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Multiple linear regression analysis showed a significantly greater increase in LVEF and decrease in LV volume index over time in the low-ePVS group. [...]the higher rates of all-cause mortality, cardiovascular mortality and HFH observed in these patients could be attributable to known and unknown clinical factors beyond residual congestion, even after meticulously executed statistical adjustments. Given the dynamic nature of congestion, it is challenging to ascertain that the adverse impact of high ePVS on long-term outcomes is simply from intravascular congestion, especially without repeated ePVS measurements. [...]using only haemoglobin and haematocrit levels in the ePVS calculation might oversimplify congestion assessment. [...]although ePVS can be easily obtained and followed longitudinally,3 the effective strategy for managing patients with high ePVS is unknown.

To determine the prevalence, right ventricular (RV) characteristics, and outcomes of primary isolated RV failure (PI-RVF) after heart transplant (HTX). PI-RVF was defined as (1) the need for mechanical circulatory support post-transplant, or (2) evidence of RVF post-transplant as measured by right atrial pressure (RAP) > 15 mmHg, cardiac index of < 2.0 L/min/m 2 or inotrope support for < 72 h, pulmonary capillary wedge pressure < 18 mmHg, and transpulmonary gradient < 15 mmHg with pulmonary systolic pressure < 50 mmHg. PI-RVF can be diagnosed from the first 24–72 h after completion of heart transplantation. A total of 122 consecutive patients who underwent HTX were reviewed. Of these, 11 were excluded because of secondary causes of graft dysfunction (GD). PI-RVF was present in 65 of 111 patients (59%) and 31 (48%) met the criteria for PGD-RV. Severity of patients with PI-RVF included 41(37%) mild, 14 (13%) moderate, and 10 (9%) severe. The median onset of PI-RVF was 14 (0–49) h and RV recovery occurred 5 (3–14) days after HTX. Severe RV failure was a predictor of 30-day mortality (HR 13.2, 95% CI 1.6–124.5%, p  < 0.001) and post-transplant dialysis (HR 6.9, 95% CI 2.0–257.4%, p  = 0.001). Patients with moderate PI-RVF had a higher rate of 30-day mortality (14% vs. 0%, p  = 0.014) and post-operative dialysis (21% vs. 2%, p  = 0.016) than those with mild PI-RVF. Among patients with mild and moderate PI-RVF, patients who did not meet the criteria of PGD-RV had worsening BUN/creatinine than those who met the PGD-RV criteria ( p  < 0.05 for all). PI-RVF was common and can occur after 24 h post-HTX. The median RV recovery time was 5 (2–14) days after HTX. Severe PI-RVF was associated with increased rates of 30-day mortality and post-operative dialysis. Moderate PI-RVF was also associated with post-operative dialysis. A revised definition of PGD-RV may be needed since patients who had adverse outcomes did not meet the criteria of PGD-RV.

Heart failure (HF) is a significant global concern, impacting patient morbidity, mortality, and healthcare costs. Guideline-directed medical therapy and various preventive measures have proven effective in improving clinical outcomes and reducing HF hospitalizations. Recent data indicates that remote HF monitoring facilitates early detection of HF decompensation by observing upstream events and parameters before clinical signs and symptoms manifest. Moreover, these innovative devices have been shown to decrease unnecessary HF hospitalizations and, in some cases, provide predictive insights before an actual HF incident. In this review, we aim to explore the data regarding smart scales and digital biomarkers and summarize both FDA-approved devices and emerging technologies by assessing their clinical utility, mechanism of HF decompensation detection, and ongoing trials. Furthermore, we also discuss the future trend of integrating these devices into routine clinical practice to improve patient clinical outcomes.

Abstract Aims Data support favourable haemodynamic benefits of glucagon-like peptide-1 receptor agonists (GLP-1 RAs) on improving cardiac structural abnormalities and function in patients with heart failure (HF). However, the direct haemodynamic effects of GLP-1 RAs remain inadequately characterized. We aim to investigate temporal trends of pulmonary artery pressure (PAP) in HF patients receiving GLP-1 RAs. Methods and results In this single-centre retrospective cohort study, we identified HF patients with a CardioMEMS device who received semaglutide or tirzepatide for at least 6 months during the monitoring period. Patients who were already on GLP-1 RAs prior to device implantation were excluded. The relationship between weight change and PAPs was assessed using Pearson correlation. A total of nine patients were included (54 years, BMI 41.4 kg/m2, 67% men, 44% with EF < 40%, 89% diabetes, 89% semaglutide). Median dose of semaglutide (or equivalent) at 6 months was 0.9 (range 0.25–1) mg/week. Body weight significantly decreased from 123.6 to 117.2 kg (P = 0.047), while guideline-directed medical therapy (GDMT) and loop diuretic uses and dosages remained unchanged. Significant reductions were observed in systolic PAP (38.9 to 34.0 mmHg, P = 0.045), diastolic PAP (20.0 to 17.8 mmHg, P = 0.019) and mean PAP (27.3 to 24.3 mmHg, P = 0.018). There was a significant correlation between weight loss and reductions in systolic PAP (r = 0.69, P = 0.04) and mean PAP (r = 0.72, P = 0.029). Conclusions GLP1-RA use in HF patients was significantly associated with reductions in body weight and PAPs at 6 months, despite no changes in GDMT and loop diuretic doses.

Abstract Despite the increasing prevalence and substantial burden of heart failure with preserved ejection fraction (HFpEF), which constitutes up to 50% of all heart failure cases, significant challenges persist in its diagnostic and therapeutic strategies. These difficulties arise primarily from the heterogeneous nature of the condition, the presence of various comorbidities and a wide range of phenotypic variations. Considering these challenges, current international guidelines endorse the utilization of invasive haemodynamic assessments, including resting and exercise haemodynamics, as the gold standard for enhancing diagnostic accuracy in cases where traditional diagnostic methods yield inconclusive results. These assessments are crucial not only for confirming the diagnosis but also for delineating the complex underlying pathophysiology, enabling the development of personalized treatment strategies, and facilitating the precise classification of HFpEF phenotypes. In this review, we summarize the haemodynamic changes observed in patients with HFpEF, comparing resting and exercise-induced parameters to those of normal subjects. Additionally, we discuss the current role of invasive haemodynamics in HFpEF assessment and highlight its utility beyond diagnosis, such as identifying HFpEF comorbidities, guiding phenotype-based personalized therapies and characterizing prognostication. Finally, we address the challenges associated with utilizing invasive haemodynamics and propose future directions, focusing on integrating these assessments into routine HFpEF care.

The aims of this study were to examine the prevalence of moderate to large (moderate–large) idiopathic pericardial effusion (i-PEF) in patients with hypertrophic cardiomyopathy (HCM) and to identify clinical and echocardiographic hemodynamic profiles associated with pericardial effusion. A total of 292 adult patients with HCM were studied. Fifteen patients with a history of factors associated with pericardial effusion including myocardial infarction, heart surgery or cardiac procedure within the last 12 months, autoimmune disease, hydralazine use, chronic kidney disease stage 3–4, tuberculosis, and malignancy were excluded. Of 277 eligible patients with HCM, 11 patients (4%) with moderate-large i-PEF were identified. Clinical tamponade was present in 1 patient. Compared to patients with HCM who had no or small pericardial effusion, patients with moderate-large i-PEF were younger and more likely to have right ventricular (RV) hypertrophy and reverse septal curvature. These patients also exhibited a greater maximal septal thickness, mean and systolic pulmonary pressure, and right atrial pressure (p < 0.05 for all). Pericardial fluid analysis and histopathological exams were performed in 7 and 3 patients, respectively. All examinations revealed transudative and nonspecific etiology of pericardial effusion. Idiopathic pericardial effusion and cardiac tamponade in patients with HCM was uncommon. The pathophysiology involved in pericardial effusion remains undetermined. Patients with moderate-large i-PEF frequently exhibited a phenotype of pulmonary hypertension and RV pressure overload.

Background There are limited data about modes of death and major adverse cardiovascular events (MACEs) in patients with hypertrophic cardiomyopathy (HCM) in South East Asian population. The aim of the study was to examine modes of death and clinical outcomes in Thai patients with HCM. Methods Between January 1, 2009 and December 31, 2013, 166 consecutive patients with HCM diagnosed in our institution were evaluated. Five patients were excluded because of non-Thai ethnic groups ( n  = 3) and diagnosis of myocardial infarction at initial presentation documented by coronary angiography ( n  = 2). The final study population consisted of 161 patients with HCM. HCM-related deaths included: (1) sudden cardiac death (SCD) – death due to sudden cardiac arrest or unexpected sudden death; (2) heart failure – death due to refractory heart failure; or (3) stroke - death due to embolic stroke associated with atrial fibrillation. MACEs included: (1) SCD, sudden unexpected aborted cardiac arrest, fatal, or nonfatal ventricular arrhythmia (ventricular fibrillation or sustained ventricular tachycardia); (2) heart failure (fatal or non-fatal), or heart transplantation; or (3) stroke - fatal or non-fatal embolic stroke associated with atrial fibrillation. Results One hundred and sixty-one Thai patients with HCM (age 66 ± 16 years, 58% female) were enrolled. Forty-two patients (26%) died over a median follow-up period of 6.8 years including 25 patients (16%) with HCM-related deaths (2%/year). The HCM-related deaths included: heart failure (52% of HCM-related deaths; n  = 13), SCD (44% of HCM-related deaths; n  = 11), and stroke (4% of HCM-related deaths, n  = 1). The SCDs occurred in 6.8% of patients (1%/year). Eighty-four major MACEs occurred in 65 patients (41, 5%/year). The MACEs included: 40 heart failures in which 2 patients underwent heart transplants; 22 SCDs and nonfatal ventricular arrhythmias; and 22 fatal or nonfatal strokes. Conclusions The most common mode of death in adult patients with HCM in Thailand was heart failure followed by SCD. About one-third of the patients experiencing heart failure died during the 6.8 years of follow-up. SCDs occurred in 7% of patients (1%/year), predominantly in the fourth decade or later.

Aims Quantitative methods have shown clinically significant heterogeneity in blood volume (BV) profiles across heart failure (HF) phenotypes. These profiles extend from hypovolaemia to normal BV and to variable degrees of BV hypervolaemia, frequently with similar clinical presentations. However, a comprehensive survey of BV profiles providing practical clinical guidance for the interpretation and management of quantitative plasma volume (PV) and red blood cell (RBC) mass findings has not been reported. The intent of this study is to advance this concept through a multicentre analysis. Methods and results A retrospective analysis of clinical and BV data was undertaken in stable NYHA class II–III HF patients (N = 546). BV was quantitated using established nuclear medicine indicator‐dilution methodology. Differing combinations of PV and RBC mass were identified contributing to marked heterogeneity in overall BV profiles. A quantitatively normal BV was identified in 32% of the cohort but of these only ~1/3 demonstrated a true normal BV (i.e., normal PV + normal RBC mass). The remaining portion of normal BV profiles reflected balanced combinations of compensatory PV expansion with RBC mass deficit (anaemia) (14% of cohort) and PV contraction with RBC mass excess (erythrocythemia) (6% of cohort). Main contributors to BV hypervolaemia were PV excess with a normal RBC mass (21% of cohort; 23% female) and PV excess with erythrocythemia (24% of cohort; 26% female). Hypovolaemia was predominately defined by RBC mass deficit with a normal PV (6% of cohort; 57% female) or RBC mass deficit with PV contraction (5% of cohort; 48% female). Conclusions Findings support the clinical relevance of identifying and accurately interpreting the varying combinations of PV and RBC mass in patients with chronic HF. This in turn helps guide appropriate individualized patient management strategies. A practical volume‐based guideline is provided in an effort to aid clinician interpretation.

Invasive exercise hemodynamics are used to diagnose heart failure with preserved ejection fraction (HFpEF), based on pulmonary artery wedge pressure (PAWP) or left atrial (LA) pressure elevations. We hypothesized that applying unsupervised cluster analysis to comprehensive hemodynamic characterization might provide data‐driven phenotypes, with pathophysiological and prognostic implications. Eighty consecutive HFpEF patients underwent right heart catheterization at rest, during passive leg raise, and at peak exercise. We performed unsupervised k ‐means clustering analysis, using eight hemodynamic variables that were not strongly correlated (Pearson correlation coefficient < 0.80). Hemodynamics and clinical characteristics, as well as event‐free survival, were assessed. k = 5 clusters were identified. Hemodynamic severity increased from Cluster 1 to Clusters 4–5 ( p < 0.01 for most of the hemodynamic variables), mirrored by different event‐free survival (log‐rank test p < 0.001). Clusters 1 and 2 presented with either steep PAWP rise or LA hypertension and pulmonary hypertension (PH) only during exercise. Cluster 3 presented with LA hypertension and PH already at rest, as well as with tall PAWP V waves during exercise. Cluster 4 presented with post‐ and precapillary PH, tall PAWP V waves, right atrial (RA) hypertension, dynamic tricuspid regurgitation (TR), and low cardiac output (CO) reserve. Cluster 5 presented with TR and RA hypertension, low CO, and a lack of decrease in PVR. Data‐driven unsupervised cluster analysis of advanced invasive hemodynamics allowed for the identification of distinct HFpEF phenotypes across the spectrum of disease severity. We found a progressive involvement of the pulmonary circulation and of the right heart, coupled with a worse prognosis.

Background We sought to examine clinical characteristics and outcomes in patients hospitalized for acute heart failure (HF) and thyrotoxicosis. Methods Patients with thyrotoxic HF were compared with age and gender‐matched patients hospitalized for acute HF (controls). Thyr‐HF was defined by the Framingham criteria for HF and clinical hyperthyroidism. Thyrotoxic cardiomyopathy was defined as left ventricular ejection fraction (LVEF) < 55%. Results Of 11 109 consecutive patients hospitalized for acute HF between 1 January 2002 and 1 January 2017, 92 patients (0.8%) had thyrotoxic HF. Clinical and echocardiographic data were available in 87 patients (age 51 ± 16 years; 74% female), representing the study population. Compared with controls, patients with Thyr‐HF had a smaller body surface area (BSA), a higher LVEF, a lower LV end‐diastolic diameter, a higher tricuspid annular plane systolic excursion (TAPSE), higher blood pressure, higher heart rate, and were more likely to have right‐sided HF at presentation (P < 0.01 for all). The survival rate among patients with thyrotoxic HF was higher than the control group (HR: 4.3; 95% CI: 2.1–9.5). Fifty‐eight percent of patients with thyrotoxic HF had thyrotoxic cardiomyopathy. In multivariate analysis, TAPSE (OR = 46; 95% CI: 1.04–2008.20; P = 0.047) and leukocytosis (OR = 16; 95% CI 1.01–259.39; P = 0.049) correlated with thyrotoxic cardiomyopathy. LV recovery was observed in 69% of these patients. Conclusions Thyrotoxic HF was uncommon among patients hospitalized for acute HF. However, after definitive therapy, these patients had a more favourable prognosis than those hospitalized for acute HF without thyrotoxic HF. Clinical phenotypes of thyrotoxic HF include small BSA, middle‐aged female, HF‐pEF, and right‐sided HF. Thyrotoxic cardiomyopathy affected over half of the patients with thyrotoxic HF with a two‐third recovery rate.