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In recent years, humanity has been confronted with a global pandemic due to coronavirus disease 2019 (COVID-19), which has caused an unprecedented health and economic crisis worldwide. Apart from the respiratory symptoms, which are considered the principal manifestations of COVID-19, it has been recognized that COVID-19 constitutes a systemic inflammatory process affecting multiple organ systems. Across the spectrum of organ involvement in COVID-19, acute liver injury (ALI) has been gradually gaining increasing attention by the international scientific community. COVID-19 associated liver impairment can affect a considerable proportion of COVID-19 patients and seems to correlate with the severity of the disease course. Indeed, COVID-19 patients hospitalized in the intensive care unit (ICU) run a greater risk of developing ALI due to the severity of their clinical condition and in the context of multi-organ failure. The putative pathophysiological mechanisms of COVID-19 induced ALI in ICU patients remain poorly understood and appear to be multifactorial in nature. Several theories have been proposed to explain the occurrence of ALI in the ICU setting, such as hypoperfusion and ischemia due to hemodynamic instability, passive liver congestion as a result of congestive heart failure, ischemia-reperfusion injury, hypoxia due to respiratory failure, mechanical ventilation itself, sepsis and septic shock, cytokine storm, endotheliitis with concomitant coagulopathy, drug-induced liver injury, parenteral nutrition and direct cytopathic viral effect. It should be noted that no specific therapy for COVID-19 induced ALI exists. Therefore, the therapeutic approach lies in preventive measures and is exclusively supportive once ALI ensues. The aim of the current review is to scrutinize the existing evidence on COVID-19 associated ALI in ICU patients, explore its clinical implications, shed light on the underlying pathophysiological mechanisms and propose potential therapeutic approaches. Ongoing research on the particular scientific field will further elucidate the pathophysiology behind ALI and address unresolved issues, in the hope of mitigating the tremendous health consequences imposed by COVID-19 on ICU patients.

Aims The current study evaluated the association of echocardiography, cardiac magnetic resonance (CMR), and ferritin data with 10-year survival in thalassemia patients. Methods Demographics, ferritin, echocardiography, and CMR parameters of stable consecutive thalassemia patients were prospectively collected. Results In total, 75 patients (mean age 37 ± 11 years, 45% male) with thalassemia were included and dichotomized based on their survival status after a median follow-up period of 10.3 [9.6-10.9] years. Older age (HR: 1.071, p = 0.001), ferritin ≥2000 ng/ml (HR: 4.682, p = 0.007) and ≥1700 ng/ml (HR: 7.817, p = 0.002), elevated LV end-diastolic pressure (HR: 1.019, p = 0.044), TR Vmax >2.8 m/s (HR: 6.845, p = 0.005), and CMR T2∗ ≤20 msec (HR: 3.602, p = 0.043) and ≤34 msec (HR: 5.854, p = 0.026) were associated with increased all-cause mortality (primary endpoint). A baseline model including age was created and became more predictive of worse survival by adding TR Vmax >2.8 m/s instead of elevated LV end-diastolic pressure (C index 0.767 vs. 0.760, respectively), ferritin ≥1700 ng/ml instead of ≥2000 ng/ml (C index 0.890 vs. 0.807, respectively), or CMR T2∗≤34 msec instead of ≤20 msec (C index 0.845 vs. 0.839, respectively). Parameters associated with the combined endpoint of cardiac mortality/cardiac hospitalization (secondary endpoint) after adjusting for age were ferritin ≥1700 ng/ml (HR 3.770, p = 0.014), ratio E/A wave >2 (HR 3.565, p = 0.04), TR Vmax >2.8 m/s (HR 4.541, p = 0.049), CMR T2∗ ≤20 ms (HR 9.462, p = 0.001), and CMR T2∗ ≤34 ms (HR 11.735, p = 0.002). The model including age and T2∗ ≤34 ms instead of T2∗ ≤20 ms was more predictive of the secondary endpoint (C-index 0.844 vs 0.838, respectively). Conclusions In thalassemia patients, TR Vmax >2.8 m/s, ferritin ≥2000 ng/ml, and CMR T2∗ ≤20 ms were associated with worse long-term survival. In the current era of advanced chelation therapy, aiming for ferritin ≤1700 ng/ml and CMR T2∗ ≥34 ms may improve their prognosis.

Heart failure (HF) is a global public health burden, characterized by frequent emergency department (ED) visits and hospitalizations. Identifying successful strategies to avoid admissions is crucial for the management of acutely decompensated HF, let alone resource utilization. The primary challenge for ED management of patients with acute heart failure (AHF) lies in the identification of those who can be safely discharged home instead of being admitted. This is an elaborate decision, based on limited objective evidence. Thus far, current biomarkers and risk stratification tools have had little impact on ED disposition decision-making. A reliable definition of a low-risk patient profile is warranted in order to accurately identify patients who could be appropriate for early discharge. A brief period of observation can facilitate risk stratification and allow for close monitoring, aggressive treatment, continuous assessment of response to initial therapy and patient education. Lung ultrasound may represent a valid bedside tool to monitor cardiogenic pulmonary oedema and determine the extent of achieved cardiac unloading after treatment in the observation unit setting. Safe discharge mandates multidisciplinary collaboration and thoughtful assessment of socioeconomic and behavioural factors, along with a clear post-discharge plan put forward and a close follow-up in an outpatient setting. Ongoing research to improve ED risk stratification and disposition of AHF patients may mitigate the tremendous public health challenge imposed by the HF epidemic.

Background It is unknown whether sex-specific differences in mortality observed in HCM are due to older age of women at presentation, or whether women have greater degree of LV myopathy than men. Methods We retrospectively compared clinical/imaging characteristics and outcomes between women and men in our overall cohort composed of 728 HCM patients, and in an age-matched subgroup comprised of 400 age-matched patients. We examined sex-specific differences in LV myopathy, and dissected the influence of age and sex on outcomes. LV myopathy was assessed by measuring LV mass, LVEF, global peak longitudinal systolic strain (LV-GLS), diastolic function (E/A, E/e′), late gadolinium enhancement (LV-LGE) and myocardial blood flow (MBF) at rest/stress. The primary endpoint was a composite outcome, comprising heart failure (HF), atrial fibrillation (AFib), ventricular tachycardia/fibrillation (VT/VF) and death; individual outcomes were defined as the secondary endpoint. Results Women in the overall cohort were older by 6 years. Women were more symptomatic and more likely to have obstructive HCM. Women had smaller LV cavity size, stroke volume and LV mass, higher indexed maximum wall thickness (IMWT), more hyperdynamic LVEF and higher/similar LV-GLS. Women had similar LV-LGE and E/A, but higher E/e′ and rest/stress MBF. Female sex was independently associated with the composite outcome in the overall cohort, and with HF in the overall cohort and age-matched subgroup after adjusting for obstructive HCM, LA diameter, LV-GLS. Conclusions Our results suggest that sex-specific differences in LV geometry, hyper-contractility and diastolic function, not greater degree of LV myopathy, contribute to a higher, age-independent risk of diastolic HF in women with HCM.

Despite considerable advances in the field, heart failure (HF) still poses a significant disease burden among affected individuals since it continues to cause high morbidity and mortality rates. Inflammation is considered to play a key role in disease progression, but the exact underlying pathophysiological mechanisms involved have not yet been fully elucidated. The gut, as a potential source of inflammation, could feasibly explain the state of low-grade inflammation seen in patients with chronic HF. Several derangements in the composition of the microbiota population, coupled with an imbalance between favorable and harmful metabolites and followed by gut barrier disruption and eventually bacterial translocation, could contribute to cardiac dysfunction and aggravate HF. On the other hand, HF-associated congestion and hypoperfusion alters intestinal function, thereby creating a vicious cycle. Based on this evidence, novel pharmaceutical agents have been developed and their potential therapeutic use has been tested in both animal and human subjects. The ultimate goal in these efforts is to reverse the aforementioned intestinal derangements and block the inflammation cascade. This review summarizes the gut-related causative pathways implicated in HF pathophysiology, as well as the associated therapeutic interventions described in the literature.

Hypertrophic cardiomyopathy (HCM) patients have a high incidence of atrial fibrillation (AF) and increased stroke risk, even with low CHAHCM patients with documented paroxysmal/persistent/permanent AF (n = 191) were considered AF cases, and the remaining patients in sinus rhythm (n = 640) were tagged as No-AF. We evaluated 93 clinical variables; the most informative variables useful for distinguishing AF from No-AF cases were selected based on the 2-sampleWe identified 18 highly informative variables that are positively (n = 11) and negatively (n = 7) correlated with AF in HCM. Next, patient records were represented via these 18 variables. Data imbalance resulting from the relatively low number of AF cases was addressed via a combination of oversampling and undersampling strategies. We trained and tested multiple classifiers under this sampling approach, showing effective classification. Specifically, an ensemble of logistic regression and naïve Bayes classifiers, trained based on the 18 variables and corrected for data imbalance, proved most effective for separating AF from No-AF cases (sensitivity = 0.74, specificity = 0.70, C-index = 0.80).Our model (HCM-AF-Risk Model) is the first machine learning-based method for identification of AF cases in HCM. This model demonstrates good performance, addresses data imbalance, and suggests that AF is associated with a more severe cardiac HCM phenotype.Les patients atteints d’une cardiomyopathie hypertrophique (CMH) présentent une forte incidence de fibrillation auriculaire (FA) et un risque accru d’accident vasculaire cérébral (AVC), malgré des scores CHANous avons considéré les patients atteints d’une CMH qui ont une FA paroxystique/persistante/permanente documentée (n = 191) comme des cas de FA, et avons étiqueté les autres patients en rythme sinusal (n = 640) comme des cas sans FA. Nous avons évalué 93 variables cliniques; nous avons sélectionné les variables les plus informatives qui sont utiles pour distinguer les cas de FA des cas sans FA en fonction du test t pour deux échantillons et du critère de gain d’information.Nous avons relevé 18 variables hautement informatives qui ont une corrélation positive (n = 11) et une corrélation négative (n = 7) avec la FA en présence d’une CMH. Ensuite, nous avons représenté les dossiers des patients au moyen de ces 18 variables. Nous avons remédié au déséquilibre des données, qui résulte du nombre relativement faible de cas de FA, grâce à une combinaison de stratégies de suréchantillonnage et de sous-échantillonnage. Nous avons formé et testé de nombreux classificateurs selon cette approche d’échantillonnage, qui montre une classification efficace. Particulièrement, un ensemble de régression logistique et de classificateurs bayésiens naïfs formés en fonction des 18 variables et corrigés en fonction du déséquilibre des données s’est révélé le plus efficace pour séparer les cas de FA des cas sans FA (sensibilité = 0,74, spécificité = 0,70, indice C = 0,80).Notre modèle (modèle de risque de CMH-FA) est la première méthode d’apprentissage automatique qui sert à déterminer les cas de FA en présence de CMH. Ce modèle permet de démontrer une bonne performance, de remédier au déséquilibre des données, et de croire que la FA est associée à un phénotype grave de CMH.

Aims: The objective was to evaluate the potential contribution of left atrial (LA) function to reduced exercise capacity in patients with hypertrophic cardiomyopathy (HCM).Methods and results: Using a case-control design we randomly selected 95 patients with confirmed HCM based on guidelines criteria and without permanent atrial arrhythmia who underwent a treadmill exercise test. We measured echo-based left ventricular (LV) and LA morphology and function including mechanics using 2D speckle tracking. Preserved exercise capacity was defined as the 25 th percentile of metabolic equivalents (METs) or > 7 METs. Of 95 HCM patients, 36 had reduced exercise capacity (£7 METs) and 59 had preserved exercise capacity (>7 METs). Reduced exercise capacity patients were more likely to be older, female, had higher BMI, and more advanced heart failure symptoms. They also had a higher E/e’ ratio and lower LA reservoir and conduit strain but similar left ventricular outflow tract (LVOT) pressure gradients. By univariate analysis, LA reservoir and conduit strain, age, gender, BMI, NYHA class, and E/e’ correlated with METs. In multivariate analysis, LA conduit strain independently determined METs after adjusting for age, gender, BMI, NYHA and E/e’ (standardized coefficients 0.17, P=0.04). This relationship was primarily noted in non- and labile-obstructive but not in obstructive HCM. History of atrial fibrillation did not impact the association of LA strain with exercise capacity.Conclusion : Even after adjusting for LVOT gradients and diastolic function, reduced LA conduit strain is an independent determinant of exercise tolerance in HCM.

Aims Diastolic dysfunction is thought to be an important pathophysiologic component of hypertrophic cardiomyopathy (HCM). However, there are conflicting data on the potential value of the mitral E/e' ratio. We examined whether left ventricular outflow tract (LVOT) obstruction influences the value of E/e' in predicting outcomes in HCM. Methods and results Patients who met diagnostic criteria for HCM were enrolled. Diastolic function was assessed with complete two-dimensional and Doppler echocardiography. A composite clinical outcome including new onset atrial fibrillation, sustained ventricular tachycardia/fibrillation, heart failure, transplantation, and death was examined over a mean follow-up period of 4.2 years. Among 604 patients, 206 patients had an E/e' level ≥20. Patients with higher septal E/e' level were older, with more severe NYHA class, and more severe LVOT obstruction. Higher E/e' was associated with worse event-free survival in non-obstructive group and total HCM cohort. In addition, E/e' and LVOT pressure gradient were highly correlated in non-obstructive and total HCM, but not in labile or obstructive group. During follow-up period, 95 patients underwent myectomy. Post-op E/e' correlated significantly with LVOT pressure gradient (R = 0.306, P = 0.004). In these patients, post-op E/e' was associated with worse event-free survival (log-rank P = 0.030). Conclusion Assessment of E/e' is useful for risk stratification in HCM patients. Nevertheless, the predictive power is confounded by dynamic LVOT obstruction. Higher E/e' predicts worse clinical outcomes in non-obstructive HCM and in labile/obstructive after myectomy.

Co-infections have an unknown impact on the morbidity and mortality of the new clinical syndrome called coronavirus disease 2019 (COVID-19). The syndrome is caused by the new pandemic coronavirus SARS-CoV-2 and it is probably connected with severe traces in the elements of the immune system. Apart from possible Aspergillus infections, particularly in patients with acute respiratory distress syndrome (ARDS), other fungal infections could occur, probably more easily, due to the immunological dysregulation and the critical condition of these patients. Probiotic preparations of Saccharomyces are broadly used for the prevention of antibiotic-associated complications, especially in the intensive care units (ICU). On the other hand, Saccharomyces organisms are reported as agents of invasive infection in immunocompromised or critically ill patients. We report two cases of bloodstream infection by Saccharomyces in two patients hospitalised in the ICU, due to severe COVID-19, after Saccharomyces supplementation.

Introduction: Hypertrophic cardiomyopathy (HCM) patients are at increased risk for heart failure (HF), stroke, death, and paroxysmal atrial fibrillation (PAF) development. There is no consensus whether atrial fibrillation (AF) is a marker or mediator of adverse outcomes in HCM patients. Hypothesis: We hypothesized that PAF and left atrial (LA) remodeling predict adverse outcomes in HCM. Methods: Echocardiography (2D and speckle tracking) was used to assess LA size, function, and mechanics in a cohort of HCM patients with history of PAF (PAF group, n=45) and age/gender-matched HCM patients without history of AF (No-AF group; n=59). AF was diagnosed by review of EKGs, event recorder/holter monitor data, and ICD interrogation. Patients were followed for a mean of 53 months for development of the composite endpoint of HF, death, and stroke. Results: Clinical/demographic characteristics were similar in the 2 groups; 67% of PAF group had a CHADS 2 VASC score ≤ 1. The PAF group had higher LA volume, lower LA ejection fraction, and higher E/A ratio (reflecting LV diastolic dysfunction) compared to the No-AF group. LA contractile and reservoir strain/strain rate (SR) were significantly lower in the PAF group (Table 1). Male gender, LA reservoir and conduit strain/SR (not PAF presence) were associated with the development of the composite endpoint in univariate analysis. Only LA conduit and reservoir strain/SR independently predicted the composite endpoint in a multivariate model. Kaplan Meier survival analysis showed greater event-free survival among HCM patients with LA conduit strain >10.2% (Figure 1a) and LA reservoir strain >23.8% (p < 0.01) (Figure 1b). Conclusions: PAF is associated with greater degree of LA myopathy in HCM. LA myopathy assessed by conduit and reservoir strain/SR may be useful for risk stratification for HF, stroke, and death in HCM.

Background Paroxysmal atrial fibrillation (PAF) and left atrial (LA) structural remodeling are common in hypertrophic cardiomyopathy (HCM) patients, who are also at risk for adverse cardiovascular outcomes. Objective We assessed whether PAF and/or LA remodeling was associated with adverse outcomes in HCM. Methods We retrospectively studied 45 HCM patients with PAF (PAF group) and 59 HCM patients without atrial fibrillation (AF; no-AF group). LA/left ventricular (LV) function and mechanics were assessed by echocardiography. Patients were followed for development of the composite endpoint comprising heart failure, stroke, and death. Results Clinical/demographic characteristics, degree of LV hypertrophy, and E/e′ were similar in the two groups The PAF group had significantly higher LA volume, but lower LA ejection fraction (LAEF), LA contractile, and reservoir strain/strain rate than the no-AF group. During follow-up, 27 patients developed the composite endpoint. Incidence of the composite endpoint was similar in the two groups. Absolute values of 23.8% for reservoir strain and 10.2% for conduit strain were the best cutoffs for the composite endpoint, using receiver operating characteristic analysis. Kaplan-Meier survival analysis showed lower event-free survival in patients with reservoir strain ≤23.8% or conduit strain ≤10.2%. Univariate Cox analysis revealed an association between female sex, LAEF, LA reservoir/conduit strain, and LV global longitudinal strain with the composite endpoint. The association between LA reservoir/conduit strain and the composite endpoint persisted after controlling for age, sex, LAEF, and LV global longitudinal strain. Conclusions In this pilot HCM patient study, PAF was associated with a greater degree of LA myopathy, and low LA reservoir and conduit strain were associated with higher risk for adverse cardiovascular outcomes.

Background Hypertrophic cardiomyopathy ( HCM ) is a common inherited cardiac disease characterized by varying degrees of left ventricular outflow tract obstruction. In a large cohort, we compare the outcomes among 3 different hemodynamic groups. Methods and Results We prospectively enrolled patients fulfilling standard diagnostic criteria for HCM from January 2005 to June 2015. Detailed phenotypic characterization, including peak left ventricular outflow tract pressure gradients at rest and after provocation, was measured by echocardiography. The primary outcome was a composite cardiovascular end point, which included new‐onset atrial fibrillation, new sustained ventricular tachycardia/ventricular fibrillation, new or worsening heart failure, and death. The mean follow‐up was 3.4±2.8 years. Among the 705 patients with HCM (mean age, 52±15 years; 62% men), 230 with obstructive HCM were older and had a higher body mass index and New York Heart Association class. The 214 patients with nonobstructive HCM were more likely to have a history of sustained ventricular tachycardia/ventricular fibrillation and implantable cardioverter defibrillator implantation. During follow‐up, 121 patients experienced a composite cardiovascular end point. Atrial fibrillation occurred most frequently in the obstructive group. Patients with nonobstructive HCM had more frequent sustained ventricular tachycardia/ventricular fibrillation events. In multivariate analysis, obstructive (hazard ratio, 2.80; 95% confidence interval, 1.64–4.80) and nonobstructive (hazard ratio, 1.94; 95% confidence interval, 1.09–3.45) HCM were associated with more adverse events compared with labile HCM . Conclusions Nonobstructive HCM carries notable morbidity, including a higher arrhythmic risk than the other HCM groups. Patients with labile HCM have a relatively benign clinical course. Our data suggest detailed sudden cardiac death risk stratification in nonobstructive HCM and monitoring with less aggressive management in labile HCM .

Neutrophil gelatinase-associated lipocalin (NGAL) and ST2 receptor, a member of the interleukin-1 receptor family, are novel biomarkers with a potential role in the diagnosis and risk stratification of patients with chronic heart failure (CHF). There is however scarce data on their relation with clinical characteristics and cardiac function in patients with CHF.Consecutive ambulatory patients with CHF were studied. All patients underwent clinical and echocardiographic assessment, and blood samples were collected for the estimation of ST2 and NGAL serum levels during the same assessment.A total of 76 patients (79% male, mean age: 63 ± 14 years), with CHF and left ventricular ejection fraction of 28 ± 7% were included. Median NGAL was 0.16 (0.09-0.275) mg/L and median ST2 was 0.0125 (0.0071-0.0176) mg/L. No association between NGAL and ST2 was observed. Multivariate analysis revealed tissue Doppler-derived right ventricular systolic velocity as an independent predictor of ST2, and the duration of HF and serum creatinine levels as independent predictors of NGAL.NGAL levels depend on the renal function and the duration of HF, while ST2 levels are affected by the right but not the left ventricular function and show no association with clinical indices of HF.

Background Recognition of cardiomyopathy in sepsis can be challenging due to the limitations of conventional measures such as ejection fraction (EF) and fractional shortening (FS) in the context of variable preload and afterload conditions. This study correlates myocardial function using strain echocardiography (SE) with cardiomyocyte oxidative stress in a murine model of sepsis. Methods C57BL/6J mice were randomized into control (n = 10), sham (n = 25), and a cecal ligation and puncture (CLP) (n = 33) model of sepsis. Echocardiography was performed pre-, 12, 24, and 48 h post-injury. Cardiac pro-inflammatory cytokines and mitochondrial redox scavenger expression were evaluated in a subset of each arm. To evaluate the influence of redox scavenger upregulation on oxidative injury and cardiac function, CLP was performed on mitochondrial catalase-upregulated C57BL/6J MCAT+/+ mice (n = 12) and wild-type (WT) animals for comparison. Results Septic C57BL/6J mice exhibited depressed longitudinal strain (LS) when compared to sham and control at 24 h (p

Global longitudinal strain (GLS) is a sensitive indicator of global left ventricular function particularly in those with normal ejection fraction. We examined the potential value of GLS in predicting outcomes in hypertrophic cardiomyopathy (HC). Conventional and strain echocardiography was performed in 400 patients with HC followed for a median 3.1 years (interquartile range 1.2 to 5.6). Peak systolic strain from 3 apical views was averaged to calculate GLS. Patients were divided based on a previously published cutoff value of -16%. Additionally, we identified 4 HC subgroups based on GLS: GLS ≤ -20%, -20%GLS ≤ -16%, -16%GLS ≤ -10%, and GLS -10%. The primary end point was a composite of new-onset sustained ventricular tachycardia/fibrillation, heart failure, cardiac transplantation, and all-cause death. Patients with GLS -16% had significantly more events (17% vs 7%, p = 0.002). In the 4-group analysis, event rates increased with worsening GLS (5%, 7%, 14%, and 33%, respectively, p = 0.001). Event-free survival was significantly superior in those with GLS ≤ -16% versus GLS -16% (p = 0.004); similarly, GLS -10% portended a significantly worse event-free survival compared with each of the other 3 groups (p0.01 for all pairwise comparisons). By univariate and multivariate Cox regression analysis, GLS remained significantly associated with the composite end point. GLS -10% had 4 times the risk of events compared with GLS ≤ -16% (p = 0.006). In conclusion, echo-based GLS is independently associated with outcomes in HC. Patients with GLS -10% have significantly higher event rates.

Hypertrophic cardiomyopathy (HCM) is traditionally classified based on a left ventricular outflow tract (LVOT) pressure gradient of 30mmHg at rest or with provocation. There are no data on whether 30mmHg is the most informative cut-off value and whether provoked gradients offer any information regarding outcomes.Resting and provoked peak LVOT pressure gradients were measured by Doppler echocardiography in patients fulfilling guidelines criteria for HCM. A composite clinical outcome including new onset atrial fibrillation, ventricular tachycardia/fibrillation, heart failure, transplantation, and death was examined over a median follow-up period of 2.1years.Among 536 patients, 131 patients had resting LVOT gradients greater than 30mmHg. Subjects with higher resting gradients were older with more cardiovascular events. For provoked gradients, a bi-modal risk distribution was found. Patients with provoked gradients90mmHg (HR 3.92, 95% CI 1.97-7.79) or30mmHg (HR 2.15, 95% CI 1.08-4.29) have more events compared to those with gradients between 30 and 89mmHg in multivariable analysis. The introduction of two cut-off points for provoked gradients allowed HCM to be reclassified into four groups: patients with "benign" latent HCM (provoked gradient 30-89mmHg) had the best prognosis, whereas those with persistent obstructive HCM had the worst outcome.Provoked LVOT pressure gradients offer additional information regarding clinical outcomes in HCM. Applying cut-off points at 30 and 90mmHg to provoked LVOT pressure gradients further classifies HCM patients into low-, intermediate- and high-risk groups.

We explored the differences in epidemiologic, clinical, laboratory and echocardiographic characteristics between idiopathic dilated (IDCM) and ischaemic cardiomyopathy (ICM). Consecutive patients with stable chronic heart failure evaluated at a tertiary cardiac centre were enrolled. Clinical examination, blood tests and echocardiographic study were performed. A total of 76 patients (43 IDCM, 33 ICM) were studied. IDCM patients were younger (p Patients with IDCM were younger, presented lower rates of right ventricular dysfunction and clinical right ventricular failure and had better functional capacity. Additional differences in clinical and laboratory findings exist pointing to a different patient population with diverse prognosis and potential need for individualized management.

Balloon aortic valvuloplasty (BAV) has been revived as a bridge to transcatheter aortic valve replacement (TAVR). The aim of the current prospective study was to define a safe time period from BAV to TAVR and to determine hemodynamic variables that predict event-free survival after BAV. The present prospective study included 68 consecutive patients with severe aortic stenosis who were treated initially with BAV from 2009 to 2012. Echocardiographic and invasive hemodynamic assessments were performed before BAV. The patients were followed up at regular intervals and events were defined as cardiac hospitalization or death. Invasive hemodynamic evaluation yielded more favorable results than echocardiographic assessment: aortic stenosis was less severe, cardiac output was higher, and pulmonary capillary wedge pressure (PCWP) was lower. Post-BAV event-free survival was 80.4 % at 30 days, 64.5 % at 6 months, 37 % at 1 year, 22.3 % at 2 years, and 9.3 % at 3 years. After excluding pre-discharge deaths (n = 7), the 30-day event-free survival rate was 90 %. Predictors of events after BAV were atrial fibrillation, cardiogenic shock, elevated euroSCORE (European System for Cardiac Operative Risk Evaluation), elevated PCWP, and elevated pulmonary artery systolic pressure. Invasively measured PCWP was the only independent predictor of events (hazard ratio, 1.07; 95 % confidence interval, 1.03–1.11; p = 0.001). A 30-day post-BAV period may be considered a bridge to TAVR. Furthermore, invasive assessment of PCWP before BAV is an independent hemodynamic predictor of events after BAV.

The aim of the present study was to examine the value of the right atrial volume index (RAVI) as predictor of functional capacity in patients with heart failure.A total of 51 patients with stable chronic heart failure of ischaemic or non-ischaemic aetiology were prospectively enrolled. The systolic function of the right ventricle was quantified using the tricuspid annular plane systolic excursion (TAPSE). Right atrial volume was measured in the apical 4-chamber view and was indexed to body surface area. The functional capacity was assessed by the Duke Activity Status Index (DASI).Patients with a low functional capacity (DASI10) had lower TAPSE (1.4 ± 0.3 cm versus 2.0 ± 0.4 cm, p0.001), higher RAVI (42 ± 15 ml/m(2) versus 22 ± 9 ml/m(2), p0.001), higher estimated right ventricular systolic pressure (61 ± 13 mmHg versus 40 ± 16 mmHg, p0.001), larger right ventricular end-diastolic diameter (4.7 ± 0.8 cm versus 3.6 ± 0.7 cm, p0.001) and lower left ventricular ejection fraction (26 ± 6% versus 30 ± 7%, p=0.022). Multivariate analysis revealed that TAPSE was the single independent predictor of DASI. In the subgroup of patients with reduced right ventricular systolic function (TAPSE2 cm), RAVI was the single independent predictor of low DASI. In the overall population RAVI=30.6 ml/m(2) had 75% sensitivity and 83% specificity in predicting DASI10. Within the subgroup of patients with TAPSE2 cm, RAVI=30.6 ml/m(2) had better sensitivity and specificity (79% and 90% respectively) in predicting DASI10.Increased right atrial volume index predicts low functional capacity quantified by the Duke Activity Status Index in patients with stable chronic heart failure.