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Literature ·

ATTR cardiomyopathy in Chicago

patients who received vutrisiran from the start of HELIOS-B have 37 percent fewer deaths or cardiovascular events through month 48 than those who began after the placebo phase, and eplontersen measurably shrinks myocardial amyloid on MRI in CARDIO-TTRansform

Two Circulation papers behind FS.11 at AHA 2026 (Monday 9 November); figures from the published abstracts. HELIOS-B open-label extension (Garcia-Pavia et al., online 3 November; Peter van der Meer of UMCG among the authors): of 654 randomised patients with transthyretin amyloid cardiomyopathy, 478 completed the double-blind phase and 466 (243 continuous vutrisiran, 223 placebo then vutrisiran 25 mg every three months) entered the extension. Through month 48, continuous vutrisiran versus placebo/vutrisiran: first cardiovascular event or all-cause death HR 0.63 (95 percent CI 0.51 to 0.79, P = 0.0001); all-cause death HR 0.63 (0.46 to 0.84, P = 0.0023); KCCQ-OS least-squares mean difference 9.0 points (5.3 to 12.6); improved or stable NYHA class OR 1.6 (1.1 to 2.2); NT-proBNP ratio 0.66, troponin I ratio 0.71; no new safety signals. The authors read it as the cost of a 33-to-36-month delay in starting treatment. CARDIO-TTRansform CMR study (Razvi, Fontana et al., online 9 November): prespecified substudy of the 1,432-patient phase 3 trial of eplontersen, 120 participants with baseline and at least one follow-up CMR (58 eplontersen, 62 placebo; mean age 76.7, 95 percent men, 12.5 percent on a stabiliser at baseline). At week 140 eplontersen versus placebo: extracellular volume minus 6.7 percentage points (minus 8.7 to minus 4.7, P less than 0.001), native T1 minus 25.9 ms, LV mass minus 19.1 g, LVEF plus 5.1 points, RVEF plus 4.6 points, better LV and RV strain; amyloid regression (ECV down 5 points or more) in 12.5 versus 0 percent, progression in 12.5 versus 76 percent. The main trial missed its clinical primary endpoint at ESC 2026; the imaging shows the biology works even where the outcomes did not separate.

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