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Sudden death (SD) in young, apparently healthy athletes under 35 is an underestimated public health problem in Belgium. This is dramatically illustrated by the case of a 28-year old ultra-trail runner who suffered cardiac arrest during training, revealing an unrecognized cardiomyopathy. This highlights the importance of pre-participation cardiovascular screening in identifying such hidden conditions. The variety of causes of SD, mainly of cardiac origin, underlines the complexity of screening and the need to tailor it to the specific risks of each individual. The central issue in screening is the relevance of the resting 12-lead electrocardiogram (ECG). While some countries have adopted it with positive results, others continue to debate its systematic inclusion. Sudden death affects not only professional athletes, but also amateurs, who are often less medically monitored. The aim of cardiovascular screening is twofold: to identify young people at risk, while not unnecessarily limiting access to sport for those with no cardiac pathology. The effectiveness of the ECG is well recognized, but the implementation of such systematic screening in Belgium must take into account certain practical aspects.

Pericardial agenesis is a rarely seen congenital defect characterised by the partial or, more rarely complete, absence of the pericardium. Most often asymptomatic, it is usually incidentally discovered following the demonstration of heart's laevorotation on imaging, in the operating room or at autopsy. In this article, we report the case of an 80-year-old patient with asymptomatic complete pericardial agenesis fortuitous discovered. Pericardial agenesis observations are extremely uncommon reported in the literature, which substantiate its original epidemiological character. In addition, this observation brings some clinical, electrical as well as iconographic elements to better understand the pathology and raises clinical suspicions. Finally, this case report confirms the exceptionally symptomatic nature of the pathology, illustrating the irrelevance of treatment or specific follow-up.

Heart failure with preserved left ventricular ejection fraction (HFpEF) is a serious condition with a constantly increasing prevalence which is in correlation with the increase of this disease's risk factors incidence (obesity, arterial hypertension, diabetes, etc.) and the aging of the population. The first challenge is the diagnosis of HFpEF. Two score-based algorithms have been proposed by the European (ESC HFA-PEFF score) and the American (ACC/AHA H2FpEF score) Cardiology Societies to help the clinician in the differential diagnosis of exertional dyspnea; these scores include the association of various signs of elevated ventricular filling pressures at rest and/or during exercise. According to the ESC recommendations, the management of HFpEF is currently based on symptomatic treatment with diuretics, treatment of co-morbidities and treatment of the underlying etiology if it is identified at the end of the diagnostic approach. The prognosis of this disease is pejorative because no treatment had demonstrated its effectiveness for all HFpEF phenotypes in controlled studies until now. The management algorithm could change soon due to the publication of the EMPEROR-Preserved study, which demonstrated the efficacy of empagliflozin, an SGLT2 inhibitor, concerning a significant reduction of the mortality rate and cardiac hospitalization, regardless of left ventricular ejection fraction. That said, there are many ongoing studies in the field, and treatment prospects will likely be more targeted on the HFpEF phenotype in a near future, due to the heterogeneous nature of this clinical entity.

Sudden cardiac death affects close to half a million people a year in Europe and accounts for 50 % of cardiovascular deaths. Unfortunately, only a minority of these events occur in front of witnesses, which reduces the chances of survival. In order to limit this risk, an internal automatic defibrillator can be implanted in patients at risk of sudden cardiac death. However, there are circumstances when the patient is at risk of sudden cardiac death and this device cannot be implanted. In order to limit this risk, certain patients can be equipped with a wearable defibrillator.

Cardiogenic shock is one of the four types of circulatory shock (cardiogenic, distributive, hypovolemic and obstructive). It is a serious complication associated with a hypoperfusion state of terminal organs and possible multivisceral failures, with a high mortality rate of nearly 50 %. It is secondary to an acute myocardial infarction in 8 out of 10 cases but only complicates it in 5 to 10 %. It is more frequently encountered in pluri-troncular coronary diseases. Coronary revascularization and supportive care are the main treatments.

Background: There are limited data on Coronavirus disease 2019 (COVID-19) in solid organ transplant patients, especially in heart transplant recipients, with only a few case reports and case series described so far. Heart transplant recipients may be at particular high risk due to their comorbidities and immunosuppressed state., Case Presentation: This report describes the clinical course and the challenging management of early COVID-19 infection in two heart transplant recipients who tested positive for the SARS-CoV-2 virus in the perioperative period of the transplant procedure. The two patients developed a severe form of the disease and ultimately died despite the initiation of an antiviral monotherapy with hydroxychloroquine coupled with the interruption of mycophenolate mofetil., Conclusions: These two cases illustrate the severity and poor prognosis of COVID-19 in the perioperative period of a heart transplant. Thorough screening of donors and recipients is mandatory, and the issue of asymptomatic carriers needs to be addressed.

Even though, it has long been considered as a passive channel allowing communication between the systemic and pulmonary circulations, it is now clearly established that the right ventricle plays an essential role in cardio-pulmonary couple physiology. Its failure results in a clinical presentation that reflects the systemic congestion and reduced cardiac output. It is the consequence of two pathological situations frequently encountered in intensive care including pulmonary vascular resistance increase and right ventricle contraction alteration. Mechanical ventilation, certain drugs and volume overload can also participate. The management of the acute right heart failure is based on the combination of supportive treatment and causal treatment, specific to the etiology. Supportive therapy aims to optimize filling pressures, reduce afterload and support cardiac contractibility. With the growing number of therapeutic options used according to co-morbidities, decision-making by a multidisciplinary heart team seems essential.

Isolated left ventricular non-compaction (LVNC) is a congenital disorder characterized by prominent myocardial trabeculations and deep intertrabecular recesses. Although LVNC is diagnosed by echocardiography and cardiac magnetic resonance, there is no evidence-based imaging diagnostic criteria. Affected individuals are at risk of left ventricular failure, life-threatening arrhythmias and cardio-embolism. The diagnosis may be difficult in the atypical forms. The management remains controversial and depends on the clinical manifestations. Familial forms exist, ordering for genetic counseling. The aim of this article is to optimize the knowledge and the management of LVNC by reminding the diagnostic criteria used.

The diagnosis of heart failure can sometimes be challenging for the clinician because presentation circumstances and heart failure phenotypes are varied. The identification and validation of sensitive and specific biomarkers for this condition are still a subject of intensive research. Among them, natriuretic peptides (ANP, BNP, NTproBNP) are widely used and validated as markers of heart failure. Their appropriate use and correct interpretation, however, require knowledge of their indications, specificities and limitations. The European Society of Cardiology has recently issued recommendations in this regard. This article summarizes them in order to facilitate the understanding and the use of natriuretic peptides in clinical practice. It also discusses their use in the etiological diagnosis of pleural effusions caused by heart failure.

Aims: To obtain the normal range for 2D echocardiographic (2DE) measurements of left ventricular (LV) layer-specific strain from a large group of healthy volunteers of both genders over a wide range of ages., Methods and Results: A total of 287 (109 men, mean age: 46 ± 14 years) healthy subjects were enrolled at 22 collaborating institutions of the EACVI Normal Reference Ranges for Echocardiography (NORRE) study. Layer-specific strain was analysed from the apical two-, three-, and four-chamber views using 2DE software. The lowest values of layer-specific strain calculated as ±1.96 standard deviations from the mean were -15.0% in men and -15.6% in women for epicardial strain, -16.8% and -17.7% for mid-myocardial strain, and -18.7% and -19.9% for endocardial strain, respectively. Basal-epicardial and mid-myocardial strain decreased with age in women (epicardial; P = 0.008, mid-myocardial; P = 0.003) and correlated with age (epicardial; r = -0.20, P = 0.007, mid-myocardial; r = -0.21, P = 0.006, endocardial; r = -0.23, P = 0.002), whereas apical-epicardial, mid-myocardial strain increased with the age in women (epicardial; P = 0.006, mid-myocardial; P = 0.03) and correlated with age (epicardial; r = 0.16, P = 0.04). End/Epi ratio at the apex was higher than at the middle and basal levels of LV in men (apex; 1.6 ± 0.2, middle; 1.2 ± 0.1, base 1.1 ± 0.1) and women (apex; 1.6 ± 0.1, middle; 1.1 ± 0.1, base 1.2 ± 0.1)., Conclusion: The NORRE study provides useful 2DE reference ranges for novel indices of layer-specific strain., (Published on behalf of the European Society of Cardiology. All rights reserved. © The Author(s) 2020. For permissions, please email: journals.permissions@oup.com.)

Several clinical reports indicate that the use of amphetaminic anorectic drugs or ergot derivatives could cause valvular heart disease (VHD). We sought to investigate whether valvular lesions develop in response to long-term oral administration of these drugs and to identify drug-targeted biological processes that may lead to VHD. Treatment of New Zealand White rabbits with pergolide, dexfenfluramine, or high-dose serotonin for 16 weeks induced valvular alterations characterized by extracellular matrix remodeling. Transcriptome profiling of tricuspid valves using RNA sequencing revealed distinct patterns of differentially expressed genes (DEGs) that clustered according to the different treatments. Genes that were affected by the three treatments were functionally enriched for reduced cell metabolism processes. The two drugs yielded more changes in gene expression than serotonin and shared most of the DEGs. These DEGs were mostly enriched for decreased biosynthetic processes, increased cell-matrix interaction, and cell response to growth factors, including TGF-β, which was associated with p38 MAPK activation. Treatment with pergolide specifically affected genes involved in homeostasis, which was corroborated by the activation of the master regulator of cell energy homeostasis, AMPK-α, as well as decreased levels of metabolism-related miR-107. Thus, both pergolide and dexfenfluramine may cause VHD through valve metabolic reprogramming and matrix remodeling., Competing Interests: The authors declare no conflict of interest. The funders had no role in the design of the study; in the collection, analyses, or interpretation of data; in the writing of the manuscript, or in the decision to publish the results.

Clinical evidence indicates that innate immune cells may contribute to acute coronary syndrome (ACS). Our prospective study aimed at investigating the association of neutrophil phenotypes with ACS. 108 patients were categorized into chronic stable coronary artery disease ( n = 37), unstable angina (UA) ( n = 19), Non-ST-Elevation Myocardial Infarction (NSTEMI) ( n = 25), and ST-Elevation Myocardial Infarction (STEMI) ( n = 27). At the time of inclusion, blood neutrophil subpopulations were analysed by flow cytometry. Differential blood cell count and plasma levels of neutrophilic soluble markers were recorded at admission and, for half of patients, at six-month follow-up. STEMI and NSTEMI patients displayed higher neutrophil count and neutrophil-to-lymphocyte ratio than stable and UA patients ( p < 0.0001), which normalized at six-month post-MI. Atypical low-density neutrophils were detected in the blood of the four patient groups. STEMI patients were characterized by elevated percentages of band cells compared to the other patients ( p = 0.019). Multivariable logistic regression analysis revealed that plasma levels of total myeloperoxidase was associated with STEMI compared to stable (OR: 1.434; 95% CI: 1.119-1.837; P < 0.0001), UA (1.47; 1.146-1.886; p = 0.002), and NSTEMI (1.213; 1.1-1.134; p = 0.0001) patients, while increased neutrophil side scatter (SSC) signal intensity was associated with NSTEMI compared to stable patients (3.828; 1.033-14.184; p = 0.045). Hence, changes in neutrophil phenotype are concomitant to ACS.

The introduction of basic treatment for heart failure dates to the late 1990s. Since that time, apart from a few new developments reserved for selected patients, there has been little progress. During these years, the epidemiology of the disease has evolved. The number of patients is constantly increasing and the prognosis is often darker than most oncological pathologies. With the arrival of the sacubitril/valsartan combination, Entresto®, a new therapeutic class has emerged. It has shown a significant reduction in mortality and hospitalizations for heart failure. The additional benefits to be expected from this molecule are still being evaluated. Significant positive remodeling seems to be a reality for many patients. This spectacular advance, however, is not the final solution. In addition, patients with preserved heart failure do not seem to benefit the same from this molecule. Other advances are being assessed. Sacubitril/valsartan is the first revolution, perhaps, in a long series.

Aim: To investigate the effects of transcatheter aortic valve implantation (TAVI) on early recovery of global and segmental myocardial function in patients with severe symptomatic aortic stenosis and preserved left ventricular ejection fraction (LVEF) and to determine if parameters of deformation correlate with outcomes., Methods: The echocardiographic (strain analysis) and outcome (hospitalizations because of heart failure and mortality) data of 62 consecutive patients with preserved LVEF (64.54 ± 7.97%) who underwent CoreValve prosthesis implantation were examined., Results: Early after TAVI (5 ± 3.9 days), no significant changes in LVEF or diastolic function were found, while a significant drop of systolic pulmonary artery pressure (PAP) occurred (42.3 ± 14.9 vs. 38.1 ± 13.9 mmHg, P = 0.028). After TAVI global longitudinal strain (GLS) did not change significantly, whereas significant improvement in global mid-level left ventricular (LV) radial strain (GRS) was found (-16.71 ± 2.42 vs. -17.32 ± 3.25%; P = 0.33; 16.57 ± 6.6 vs. 19.48 ± 5.97%, P = 0.018, respectively). Early significant recovery of longitudinal strain was found in basal lateral and anteroseptal segments (P = 0.038 and 0.048). Regional radial strain at the level of papillary muscles [P = 0.038 mid-lateral, P < 0.001 mid-anteroseptum (RSAS)] also improved. There was a significant LV mass index reduction in the late follow-up (152.42 ± 53.21 vs. 136.24 ± 56.67 g/m, P = 0.04). Mean follow-up period was 3.5 ± 1.9 years. Parameters associated with worse outcomes in univariable analysis were RSAS pre-TAVI, LV end-diastolic diameter after TAVI, relative wall thickness, and mitral E and E/A after TAVI., Conclusion: Global and regional indices of myocardial function improved early after TAVI, suggesting the potential of myocardium to recover with a reduced risk for clinical deterioration.

The «Prospective Comparison of ARNI with ARB Global Outcomes in HF with Preserved Ejection Fraction» (PARAGON HF) trial is a multicenter, randomized, double-blind study comparing the incidence of heart failure hospitalization and cardiovascular mortality in patients with heart failure with preserved ejection fraction (HFpEF) treated with sacubitril/valsartan (Entresto®) versus valsartan alone. After a median follow-up of 35 months, the primary endpoint was reduced by 13 % in the sacubitril/valsartan group compared to the valsartan group (relative risk: 0.87, 95 % IC: 0.753-1.005, p = 0.058). Despite this lack of significance, the incidence of hospitalizations for heart failure was reduced (RR 0.85, 95 % CI: 0.72-1.00), whereas no benefit was observed on cardiovascular mortality. A subgroup analysis suggested that women and patients with an intermediate ejection fraction could get more benefit from the treatment. Concerning secondary criteria, a significant improvement in quality of life and in heart failure symptoms was observed in the group sacubitril/valsartan. There was a greater incidence of arterial hypotension and angioneurotic edema, but a lower incidence of hyperkalemia in the group sacubitril/valsartan.

Aim: Heart failure (HF) poses a unique medical burden of high morbidity and mortality. Elevated resting heart rate (HR) is associated with worse outcomes in chronic HF, but little is known about the prognostic impact of serial HR measurement during hospital stay after acute HF. We examined the association between HR obtained at admission at Day 4 and at discharge and long-term mortality in a cohort of 672 patients discharge from hospital after management of acute HF., Methods and Results: All patients examined were in sinus rhythm. HR was derived from electrocardiogram and was defined as the first reported HR in the medical record. At 1 year follow up, 60 patients died. Median HR was 86 ± 17 b.p.m. (first tertile: 75 b.p.m., third tertile: 97 b.p.m.) at admission, 76 ± 14 b.p.m. (first tertile: 67 b.p.m., third tertile 85 b.p.m.) at Day 4, and 72 ± 11 b.p.m. (first tertile: 64 b.p.m., third tertile 80 b.p.m.) at discharge. Patients who died were significantly older (75 ± 11 vs. 71 ± 12 years; P = 0.027), had more frequently a history of ischemic cardiomyopathy (n = 34/60, P = 0.012) and of chronic obstructive pulmonary disease (n = 26/60, P = 0.027), had higher admission N terminal pro brain natriuretic peptide (14 572 ± 21 600 vs. 7647 ± 7964 pg/ml; P = 0.027), had lower systolic and diastolic blood pressures (P < 0.05), haemoglobin level (10.6 ± 2.2 vs. 12.2 ± 2.2 g/L; P = 0.005), albumin level (35.2 ± 4.3 vs 37.1 ± 4.1 g/dl; P = 0.003) and estimated glomerular filtration rate (47 ± 21 vs. 60 ± 28 ml/min/1.73 m 2 ; P = 0.0017). There were no significant differences between survivors and nonsurvivors in left ventricular ejection, the use of beta-blocker and angiotensin-converting enzyme-inhibitor, and the rate of comorbidities (hypertension, diabetes) (P=NS, for all). HR at admission was not significantly associated with 1 year mortality (P = 0.20), whereas there was a significant increase in 1 year mortality for HRs>85 b.p.m. at Day 4 (P < 0.0001) and > 80 b.p.m. at discharge (P < 0.0001). In the multivariable model that included the third tertile at Day 4 and discharge HR and adjusted for all other significant covariates, haemoglobin (P = 0.019), and HR at Day 4 (P = 0.023) were independently associated with 1 year mortality. When only discharge HR was included haemoglobin (P = 0.0004) and HR at discharge (P = 0.00053) remained independently associated with 1 year mortality., Conclusions: In patients surviving the acute HF phase, a high HR at Day 4, and at a lesser degree at discharge, but not at admission, is a strong predictor of 1 year mortality., (© 2019 The Authors. ESC Heart Failure published by John Wiley & Sons Ltd on behalf of the European Society of Cardiology.)

Anemia and iron deficiency are two common comorbidities in heart failure with reduced ejection fraction (HFrEF) and are associated with a poor prognosis. In contrast to iron oral supplementation, administration of intravenous ferric carboxymaltose (Injectafer®) improves quality of life, exercise capacity, and seems to reduce hospitalizations for heart failure. Unfortunately, although anaphylactic reactions are extremely rare, it is recommended to administer Injectafer® in a suitable medical environment. This limitation hinders Injectafer® administration and may cause reluctance from both physician and patient. The aim of this article is to optimize and harmonize management of iron deficiency in heart failure, by proposing a simple solution for the patient and the practitioner.

The functional integrity of the endothelium is essential for vascular health. In addition to maintaining a delicate balance between vasodilation and vasoconstriction, the endothelium has numerous other complex roles involved in the maintenance of vascular homeostasis. Chronic exposure to cardiovascular risk factors and oxidative stress results in an imbalance in these functions, creating an environment that favors reduced vasodilation and a proinflammatory and prothrombic state. The involvement of endothelial dysfunction in all stages of the cardiovascular continuum makes it an important target for treatment. One of the major endothelial-derived factors involved in the maintenance of endothelial function is nitric oxide (NO). Angiotensin-converting enzyme (ACE) inhibitors increase NO production both directly and indirectly by preventing production of angiotensin II (which diminishes NO production) and inhibiting the degradation of bradykinin (which stimulates local release of NO). Among the ACE inhibitors, perindopril appears to have the greatest effects on bradykinin and has demonstrated efficacy in a number of markers of endothelial dysfunction including arterial stiffness and progression of atherosclerosis. There is also strong evidence supporting the use of perindopril-based therapy for the treatment of hypertension and for reducing the risk of cardiovascular morbidity and mortality in a wide range of patients across the cardiovascular continuum.Funding: The journal's Rapid Service Fee was funded by Servier.

Alcohol consumption is a serious problem in terms of public health because it remains a major cause of illness and premature death. The effects of alcohol on cardiovascular system are particularly complex. Current data report both favourable and adverse effects depending on the level of consumption, the type of alcohol consumed and the pathology considered. The goal of this review is to describe the spectrum of cardiovascular events associated with alcohol consumption.

Numerous epidemiological studies have shown that a high resting heart rate is associated with an increased cardiovascular morbidity and mortality, particularly in heart failure. The resting heart rate is not only a risk marker in heart failure, but it is also a risk factor, i.e., modifying heart rate also modifies the risk. Chronotropic drugs have shown benefits in terms of morbidity and mortality. Nevertheless, there is a major difference between the recommended heart rate and the patients’ everyday life heart rate. Indeed, even if the proportion of heart failure patients on beta-blockers is satisfactory, the number of patients with an optimal heart rate remains insufficient. The aim of this article is to examine the deleterious effect of an elevated resting heart rate in heart failure with systolic dysfunction, in order to overcome the therapeutic inertia and to improve the outcome in this patient group.

Behçet's disease is a relapsing, immune-mediated systemic vasculitis that may affect blood vessels of all types and sizes. Nowadays, the etiology remains unclear. In the absence of a biological marker or pathognomonic radiology, the diagnosis is mainly based on clinical manifestations. The cardiovascular involvement, known as "angio-Behçet", is relatively common and affects up to 40% of patients. It typi- cally occurs in a young male, usually during the onset of the disease. In general, immunosuppressive and anticoagulant therapies initiated early are likely to induce a remarkable cli- nical improvement. Nevertheless, prompt recognition of the polymorphous cardiovascular manifestations of the disease is challenging and may be responsible for some considerable delay prior to initiation of adequate therapy. The aim of this article is to describe the spectrum of cardiovascular involve- ments of Behçet's disease in order to optimize detection and therapeutic management.