The Vulnerable Phase of Heart Failure.
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ABSTRACT:
SUBMITTER: Gracia E
PROVIDER: S-EPMC6047520 | biostudies-literature | 2018 Jul/Aug
REPOSITORIES: biostudies-literature
Publications
The Vulnerable Phase of Heart Failure.
Gracia Ely E Singh Prabhjot P Collins Sean S Chioncel Ovidiu O Pang Peter P Butler Javed J
American journal of therapeutics 20180701 4
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Project description:Heart failure (HF) is a life-threating cardiac disease that develops progressively for the reduced ability of the left ventricle (LV) to pump blood into the circulation during systole. HF can also develop in patients with a preserved systolic function, typically in presence of hypertrophic cardiomyopathy (HCM). This type of HF is sometimes termed as diastolic HF, but its biomechanical origin is still unclear. This study employs a physics-based analysis of both the LV and left atrium (LA) in selected HCM patients and matched healthy subjects using 3D echocardiography and demonstrates that alteration on the LV side (stiffening) reduces the elastic recovery of the LA. Moreover, the analysis of the forces exchanged between the two chambers demonstrates that they result unbalanced, keeping the LA in a sustained stretched condition that leads to dilation. This scenario clarifies the diastolic root of the dysfunction that may likely be the cause of the spiraling of events progressing toward failure of both LA emptying and LV filling. This deeply interdisciplinary study provides a physics-based basis for both physics/engineering modeling of heart function and to cardiologists for the design of clinical studies.
| S-EPMC11445582 | biostudies-literature
Project description:Acute heart failure (AHF), a global pandemic with high morbidity and mortality, exerts a considerable economic burden. AHF includes a broad spectrum of clinical presentations ranging from new-onset heart failure to cardiogenic shock. Key elements of the management rely on the clinical diagnosis confirmed on, both, increased natriuretic peptides and echocardiography, and on the prompt initiation of oxygen therapy, including non-invasive positive pressure ventilation, vasodilators, and diuretics. A care pathway is essential, specifically when an acute coronary syndrome is suspected or in the case of cardiogenic shock. Association or increasing doses of vasopressors despite an adequate volume status are markers of progression toward a refractory cardiogenic shock state. For the latter, mechanical circulatory support should be initiated early, optimally before the onset of renal or liver failure. Thus, a tertiary care center is recommended for the management of patients with AHF who require percutaneous coronary intervention or mechanical circulatory support. This narrative review provides multidisciplinary guidance for the management of AHF and cardiogenic shock from pre-hospital to intensive care unit/cardiac care unit, based on contemporary evidence and expert opinion.
| S-EPMC9536658 | biostudies-literature
Project description:Hospitalization for acute heart failure (HF) is associated with a substantial morbidity burden and with associated healthcare costs and an increased mortality risk. However, few if any major medical innovations have been witnessed in this area in recent times. Levosimendan is a first-in-class calcium sensitizer and potassium channel opener indicated for the management of acute HF. Experience in several clinical studies has indicated that administration of intravenous levosimendan in intermittent cycles may reduce hospitalization and mortality rates in patients with advanced HF; however, none of those trials were designed or powered to give conclusive insights into that possibility. This paper describes the rationale and protocol of LeoDOR (levosimendan infusions for patients with advanced chronic heart failure), a randomized, double-blind, placebo-controlled, international, multicentre trial that will explore the efficacy and safety of intermittent levosimendan therapy, in addition to optimized standard therapy, in patients following hospitalization for acute HF. Salient features of LeoDOR include the use of two treatment regimens, in order to evaluate the effects of different schedules and doses of levosimendan during a 12 week treatment phase, and the use of a global rank primary endpoint, in which all patients are ranked across three hierarchical groups ranging from time to death or urgent heart transplantation or implantation of a ventricular assist device to time to rehospitalization and, lastly, time-averaged proportional change in N-terminal pro-brain natriuretic peptide. Secondary endpoints include changes in HF symptoms and functional status at 14 weeks.
| S-EPMC6351894 | biostudies-literature
Project description:Acute heart failure (HF) is associated with poor prognosis. After the acute event, there is a vulnerable period during which the patient has a marked risk of readmission or death. Therefore, early optimization of treatment is mandatory during the vulnerable period. The objective of this article is to provide recommendations to address the management of patients with HF during the vulnerable period from a practical point of view. A group of Mexican experts met to prepare a consensus document. The vulnerable period, with a duration of up to 6 months after the acute event - either hospitalization, visit to the emergency department or the outpatient clinic/day hospital - represents a real window of opportunity to improve outcomes for these patients. To best individualize the recommendations, the management strategies were divided into three periods (early, intermediate and late vulnerable period), including not only therapeutic options but also evaluation and education. Importantly, the recommendations are addressed to the entire cardiology team, including physicians and nurses, but also other specialists implicated in the management of these patients. In conclusion, this document represents an opportunity to improve the management of this population at high risk, with the aim of reducing the burden of HF.
| S-EPMC10803129 | biostudies-literature
Project description:AimsPatients with acute heart failure (AHF) often present with an increased heart rate (HR), and the HR changes dramatically after initial treatment for AHF. However, the HR change after admission and the relationship between HR change in the early phase and prognosis have not been fully elucidated.Methods and resultsFrom a multicentre AHF registry, we retrospectively evaluated 1527 consecutive patients admitted with AHF. HR change (%) was calculated by [HR (at admission) - HR (24 h after admission)] × 100∕HR (at admission). The median HR change was 15.1% (range, 2.0-28.4%). The HR decreased most in the first 24 h and then gradually thereafter [admission: 98 (81-117) b.p.m., 24 h: 80 (70-92) b.p.m., 48 h: 78 (68-90) b.p.m., and 72 h: 77 (67-88) b.p.m.]. In Kaplan-Meier analysis, the cumulative event-free rates in the composite endpoint of death and rehospitalization due to AHF showed better according to larger HR change (P = 0.012, log rank). Cox proportional hazards analysis showed that HR change was a prognostic factor for composite endpoint adjusted by age and sex [hazard ratio, 0.995; 95% confidence interval (CI), 0.991-0.998; P = 0.006]. HR change was associated with outcome adjusted by age and sex in patients with sinus rhythm (hazard ratio, 0.993; 95% CI, 0.988-0.999; P = 0.015), but not in patients with atrial fibrillation (hazard ratio, 0.996; 95% CI, 0.990-1.002; P = 0.15).ConclusionsA decrease in HR in the first 24 h after admission indicates better prognosis in patients with AHF, although the prognostic influence may differ between patients with sinus rhythm and those with atrial fibrillation.
| S-EPMC8318482 | biostudies-literature
Project description:BackgroundHeart failure (HF), which is the terminal stage of many cardiovascular diseases, is associated with low survival rates and a severe financial burden. The mechanisms, especially the molecular mechanism combined with new theories, underlying the pathogenesis of HF remain elusive. We demonstrate that phosphorylation-regulated dynamic liquid-liquid phase separation of HIP-55 (hematopoietic progenitor kinase 1-interacting protein of 55 kDa) protects against HF.MethodsFluorescence recovery after photobleaching assay, differential interference contrast analysis, pull-down assay, immunofluorescence, and immunohistochemical analysis were used to investigate the liquid-liquid phase separation capacity of HIP-55 and its dynamic regulation in vivo and in vitro. Mice with genetic deletion of HIP-55 and mice with cardiac-specific overexpression of HIP-55 were used to examine the role of HIP-55 on β-adrenergic receptor hyperactivation-induced HF. Mutation analysis and mice with specific phospho-resistant site mutagenesis were used to identify the role of phosphorylation-regulated dynamic liquid-liquid phase separation of HIP-55 in HF.ResultsGenetic deletion of HIP-55 aggravated HF, whereas cardiac-specific overexpression of HIP-55 significantly alleviated HF in vivo. HIP-55 possesses a strong capacity for phase separation. Phase separation of HIP-55 is dynamically regulated by AKT-mediated phosphorylation at S269 and T291 sites, failure of which leads to impairment of HIP-55 dynamic phase separation by formation of abnormal aggregation. Prolonged sympathetic hyperactivation stress induced decreased phosphorylation of HIP-55 S269 and T291, dysregulated phase separation, and subsequent aggregate formation of HIP55. Moreover, we demonstrated the important role of dynamic phase separation of HIP-55 in inhibiting hyperactivation of the β-adrenergic receptor-mediated P38/MAPK (mitogen-activated protein kinase) signaling pathway. A phosphorylation-deficient HIP-55 mutation, which undergoes massive phase separation and forms insoluble aggregates, loses the protective activity against HF.ConclusionsOur work reveals that the phosphorylation-regulated dynamic phase separation of HIP-55 protects against sympathetic/adrenergic system-mediated heart failure.
| S-EPMC11404759 | biostudies-literature
Project description:BackgroundSevere heart failure (HF) has a higher mortality during vulnerable period while targeted predictive tools, especially based on drug exposures, to accurately assess its prognoses remain largely unexplored. Therefore, this study aimed to utilize drug information as the main predictor to develop and validate survival models for severe HF patients during this period.MethodsWe extracted severe HF patients from the MIMIC-IV database (as training and internal validation cohorts) as well as from the MIMIC-III database and local hospital (as external validation cohorts). Three algorithms, including Cox proportional hazards model (CoxPH), random survival forest (RSF), and deep learning survival prediction (DeepSurv), were applied to incorporate the parameters (partial hospitalization information and exposure durations of drugs) for constructing survival prediction models. The model performance was assessed mainly using area under the receiver operator characteristic curve (AUC), brier score (BS), and decision curve analysis (DCA). The model interpretability was determined by the permutation importance and Shapley additive explanations values.ResultsA total of 11,590 patients were included in this study. Among the 3 models, the CoxPH model ultimately included 10 variables, while RSF and DeepSurv models incorporated 24 variables, respectively. All of the 3 models achieved respectable performance metrics while the DeepSurv model exhibited the highest AUC values and relatively lower BS among these models. The DCA also verified that the DeepSurv model had the best clinical practicality.ConclusionsThe survival prediction tools established in this study can be applied to severe HF patients during vulnerable period by mainly inputting drug treatment duration, thus contributing to optimal clinical decisions prospectively.
| S-EPMC11302109 | biostudies-literature
Project description:Rats overexpressing the human renin and angiotensinogen genes die after seven weeks of end organ damage. They develop hypertension, heart hypertrophy and proteinuria.We compared terminal heart failure, these are indeed terminally ill to double transgenic animals suffering on hypertension, proteinuria and heart hypertrophy. In addition, Losartan-treated animals (10 mg/kg/d)showed similar physiological parameters (normotension, no proteinuria and no heart hypertrophy compared to control sprague dawley rats. Keywords: other
2005-01-03 | GSE1557 | GEO
Project description: Not available
| S-EPMC6688717 | biostudies-literature
Project description:BackgroundThe phase angle (PhA) in bioelectrical impedance analysis (BIA) reflects the cell membrane integrity or body fluid equilibrium. We examined how the PhA aligns with previously known markers of acute heart failure (HF) and assessed its value as a screening tool.MethodsPhA was measured in 50 patients with HF and 20 non-HF controls along with the edema index (EI), another BIA parameter suggestive of edema. Chest computed tomography-measured lung fluid content (LFC) was used to assess pulmonary congestion. A correlation analysis was conducted to evaluate the relationships between PhA and EI, NT-proBNP, and LFC. Receiver operating characteristic (ROC) curve analysis was used to determine the cut-off values for PhA and EI for classifying patients with HF. The area under the curve (AUC) was compared using the DeLong test to evaluate the performance of PhA and EI compared to that of LFC in correctly classifying HF.ResultsThe PhA levels were significantly lower in the HF group. Whole-body PhA was 4.49° in the HF group and 5.68° in the control group. Moderate and significant correlation was observed between PhA measured at 50-kHz and both NT-proBNP (-0.56 to -0.27, all p-values<0.05) and LFC (-0.52 to -0.41, all p-values <0.05). The AUC for whole-body PhA was 0.827 (confidence interval [CI] 0.724-0.931, p<0.01) and was 0.883 (CI 0.806-0.961, p<0.01) for EI, and the optimal cutoffs were estimated as 5° (sensitivity 0.84, specificity 0.80) and 0.394 (sensitivity 0.78, specificity 0.95), respectively. When both PhA and EI were included in the model, the AUC increased to 0.905, and this was comparable to that of LFC (AUC = 0.913, p = 0.857).ConclusionsPhA exhibited a correlation with known markers of HF and demonstrated its potential as a non-invasive screening tool for the early detection of HF exacerbation. The combined use of PhA and EI can provide a robust alternative for routine self-monitoring in patients with HF, thereby enhancing early intervention.
| S-EPMC11759352 | biostudies-literature