Early right heart failure (RHF) remains common after left ventricular assist device (LVAD) implantation and is associated with substantial morbidity and mortality. Definition and time window determine reported incidence and complicate risk‐model comparison. Established risk models perform differently across cohorts and device eras, and temporary support should be matched to the dominant physiology. LV unloading alters venous return, septal geometry, and right ventricular (RV) loading, whereas perioperative stress exposes limited RV reserve. No single clinical, imaging, or hemodynamic measure reliably predicts early RHF, and existing scores perform variably on external validation. Dynamic hemodynamic assessment adds information about RV reserve and warrants prospective threshold validation. Management begins by addressing reversible causes and optimizing LVAD support. When temporary mechanical support is required, RV‐specific bypass restores pulmonary forward flow, an oxygenated right atrial‐to‐pulmonary arterial RVAD adds gas exchange, and venoarterial extracorporeal membrane oxygenation provides broader rescue for combined circulatory and respiratory failure. Comparative evidence on timing and configuration remains observational.
Proprotein convertase subtilisin/kexin type 9 (PCSK9) has emerged as a novel contributor to atrial fibrillation (AF) pathophysiology. Recent studies suggest that elevated PCSK9 levels may promote AF through multiple mechanisms, including platelet activation, oxidative stress, vascular calcification, and structural atrial remodeling. PCSK9 inhibitors such as alirocumab, evolocumab, and newer agents like inclisiran have shown potential in reducing AF incidence and cardiovascular events, particularly in high-risk populations. However, evidence from randomized controlled trials with AF as a primary clinical endpoint is limited. Further mechanistic and interventional research is warranted to establish optimized therapeutic strategies targeting PCSK9 in AF prevention and management.
Dual antiplatelet therapy (DAPT) with aspirin and a P2Y12 inhibitor is standard for patients with acute coronary syndrome (ACS) undergoing percutaneous coronary intervention (PCI), yet real-world comparisons of ticagrelor and prasugrel remain limited. We evaluated their relative effectiveness and safety using the TriNetX Global Collaborative Network (2010–2024). Adult ACS patients receiving prasugrel or ticagrelor within 24 h post-PCI were included. The primary endpoint was a 1-year composite of all-cause mortality, myocardial infarction (MI), and cerebral infarction; secondary endpoints included individual components, major bleeding, and repeat revascularization. Propensity score matching balanced baseline characteristics, with subgroup and sensitivity analyses assessing robustness. Among 14,895 matched pairs (n=29,790) from 126,273 patients, prasugrel was associated with lower risk of the composite endpoint (HR 0.641; 95% CI 0.613–0.671), all-cause mortality (HR 0.557; 95% CI 0.487–0.637), and MI (HR 0.648; 95% CI 0.616–0.680), without increased bleeding (HR 0.945; 95% CI 0.824–1.084). Repeat revascularization was higher with prasugrel (HR 1.791; 95% CI 1.639–1.957). Effects were consistent across subgroups. In this real-world setting, prasugrel demonstrated superior effectiveness over ticagrelor in reducing mortality and ischemic events without increasing the risk of bleeding, although higher rates of repeat revascularization warrant further study. These findings support prasugrel as a potentially preferred P2Y12 inhibitor in selected ACS patients undergoing PCI.
Background Propofol (PPF) alleviates myocardial ischemia/reperfusion injury (MIRI), yet no existing studies have clarified the function of microRNA‐511‐3p (miR‐511‐3p) in cardiac injury or its link to PPF′s cardioprotection. Purpose This study clarified how the miR‐511‐3p/ATPase sarcoplasmic/endoplasmic reticulum Ca 2+ transporting 2 (ATP2A2) signaling cascade mediated PPF‐induced relief against hypoxia/reoxygenation (H/R) cardiac damage. Methods H/R damage models were established in H9c2 cells. Cell viability was measured via the CCK‐8 assay, and flow cytometry was used to quantify the proportion of apoptotic cells. Cellular reactive oxygen species (ROS) levels were assessed using the DCFH‐DA fluorescent staining method. ELISA and colorimetric tests were combined to measure cardiac injury markers, inflammatory mediators, and oxidative stress‐related molecules. RT‐qPCR was applied to test the expression levels of miR‐511‐3p and ATP2A2. Dual‐luciferase reporter assays were carried out to confirm the direct binding interaction between the two molecules. Results PPF markedly boosted the viability and restrained apoptosis of H9c2 cells subjected to H/R treatment. It also reduced the release of cardiac injury markers and eased excessive oxidative stress and inflammatory responses. H/R exposure raised miR‐511‐3p abundance, an alteration that PPF treatment could reverse. Forced miR‐511‐3p expression partially abolished the cardioprotective benefits brought by PPF. ATP2A2 was verified as a direct target of miR‐511‐3p, whose expression was suppressed by this miRNA. Upregulating ATP2A2 counteracted cell damage triggered by miR‐511‐3p overexpression. Conclusions PPF might mitigate H/R‐triggered cardiomyocyte damage, possibly through inhibiting miR‐511‐3p and increasing its target ATP2A2, and this molecular axis may offer a tentative therapeutic reference for MIRI.
