ArticleCJC open2026
Atorvastatin Prevents Early Lipotoxic Remodelling in Right Ventricular Pacing-Induced Cardiomyopathy.
Article in CJC open, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Authors and funding
11 authors.
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No grant is acknowledged in the PubMed record.
Abstract
Background: Right ventricular (RV) pacing can induce metabolic and structural alterations in left ventricular (LV) myocardium, including lipid accumulation, glycogen depletion, and increased endoplasmic reticulum (ER) stress. This study evaluated protective effects of atorvastatin on RV pacing-induced metabolic dysfunction. Methods: Fifteen male Lanyu miniature pigs were randomized into sham control (n = 5), RV pacing (n = 5), and RV pacing with atorvastatin treatment (n = 5) groups. RV pacing was achieved via ventricular lead implantation at the RV outflow tract, followed by complete atrioventricular block, with ventricular pacing maintained for at least 80 beats/min in dual-chamber, dual-sensing, dual-response, rate-responsive mode to provide atrial-synchronous ventricular pacing while allowing atrial sensing or pacing. The RV pacing with atorvastatin treatment group received atorvastatin (40 mg/d) starting 2 weeks before surgery until euthanasia at 6 months. Metabolic, histologic, and molecular parameters were assessed in LV myocardial tissue. Results: Compared with sham controls, RV pacing significantly increased myocardial lipid accumulation, with higher triglyceride (2.43 ± 0.17 vs 1.74 ± 0.14 μg/mg, Conclusions: RV pacing induces lipid accumulation, glycogen loss, and increased ER stress in the LV myocardium. Atorvastatin partially mitigated these effects by normalizing fatty acid metabolism and reducing ER stress and apoptosis, suggesting a potential role in attenuating early/subclinical RV pacing-induced metabolic remodelling.
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