Background and aims There is a gap in knowledge about implementing diagnostic tools and therapy for heart failure with preserved ejection fraction (HFpEF) in clinical practice. This survey aimed to assess real-world practice in HFpEF diagnosis and treatment in the international medical community. Methods An independent academic web-based 29-question survey was designed by a group of heart failure specialists and posted by email and through scientific societies and social networks to a broad community of physicians worldwide. Results 1.460 physicians from 95 countries answered the survey, with a mean age of 42.2±10.4 years, 39.4 % females, and 85.1% were cardiologists. The left ventricular ejection fraction cut-off value selected for HFpEF diagnosis was 50% for 89% of participants. The scores for the probability of diagnosis of HFpEF were used only by 47.2%, and H2FPEF was the most used score (31%). Natriuretic peptides were used by 87.4% of participants for the diagnostic workup, while the diastolic stress test was only used by 26.2%. 54.4% of participants chose SGLT2 inhibitors as their first drug treatment, followed by diuretics (18.6%) and ACE inhibitors (8.4%). Conclusions In an international academic survey on HFpEF management, the criteria for screening and diagnosis of HFpEF patients remain aligned with classic international guidelines with a low use of diagnostic scores. SGLT2i is the leading therapeutic drug class used for this heterogeneous patient population. These results raise the need to improve education and awareness on diagnosing and managing HFpEF patients.

Abstract Background/Introduction Contemporary data that describe underlying causes of acute heart failure (AHF) epidemiology in a nation-wide unselected real-life cohort is lacking. Advances in diagnostics, including imaging and genetics, have facilitated the identification of the underlying cause of heart failure (HF). This is the first Icelandic nation-wide study on HF epidemiology of patients hospitalised for AHF. Purpose Investigate the underlying causes of AHF in Iceland and the patients‘ prognosis according to phenotypes. Methods This study used data from the Icelandic Heart Failure Registry (IHFR) and included all hospital admissions for AHF at Landspitali University Hospital from January 2020 to June 2022 (n = 1723). Differences in survival between HF phenotypes were analysed using a multivariate log-rank test, both after diagnosis and after the first discharge. Results The study found that 39.8% of the cases had heart failure with reduced ejection fraction (HFrEF), 17.4% had HF with mildly reduced ejection fraction (HFmrEF), 40.3% had HF with preserved ejection fraction (HFpEF), 0.9% had HF with improved ejection fraction (HFimpEF), and 1.5% had unknown ejection fraction (EF). The average length of hospital admission varied by phenotype, ranging from 8.1 to 15.9 days. Women accounted for 41.15% of all admissions, with the most common phenotype amongst women being HFpEF (57.8%) and the least common being HFrEF (25.1%). The mean age at admission was 75.8 years. Roughly 79% of the whole cohort had NYHA class III-IV at admission; 33% of HFrEF, 13% of HFmrEF and 32% of HFpEF admissions. The most common underlying cause of AHF was coronary artery disease (CAD, 30.9%) followed by atrial fibrillation (15.0%), hypertension (9.8%), diastolic dysfunction (9.4%) and valvular heart disease (9.2%). Other more rare causes were dilated cardiomyopathy (4.4%), amyloidosis (3.2%), broken heart disease (1.5%), myocarditis (0.4%), postpartum cardiomyopathy (0.2%) and Fabry disease (0.1%). During the study period, 422 mortalities were recorded, with 106 in-hospital deaths. After excluding in-hospital mortalities, no significant difference in survival between phenotypes was observed after the first discharge. However, a significant difference in survival was observed with respect to the date of diagnosis (p = 0.0191). Conclusion This study provides new insights into the underlying causes of AHF and patients' prognosis according to phenotypes in Iceland. Our results demonstrate that the most common underlying cause of AHF was CAD, followed by atrial fibrillation and hypertension and that the cohort was highly symptomatic, with a large proportion of patients having NYHA class III-IV at admission. Our findings also highlight significant differences in the prevalence of HF phenotypes between genders, with women more commonly presenting with HFpEF and less commonly with HFrEF.

BACKGROUND:To minimize blood loss during hepatic surgery, various methods are used to reduce pressure and flow within the hepato-splanchnic circulation. In this study, the effect of low- to moderate doses of vasopressin, a potent splanchnic vasoconstrictor, on changes in portal and hepatic venous pressures and splanchnic and hepato-splanchnic blood flows were assessed in elective liver resection surgery.METHODS:Twelve patients were studied. Cardiac output (CO), stroke volume (SV), mean arterial (MAP), central venous (CVP), portal venous (PVP) and hepatic venous pressures (HVP) were measured, intraoperatively, at baseline and during vasopressin infusion at two infusion rates (2.4 and 4.8 U/h). From arterial and venous blood gases, the portal (splanchnic) and hepato-splanchnic blood flow changes were calculated, using Fick's equation.RESULTS:CO, SV, MAP and CVP increased slightly, but significantly, while systemic vascular resistance and heart rate remained unchanged at the highest infusion rate of vasopressin. PVP was not affected by vasopressin, while HVP increased slightly. Vasopressin infusion at 2.4 and 4.8 U/h reduced portal blood flow (-26% and -37%, respectively) and to a lesser extent hepato-splanchnic blood flow (-9% and -14%, respectively). The arterial-portal vein lactate gradient was not significantly affected by vasopressin. Postoperative serum creatinine was not affected by vasopressin.CONCLUSION:Short-term low to moderate infusion rates of vasopressin induced a splanchnic vasoconstriction without metabolic signs of splanchnic hypoperfusion or subsequent renal impairment. Vasopressin caused a centralization of blood volume and increased cardiac output. Vasopressin does not lower portal or hepatic venous pressures in this clinical setting.

Divergent regional filling characteristics of the lung may explain ventilator-induced lung injury. In this descriptive study, the potential of electrical impedance tomography (EIT) to determine progressive changes in regional filling characteristics during acute lung injury was explored.