Interventional Cardiology Research Updates

This American Heart Association scientific statement reviews evidence on optimizing care for older adults (≥65 years) with heart failure, noting that guideline-directed therapies have consistent treatment effects and safety profiles in this population but are underused due to multimorbidity, polypharmacy, frailty, and social barriers. The statement presents a structured, shared decision-making framework to weigh benefit–risk in the context of comorbidities, offers practical guidance for patients often underrepresented in trials, and discusses implementation strategies and health services tools to improve care and outcomes for older adults with heart failure.

Review highlighting polycystin-1 (PC1) as a central regulator of cardiovascular mechanobiology, supported by recent structural elucidation of the PC1/PC2 complex showing a mechanically sensitive ectodomain, regulated proteolysis, and functional coupling with PC2. The authors summarize evidence that PC1 independently governs vascular homeostasis, endothelial shear responsiveness, smooth muscle phenotype, and myocardial mechanotransduction, and that PC1 dysfunction disrupts nitric oxide signaling, cytoskeletal remodeling, excitation–contraction coupling, and hypertrophic transcriptional programs with consequences for cardiac morphogenesis and adult myocardial integrity. The review identifies knowledge gaps and emerging therapeutic opportunities, including roles for structure-guided approaches and artificial intelligence in PC1-targeted drug discovery.

Review synthesizing human cohort, genetic, and experimental data that link circulating suPAR (soluble urokinase plasminogen activator receptor) to incident cardiovascular events, heart failure, diabetes, and kidney disease progression and supporting a causal role. Mechanistic work shows membrane-tethered uPAR forms signaling complexes with coreceptors (including αvβ3 integrin and RAGE) to drive vascular inflammation, remodeling, and fibrosis, while proteolytic release of suPAR converts local signaling into systemic agonist activity that activates podocyte αvβ3/RAGE and a Rac1/NOX2-Src-TRPC6 cascade causing proteinuria/glomerulosclerosis; a D2D3 fragment induces insulin-dependent diabetes in transgenic mice reversible by anti-uPAR antibody. The review outlines pharmacologically tractable nodes—transcriptional suppression, suPAR neutralization, receptor-interface disruption, and downstream kinase/channel inhibition—and proposes matching interventions to signaling modes across organ systems.