scholarly journals Pulmonary vascular mechanical consequences of ischemic heart failure and implications for right ventricular function

2019 ◽  
Vol 316 (5) ◽  
pp. H1167-H1177 ◽  
Author(s):  
Jennifer L. Philip ◽  
Thomas M. Murphy ◽  
David A. Schreier ◽  
Sydney Stevens ◽  
Diana M. Tabima ◽  
...  
Keyword(s):  
Heart Failure ◽  
Pulmonary Hypertension ◽  
Pulmonary Fibrosis ◽  
Ejection Fraction ◽  
Right Ventricle ◽  
Pulmonary Vasculature ◽  
Left Heart ◽  
Left Heart Failure ◽  
Reduced Ejection Fraction ◽  
Pathologic Features

Left heart failure (LHF) is the most common cause of pulmonary hypertension, which confers an increase in morbidity and mortality in this context. Pulmonary vascular resistance has prognostic value in LHF, but otherwise the mechanical consequences of LHF for the pulmonary vasculature and right ventricle (RV) remain unknown. We sought to investigate mechanical mechanisms of pulmonary vascular and RV dysfunction in a rodent model of LHF to address the knowledge gaps in understanding disease pathophysiology. LHF was created using a left anterior descending artery ligation to cause myocardial infarction (MI) in mice. Sham animals underwent thoracotomy alone. Echocardiography demonstrated increased left ventricle (LV) volumes and decreased ejection fraction at 4 wk post-MI that did not normalize by 12 wk post-MI. Elevation of LV diastolic pressure and RV systolic pressure at 12 wk post-MI demonstrated pulmonary hypertension (PH) due to LHF. There was increased pulmonary arterial elastance and pulmonary vascular resistance associated with perivascular fibrosis without other remodeling. There was also RV contractile dysfunction with a 35% decrease in RV end-systolic elastance and 66% decrease in ventricular-vascular coupling. In this model of PH due to LHF with reduced ejection fraction, pulmonary fibrosis contributes to increased RV afterload, and loss of RV contractility contributes to RV dysfunction. These are key pathologic features of human PH secondary to LHF. In the future, novel therapeutic strategies aimed at preventing pulmonary vascular mechanical changes and RV dysfunction in the context of LHF can be tested using this model. NEW & NOTEWORTHY In this study, we investigate the mechanical consequences of left heart failure with reduced ejection fraction for the pulmonary vasculature and right ventricle. Using comprehensive functional analyses of the cardiopulmonary system in vivo and ex vivo, we demonstrate that pulmonary fibrosis contributes to increased RV afterload and loss of RV contractility contributes to RV dysfunction. Thus this model recapitulates key pathologic features of human pulmonary hypertension-left heart failure and offers a robust platform for future investigations.

scholarly journals Sildenafil improves clinical and functional status of an elderly postmenopausal female with ‘out of proportion’ PH associated with left heart disease

2013 ◽  
Vol 80 (4) ◽  
Author(s):  
Michele Correale ◽  
Antonio Totaro ◽  
Armando Ferraretti ◽  
Matteo Di Biase ◽  
Natale Daniele Brunetti
Keyword(s):  
Heart Failure ◽  
Pulmonary Hypertension ◽  
Heart Disease ◽  
Ejection Fraction ◽  
Elderly Woman ◽  
Preserved Ejection Fraction ◽  
Left Heart ◽  
Left Heart Failure ◽  
Clinical And Functional Status ◽  
Postmenopausal Female

We report a case of an elderly woman with heart failure with preserved ejection fraction and pulmonary hypertension (HFpEF-PH), refractory to conventional therapy for left heart failure and successfully treated by sildenafil.

scholarly journals GAGAL JANTUNG KIRI DAN HIPERTENSI PULMONAL

2017 ◽  
Vol 1 (1) ◽  
pp. 9-21
Author(s):  
Djanggan Sargowo
Keyword(s):  
Heart Failure ◽  
Pulmonary Hypertension ◽  
Ejection Fraction ◽  
Right Ventricular Dysfunction ◽  
Left Heart ◽  
Left Heart Failure ◽  
Non Invasive ◽  
Hemodynamic Variables ◽  
History Of ◽  
The Right

In patients with left heart failure, pulmonary hypertension and right ventricular dysfunction is a common condition and has important implications in the development of disease, disability and death, so it required special attention. Pulmonary hypertension is the most common form with approximately 65-80% of cases. Although today is already highly developed understanding of the pathophysiology and clinical assessment, as well as setting the hemodynamic definition and classification of pulmonary hypertension in left heart failure, but the interrelation hemodynamics in pulmonary hypertension combination of pre- and post-capillary is still very complex, and there is no evidence-based recommendations the handling of pulmonary hypertension is left heart failure. Here, we will discuss the prevalence and significance of pulmonary hypertension and cardiac dysfunction Right in patients with both heart failure with ejection fraction decreased, as well as heart failure with ejection fraction, as well as provides an overview of the pathophysiology of the complex due to the interaction of cardiopulmonary left heart failure, which can supports the evolution of the phenotype of the left ventricle into the right ventricle phenotype through the travel history of heart failure. Next, we will discuss fenoitp pulmonary hypertension by combining the clinical context, the assessment of non-invasive and invasive hemodynamic variables in a structured diagnostic assessment.

scholarly journals Chamber-enriched gene expression profiles in failing human hearts with reduced ejection fraction

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Xin Luo ◽  
Jun Yin ◽  
Denise Dwyer ◽  
Tracy Yamawaki ◽  
Hong Zhou ◽  
...  
Keyword(s):  
Heart Failure ◽  
Ejection Fraction ◽  
Human Genetics ◽  
Expression Profiles ◽  
Gene Expression Profiles ◽  
Left Heart ◽  
Reduced Ejection Fraction ◽  
Cell Type Composition ◽  
Type Composition ◽  
Underlying Mechanisms

AbstractHeart failure with reduced ejection fraction (HFrEF) constitutes 50% of HF hospitalizations and is characterized by high rates of mortality. To explore the underlying mechanisms of HFrEF etiology and progression, we studied the molecular and cellular differences in four chambers of non-failing (NF, n = 10) and HFrEF (n = 12) human hearts. We identified 333 genes enriched within NF heart subregions and often associated with cardiovascular disease GWAS variants. Expression analysis of HFrEF tissues revealed extensive disease-associated transcriptional and signaling alterations in left atrium (LA) and left ventricle (LV). Common left heart HFrEF pathologies included mitochondrial dysfunction, cardiac hypertrophy and fibrosis. Oxidative stress and cardiac necrosis pathways were prominent within LV, whereas TGF-beta signaling was evident within LA. Cell type composition was estimated by deconvolution and revealed that HFrEF samples had smaller percentage of cardiomyocytes within the left heart, higher representation of fibroblasts within LA and perivascular cells within the left heart relative to NF samples. We identified essential modules associated with HFrEF pathology and linked transcriptome discoveries with human genetics findings. This study contributes to a growing body of knowledge describing chamber-specific transcriptomics and revealed genes and pathways that are associated with heart failure pathophysiology, which may aid in therapeutic target discovery.

scholarly journals Heart rate variability in severe right or left heart failure: the role of pulmonary hypertension and resistances

2004 ◽  
Vol 6 (2) ◽  
pp. 181-185 ◽  
Author(s):  
Laurent Fauchier ◽  
Dominique Babuty ◽  
Alexandre Melin ◽  
Pierre Bonnet ◽  
Pierre Cosnay ◽  
...  
Keyword(s):  
Heart Failure ◽  
Heart Rate ◽  
Pulmonary Hypertension ◽  
Heart Rate Variability ◽  
Left Heart ◽  
Left Heart Failure

1409Use of phenomapping to determine response of treatment by sacubitril/valsartan in patients with heart failure with reduced ejection fraction

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
M Godet ◽  
O Raitiere ◽  
H Chopra ◽  
P Guignant ◽  
C Fauvel ◽  
...  
Keyword(s):  
Heart Failure ◽  
Pulmonary Hypertension ◽  
Ejection Fraction ◽  
Left Ventricular ◽  
Heat Map ◽  
Reduced Ejection Fraction ◽  
Patients With Heart Failure ◽  
Group 3 ◽  
Group 2 ◽  
Group 1

Abstract Background Treatment by sacubitril/valsartan decreases mortality, improves KCCQ score and ejection fraction in patients with heart failure with reduced ejection fraction (HF REF), but there is currently no data to predict response to treatment. Purpose The purpose of our work was to assess whether unbiased clustering analysis, using dense phenotypic data, could identify phenotypically distinct HF-REF subtypes with good or no response after 6 months of sacubitril/valsartan administration. Methods A total of 78 patients in NYHA functional class 2–3 and treated by ACE inhibitor or AAR2, were prospectively assigned to equimolar sacubitril/valsartan replacement. We collected demographic, clinical, biological and imaging continuous variables. Phenotypic domains were imputed with 5 eigenvectors for missing value, then filtered if the Pearson correlation coefficient was >0.6 and standardized to mean±SD of 0±1. Thereafter, we used agglomerative hierarchical clustering for grouping phenotypic variables and patients, then generate a heat map (figure 1). Subsequently, participants were categorized using Penalized Model-Based Clustering. P<0,05 was considered significant. Results Mean age was 60.4±13.4 yo and 79.0% patients were males. Mean ejection fraction was 29.3±7.0%. Overall, 16 phenotypic domains were isolated (figure 1) and 3 phenogroups were identified (Table 1). Phenogroup 1 was remarkable by isolated left ventricular involvement (LVTDD 64.3±5.9mm vs 73.9±8.7 in group 2 and 63.8±5.7 in group3, p<0.001) with moderate diastolic dysfunction (DD), no mitral regurgitation (MR) and no pulmonary hypertension (PH). Phenogroups 2 and 3 corresponded to patients with severe PH (TRMV: 2.93±0.47m/s in group 2 and 3.15±0.61m/s in groupe 3 vs 2.16±0.32m/s in group 1), related to severe DD (phenogroup 2) or MR (phenogroup 3). In both phenogroups, the left atrium was significantly enlarged and the right ventricle was remodeled, compared with phenogroup 1. Despite more severe remodeling and more compromised hemodynamic in phenogroups 2 and 3, the echocardiographic response to sacubitril/valsartan was comparable in all groups with similar improvement of EF and reduction of cardiac chambers dimensions (response of treatment, defined by improvement of FE +15% and/or decreased of indexed left ventricule diastolic volume −15% = group 2: 22 (76%); group 3: 18 (60%); group 1: 9 (50%); p=0.17; OR group 2 vs 1: OR=3.14; IC95% [0.9–11.03]; p=0.074; OR group 3 vs 1: OR=1.5; IC95% [0.46–4.87]; p=0.5)). The clinical response was even better in phenogroups 2 and 3 (Group 2: 19 (66%); group 3: 21 (78%) vs group 1: 9 (50%); p=0.05). Heat map Conclusion HF-REF patients with severe diastolic dysfunction, significant mitral regurgitation and elevated pulmonary hypertension by echocardiographic had similar reverse remodeling but better clinical improvement than patients with isolated left ventricular systolic dysfunction.

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