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Chronic heart failure (HF) is rare in the young and common in the elderly in the Western world. HF in the young is usually due to specific causes, predominantly or exclusively affecting the heart (adult congenital heart disease, different types of cardiomyopathies, myocarditis, or cardiotoxicity). In contrast, the mechanisms underlying HF development in the elderly have not been completely delineated. We propose that in most elderly patients, HF, regardless of the left ventricular ejection fraction (LVEF), is the consequence of the acceleration of cardiovascular aging by specific risk factors (usually hypertension, obesity, type 2 diabetes mellitus [T2DM], coronary artery disease [CAD], and valvular heart disease [VHD]), most affecting both the heart and the vasculature. These risk factors act individually or more commonly in groups, directly or indirectly (hypertension, obesity, and T2DM may lead to HF through an intervening myocardial infarction). The eventual HF phenotype and outcomes in the elderly are additionally dependent on the presence and/or development of comorbidities (atrial fibrillation, anemia, depression, kidney disease, pulmonary disease, sleep disordered breathing, other) and disease modifiers (race, sex, genes, other). The clinical implications of this paradigm are that aggressive treatment of hypertension, obesity, T2DM (preferably with metformin and sodium-glucose cotransporter-2 inhibitors), CAD, and VHD on top of measures that retard cardiovascular aging are the steadfast underpinning for HF prevention in the elderly, which represent the vast majority of HF patients.

As the prevalence of heart failure (HF) continues to rise, prompt diagnosis and management of various medical conditions, which may lead to HF exacerbation and result in poor patient outcomes, are of paramount importance. Infection has been identified as a common, though under-recognized, precipitating factor of acute heart failure (AHF), which can cause rapid development or deterioration of HF signs and symptoms. Available evidence indicates that infection-related hospitalizations of patients with AHF are associated with higher mortality, protracted length of stay, and increased readmission rates. Understanding the intricate interaction of both clinical entities may provide further therapeutic strategies to prevent the occurrence of cardiac complications and improve prognosis of patients with AHF triggered by infection. The purpose of this review is to investigate the incidence of infection as a causative factor in AHF, explore its prognostic implications, elucidate the underlying pathophysiological mechanisms, and highlight the basic principles of the initial diagnostic and therapeutic interventions in the emergency department.

Background Incretin-based therapies are used in the treatment of type 2 diabetes mellitus (T2DM) and obesity. We investigated the changes in arterial stiffness and left ventricular (LV) myocardial deformation after 6-month treatment with the GLP-1 analogue liraglutide in subjects with newly diagnosed T2DM. Methods We randomized 60 patients with newly diagnosed and treatment-naive T2DM to receive either liraglutide (n = 30) or metformin (n = 30) for 6 months. We measured at baseline and after 6-month treatment: (a) carotid-femoral pulse wave velocity (PWV) (b) LV longitudinal strain (GLS), and strain rate (GLSR), peak twisting (pTw), peak twisting velocity (pTwVel) and peak untwisting velocity (pUtwVel) using speckle tracking echocardiography. LV untwisting was calculated as the percentage difference between peak twisting and untwisting at MVO (%dpTw–Utw MVO ), at peak (%dpTw–Utw PEF ) and end of early LV diastolic filling (%dpTw–Utw EDF ) (c) Flow mediated dilatation (FMD) of the brachial artery and percentage difference of FMD (FMD%) (d) malondialdehyde (MDA), protein carbonyls (PCs) and NT-proBNP. Results After 6-months treatment, subjects that received liraglutide presented with a reduced PWV (11.8 ± 2.5 vs. 10.3 ± 3.3 m/s), MDA (0.92 [0.45–2.45] vs. 0.68 [0.43–2.08] nM/L) and NT-proBNP (p < 0.05) in parallel with an increase in GLS (− 15.4 ± 3 vs. − 16.6 ± 2.7), GLSR (0.77 ± 0.2 vs. 0.89 ± 0.2), pUtwVel (− 97 ± 49 vs. − 112 ± 52°, p < 0.05), %dpTw–Utw MVO (31 ± 10 vs. 40 ± 14), %dpTw–Utw PEF (43 ± 19 vs. 53 ± 22) and FMD% (8.9 ± 3 vs. 13.2 ± 6, p < 0.01). There were no statistically significant differences of the measured markers in subjects that received metformin except for an improvement in FMD. In all subjects, PCs levels at baseline were negatively related to the difference of GLS (r = − 0.53) post-treatment and the difference of MDA was associated with the difference of PWV (r = 0.52) (p < 0.05 for all associations) after 6-month treatment. Conclusions Six-month treatment with liraglutide improves arterial stiffness, LV myocardial strain, LV twisting and untwisting and NT-proBNP by reducing oxidative stress in subjects with newly diagnosed T2DM. ClinicalTrials.gov Identifier NCT03010683

Cognitive impairment (CI) is an important comorbidity in patients with heart failure (HF). Its prevalence parallels the severity of heart failure, while it is an independent prognostic marker of adverse events. Various factors contribute to cognitive decline in HF, influencing self-care. There are no standardized screening methods for the diagnosis and management of these patients. The aim of the present manuscript is to provide an overview of the impact of cognitive impairment in HF, describe the utility of assessment tools and imaging methods for the evaluation of CI, and propose a comprehensive diagnostic and management approach.

We compared the effects of Heat-not-Burn cigarette (HNBC) to those of tobacco cigarette (Tcig), on myocardial, coronary and arterial function as well as on oxidative stress and platelet activation in 75 smokers. In the acute study, 50 smokers were randomised into smoking a single Tcig or a HNBC and after 60 min were crossed-over to the alternate smoking. For chronic phase, 50 smokers were switched to HNBC and were compared with an external group of 25 Tcig smokers before and after 1 month. Exhaled carbon monoxide (CO), pulse wave velocity (PWV), malondialdehyde (MDA) and thromboxane B2 (TxB2) were assessed in the acute and chronic study. Global longitudinal strain (GLS), myocardial work index (GWI), wasted myocardial work (GWW), coronary flow reserve (CFR), total arterial compliance (TAC) and flow-mediated dilation (FMD) were assessed in the chronic study. Acute HNBC smoking caused a smaller increase of PWV than Tcig (change 1.1 vs 0.54 m/s, p < 0.05) without change in CO and biomarkers in contrast to Tcig. Compared to Tcig, switching to HNBC for 1-month improved CO, FMD, CFR, TAC, GLS, GWW, MDA, TxB2 (differences 10.42 ppm, 4.3%, 0.98, 1.8 mL/mmHg, 2.35%, 19.72 mmHg%, 0.38 nmol/L and 45 pg/mL respectively, p < 0.05). HNBCs exert a less detrimental effect on vascular and cardiac function than tobacco cigarettes. Trial registration Registered on https://clinicaltrials.gov/ (NCT03452124, 02/03/2018).

Sepsis and septic shock are life-threatening emergencies associated with increased morbidity and mortality. Hence, early diagnosis and management of both conditions is of paramount importance. Point-of-care ultrasound (POCUS) is a cost-effective and safe imaging modality performed at the bedside, which has rapidly emerged as an excellent multimodal tool and has been gradually incorporated as an adjunct to physical examination in order to facilitate evaluation, diagnosis and management. In sepsis, POCUS can assist in the evaluation of undifferentiated sepsis, while, in cases of shock, it can contribute to the differential diagnosis of other types of shock, thus facilitating the decision-making process. Other potential benefits of POCUS include prompt identification and control of the source of infection, as well as close haemodynamic and treatment monitoring. The aim of this review is to determine and highlight the role of POCUS in the evaluation, diagnosis, treatment and monitoring of the septic patient. Future research should focus on developing and implementing a well-defined algorithmic approach for the POCUS-guided management of sepsis in the emergency department setting given its unequivocal utility as a multimodal tool for the overall evaluation and management of the septic patient.

Aims The purpose of this study is to identify echocardiography predictors of clinical response and reverse left ventricular (LV) remodelling in patients with functional mitral regurgitation (FMR) treated with MitraClip. Method and results We retrospectively analysed 86 high surgical risk patients with severe FMR; of those, 58 were implanted a MitraClip, and 28 received medical treatment and served as controls. At baseline and at 1‐year follow‐up, we performed clinical and echocardiography evaluation to assess global longitudinal strain (GLS) and myocardial work [global work index (GWI), global constructive work (GCW), global wasted work (GWW), global work efficiency (GWE)]. Mitral regurgitation was significantly reduced after MitraClip implantation (3.7 ± 0.4 vs. 1.7 ± 0.8, P < 0.001), and the procedure was associated with improvement in brain natriuretic peptide levels (980 ± 1027 vs. 420 ± 338 pg/mL, P < 0.001), New York Heart Association class status (3.2 ± 0.55 vs. 2.0 ± 0.6, P < 0.001), 6‐min walking test (233 ± 154 vs. 286 ± 114 m, P = 0.01) at follow‐up and reduction of left ventricle end‐systolic (LVESV) and left ventricle end‐diastolic volumes (LVEDV) (152 ± 68 vs. 136 ± 43 mL, P = 0.004 & 219 ± 74 vs. 193 ± 66 mL, P = 0.001, respectively). MitraClip procedure was associated with improvement of LV performance and significant increase of GWI (607 ± 282 vs. 650 ± 260 mmHg%, P = 0.045) and GCW (854 ± 288 vs. 949 ± 325 mmHg%, P < 0.001). Baseline ejection fraction (EF), GLS, GWI, GCW, and effective regurgitant orifice area were the variables that were associated with reduction of LVEDV 1 year after intervention (P < 0.05 for all) and baseline GCW of the LV was the only variable associated with reduction of LVESV (P = 0.002). Receiver operating characteristic curve analysis identified that a GLS cut‐off value of −8.65% (AUC 0.815, P = 0.007) was associated with a 20% reduction of the LVEDV with a sensitivity and specificity of 72% and 70%, respectively, and that a GCW cut‐off value of 846 mmHg% (AUC 0.759, P = 0.007) was associated with a 10% reduction of LVESV with sensitivity and specificity 79% and 74%, respectively. Conclusions Mitral valve repair with MitraClip has positive clinical and echocardiographic impact in patients with FMR 1 year after implantation. Preserved GLS and GCW values appear to be associated with LV reverse remodelling post intervention.

Cardiogenic shock (CS) is increasingly recognized in patients with malignancies, while cancer is independently associated with worse prognosis in CS. A number of conditions may lead to CS in cancer, including acute coronary syndromes, cardiomyopathy, takotsubo syndrome, myocarditis, pulmonary embolism, tamponade, and cardiac herniation. In these conditions, CS may be related to cancer itself or to cancer therapy, including surgery, chemotherapy, or radiotherapy. Given the significantly improved overall survival of patients with malignancies, the early recognition and proper management of CS in cancer become increasingly important. In the present paper, we review the available evidence on CS in patients with malignancies and highlight issues related to its management.

Atrial fibrillation (AF) and acute heart failure (AHF) are two closely interrelated conditions that frequently coexist in a manifold manner, with AF serving either as the causative factor or as the consequence or even as an innocent bystander. The interplay between these two clinical conditions is complex, given that they share common pathophysiological pathways and they can reciprocally exacerbate each other, thus triggering a vicious cycle that worsens the prognosis and increases the thromboembolic risk. The optimal management of AF in the context of AHF in the emergency department remains a challenge depending on the time onset, as well as the nature and the severity of the associated symptoms. Acute rate control, along with early rhythm control, when indicated, and anticoagulation represent the main pillars of the therapeutic intervention. The purpose of this review is to elucidate the pathophysiological link between AF and AHF and accordingly present a stepwise algorithmic approach for the management of AF in AHF patients in the emergency setting.

Heart failure (HF) and atrial fibrillation (AF) often coexist, being closely interrelated as the one increases the prevalence and incidence and worsens the prognosis of the other. Their frequent coexistence raises several challenges, including under-diagnosis of HF with preserved ejection fraction in AF and of AF in HF, characterization and diagnosis of atrial cardiomyopathy, target and impact of rate control therapy on outcomes, optimal rhythm control strategy in the era of catheter ablation, HF-related thromboembolic risk and management of anticoagulation in patients with comorbidities, such as chronic kidney disease or transient renal function worsening, coronary artery disease or acute coronary syndromes, valvular or structural heart disease interventions and cancer. In the present document, derived by an expert panel meeting, we sought to focus on the above challenging issues, outlining the existing evidence and identifying gaps in knowledge that need to be addressed.