While retaining normal systemic iron levels, this model developed PAH and right heart failure as a consequence of intracellular iron deficiency and increased expression of the vasoconstrictor endothelin-1 (ET-1) within PASMCs.PAH was prevented and reversed by i.v. iron and by the ET receptor antagonist BQ-123.
Based on current evidence, we suggest the potential utility of ST2, sST2, Gal-3, CRP, hs-cTn, and NT-proBNP in predicting and detecting RVF in cardiac surgery patients, as they encompass the multifaceted nature of perioperative RVF and warrant further investigation to establish their clinical utility.
However, positive staining for ET-1 was also seen in rats' hearts that suffered from arrhythmias after electric shock and in the myocardium of the right ventricle in human control cases in which a right heart failure has to be discussed.
Furthermore, right ventricle-targeted therapies, aimed at mitigating the effects of functional right ventricular failure, include β-adrenoceptor (β-AR) blockers, angiotensin-converting enzyme (ACE) inhibitors, antioxidants, modulators of metabolism, and 5-hydroxytryptamine-2B (5-HT2B) receptor antagonists.
Current management of patients with pulmonary arterial hypertension and symptoms of right heart failure includes use of mineralocorticoid receptor antagonists for their diuretic and natriuretic effects.
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.
Furthermore, right ventricle-targeted therapies, aimed at mitigating the effects of functional right ventricular failure, include β-adrenoceptor (β-AR) blockers, angiotensin-converting enzyme (ACE) inhibitors, antioxidants, modulators of metabolism, and 5-hydroxytryptamine-2B (5-HT2B) receptor antagonists.
This study aimed to compare von Willebrand factor (vWF) levels, ristocetin cofactor levels, platelet counts, aortic valve movements, and right heart failure (RHF) as risk factors of gastrointestinal (GI) bleeding in patients with continuous flow left ventricular assist device (cf-LVAD).
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.
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.
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).
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.
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.