Using an integrated systems genomic and functional biology approach, we identified an RVF-specific gene module, for which WIPI1 served as a hub and HSPB6 and MAP4 as drivers, and confirmed the ventricular specificity of Wipi1, Hspb6, and Map4 transcriptional changes in adult murine models of pressure overload induced RV- versus LV- failure.
Preimplant Phosphodiesterase-5 Inhibitor Use Is Associated With Higher Rates of Severe Early Right Heart Failure After Left Ventricular Assist Device Implantation.
This review focusses on the studies in PH and RHF that investigated the gene families that write (histone acetyltransferases, HATs), read (bromodomain-containing proteins, BRDPs) or erase (histone deacetylases, HDACs and Sirtuins, SIRT) acetyl moieties from the ε-amino group of lysine residues of histones and non-histone proteins.
Independent predictors for RHF were preoperative right ventricular ejection fraction <25% [odds ratio (OR) 4.68, 95% confidence interval (CI) 1.41-15.5; P = 0.01], right ventricular stroke work index <400 mmHg ml-1 (OR 3.73, 95% CI 1.01-13.7; P = 0.04), right ventricular outflow tract systolic excursion <7 mm (OR 1.55, 95% CI 0.31-0.84; P = 0.002), right ventricular outflow tract fractional shortening <15% (OR 1.62, 95% CI 0.34-0.78; P = 0.02), right ventricular free wall longitudinal strain ≤19% (OR 3.13, 95% CI 1.01-2.43; P = 0.003), right ventricular fractional area change <27% (OR 3.71, 95% CI 1.15-11.9; P = 0.02) and prealbumin <14 mg/dl (OR 3.45, 95% CI 1.07-11.03; P = 0.03).
Preimplant Phosphodiesterase-5 Inhibitor Use Is Associated With Higher Rates of Severe Early Right Heart Failure After Left Ventricular Assist Device Implantation.
Together with our human transcriptomic analysis and corroborating studies in an RVF mouse model, these data render Wipi1 a potential target for RV-directed HF therapy.
These studies also reveal potential indirect effects of MuRF1 through regulating Rreb-1, and they reveal mechanisms by which MuRF1 may transcriptionally regulate anti-oxidant systems in the face of right heart failure.
Our findings indicate that the myocardium of rats with monocrotaline-induced right ventricular failure is deficient with activation of local RAS and therefore expresses blunted SFR, very similar to the depression of SFR observed in normal myocardium under inhibition of AT1 receptors.
These findings demonstrate that pharmacological inhibition of HIF-2α is a promising novel therapeutic strategy for the treatment of severe vascular remodeling and right heart failure in patients with PAH.
The RHF section comprises definition and pathophysiology, diagnosis and monitoring, identification of triggering factors and supportive therapy of RHF, volume management as well as PAH targeting therapy, therapy with inotropic, inodilator and vasopressor drugs, extracorporeal support and transplantation.
Our findings indicate that the myocardium of rats with monocrotaline-induced right ventricular failure is deficient with activation of local RAS and therefore expresses blunted SFR, very similar to the depression of SFR observed in normal myocardium under inhibition of AT1 receptors.
Our findings indicate that the myocardium of rats with monocrotaline-induced right ventricular failure is deficient with activation of local RAS and therefore expresses blunted SFR, very similar to the depression of SFR observed in normal myocardium under inhibition of AT1 receptors.
In addition, under-expression of CCR3 to CCR8 was independently associated with an increased risk of mortality at 1 year, even after adjusting for RVF.
Expression levels of miR-421, miR-1233-3p and miR-625-5p are lower in TOF patients with symptomatic right heart failure and thus may indicate disease progression in these patients.
The area under the receiver operating characteristic curve (AUC) for miR-181d-5p, miR-206 and miR-625-5p were 0.987, 0.993 and 0.769 in TOF-all and 0.990, 0.994 and 0.749 in TOF-noHF, respectively.