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C. Montalto

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Review Open access Sep 2026

Moderate aortic stenosis: diagnostic pitfalls and the role of multimodality imaging in risk stratification and clinical management

Moderate aortic stenosis (AS) has traditionally been considered a transitional and relatively benign stage of valvular disease. Yet, contemporary evidence shows that it is associated with substantial morbidity and mortality even before progression to severe AS. This paper synthesizes current evidence on the limitations of standard echocardiography, highlights the role of advanced imaging and artificial intelligence, and outlines evolving strategies for risk stratification and clinical management. Multimodality imaging provides a more accurate assessment of disease severity beyond conventional echocardiographic parameters: computed tomography aortic valve calcium scoring, cardiac magnetic resonance, and 18 F-sodium fluoride positron emission tomography reveal early myocardial injury and identify rapid progressors. AI further enhances reproducibility and supports the development of emerging prognostic models. A staging approach that integrates ventricular, atrial, and right-sided involvement correlates more closely with clinical outcomes than valve metrics alone, enabling a more comprehensive characterization of disease burden. Although guideline-directed surveillance remains the standard strategy for most patients, selected high-risk individuals, particularly those with adverse remodeling, elevated biomarkers, or recurrent heart failure admissions, may benefit from earlier intervention. While waiting for the results of ongoing randomized trials cardiologist should implement all the imaging multimodality tools available in order to individuate patients in which an earlier treatment of moderate AS will more probably improve long-term outcomes.

G. Santangelo, Alessandro Maloberti, C. Tognola et al. · 0 citations
Aug 2026

De-escalation of antiplatelet therapy to evaluate platelet reactivity and clinical outcomes after coronary stenting in patients at high bleeding risk and recent acute coronary syndrome: Rationale and design of the DESC-HBR trial.

BACKGROUND Patients at high bleeding risk (HBR) presenting with acute coronary syndrome (ACS) and treated with percutaneous coronary intervention (PCI) have competing hazards of ischemic and bleeding events. In unselected ACS populations, trials of unguided de-escalation of P2Y12 inhibition reduce bleeding without excess ischemia; however, HBR patients were largely underrepresented in these studies. Comparative evidence across multiple de-escalation regimens in this vulnerable cohort is currently lacking. STUDY DESIGN DESC-HBR is a prospective, multicenter, randomized, open-label trial with blinded endpoint adjudication enrolling 200 HBR patients (PRECISE-DAPT ≥25 or ARC-HBR criteria) at 30 ± 7 days after ACS-PCI. Following one month of dual antiplatelet therapy (DAPT) with prasugrel 10 mg once daily or ticagrelor 90 mg twice daily, on a background of aspirin 100 mg, patients are randomized (1: 1:1:1) to clopidogrel 75 mg once daily, prasugrel 5 mg once daily, ticagrelor 60 mg twice daily, or continuation of full-dose potent therapy. The primary endpoint is the proportion of patients achieving optimal platelet reactivity (VerifyNow PRU 85-208) at 14 ± 2 days post-randomization, 2-h after maintenance dose. Key secondary outcomes include BARC bleeding, net adverse clinical events, quality of life and adherence. Pharmacodynamic profiling incorporates VerifyNow and Total Thrombus Formation Analysis (T-TAS). A total sample of 200 patients allows >80% power to detect superiority of each de-escalation arm versus control (α = 0.017). CONCLUSIONS DESC-HBR is the first randomized trial directly comparing multiple P2Y12 inhibitor de-escalation strategies in HBR patients post-ACS. By integrating pharmacodynamic, clinical, and patient-reported outcomes, it will provide information to guide individualized antiplatelet strategies balancing ischemic protection and bleeding mitigation in HBR patients. CLINICAL TRIAL REGISTRATION UNIQUE IDENTIFIER NCT05903976, EudraCT 2023-000029-10.

Francesco Costa, Gianpiero Vizzari, S. Zecchino et al. · 0 citations

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