sinus rhythm, highlighting the current gaps in knowledge, which may guide the design of future randomized clinical trials focusing on the efficacy and safety of anticoagulant therapy in this HF population.

Predictors of Post-discharge Mortality Among Patients Hospitalized for Acute Heart Failure.

Acute Heart Failure (AHF) is a " multi-event disease" and hospitalisation is a critical event in the clinical course of HF. Despite relatively rapid relief of symptoms, hospitalisation for AHF is followed by an increased risk of death and re-hospitalisation. In AHF, risk stratification from clinically available data is increasingly important in evaluating long-term prognosis. From the perspective of patients, information on the risk of mortality and re-hospitalisation would be helpful in providing patients with insight into their disease. From the perspective of care providers, it may facilitate management decisions, such as who needs to be admitted and to what level of care (i.e. floor, step-down, ICU). Furthermore, risk-stratification may help identify patients who need to be evaluated for advanced HF therapies (i.e. left-ventricle assistance device or transplant or palliative care), and patients who need early a post-discharge follow-up plan. Finally, risk stratification will allow for more robust efforts to identify among risk markers the true targets for therapies that may direct treatment strategies to selected high-risk patients. Further clinical research will be needed to evaluate if appropriate risk stratification of patients could improve clinical outcome and resources allocation.