ArticleCardiovascular research2019
An N-/L-type calcium channel blocker, cilnidipine, suppresses autonomic, electrical, and structural remodelling associated with atrial fibrillation.
Article in Cardiovascular research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 20 citations in OpenAlex.
- Bidirectional relationships between increased arterial stiffness and atrial fibrillation.Frontiers in cardiovascular medicine · 2026Article
- Autonomic dysregulation and atrial arrhythmias.American journal of physiology. Cell physiology · 2025Review
- Targeting atrial fibrillation in HFpEF: the emerging role of pulsed field ablation.Frontiers in physiology · 2025Review
- An L-type calcium channel blocker nimodipine exerts anti-fibrotic effects by attenuating TGF-β1 induced calcium response in an in vitro model of thyroid eye disease.Eye and vision (London, England) · 2024Article
- Article
- Increased vulnerability to atrial and ventricular arrhythmias caused by different types of inhaled tobacco or marijuana products.Heart rhythm · 2023Article
- Targeting autonomic nervous system as a biomarker of well-ageing in the prevention of stroke.Frontiers in aging neuroscience · 2022Review
- Screening and functional analysis of differentially expressed lncRNAs in rapid atrial pacing dog atrial tissue.Journal of interventional cardiac electrophysiology : an international journal of arrhythmias and pacing · 2021Article
- Why translation from basic discoveries to clinical applications is so difficult for atrial fibrillation and possible approaches to improving it.Cardiovascular research · 2021Review
- Autonomic Dysfunction and Neurohormonal Disorders in Atrial Fibrillation.Cardiac electrophysiology clinics · 2021Review
- Does cilnidipine, a dual L- and N-type CaHypertension research : official journal of the Japanese Society of Hypertension · 2020Article
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Authors and funding
9 authors at 3 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimsAutonomic dysfunction can promote atrial fibrillation (AF) and results from AF-related remodelling. N-type Ca2+-channels (NTCCs) at sympathetic nerve terminals mediate Ca2+-entry that triggers neurotransmitter release. AF-associated remodelling plays an important role in AF pathophysiology but the effects of NTCC inhibition on such remodelling is unknown. Here, we investigated the ability of a clinically available Ca2+-channel blocker (CCB) with NTCC-blocking activity to suppress the arrhythmogenic effects of AF-promoting remodelling in dogs. METHODS AND
resultsMongrel dogs were kept in AF by right atrial tachypacing at 600 bpm. Four groups were studied under short-term AF (7 days): (i) Shams, instrumented but without tachypacing (n = 5); (ii) a placebo group, tachypaced while receiving placebo (n = 6); (iii) a control tachypacing group receiving nifedipine (10 mg orally twice-daily; n = 5), an L-type CCB; and (iv) a cilnidipine group, subjected to tachypacing and treatment with cilnidipine (10 mg orally twice-daily; n = 7), an N-/L-type CCB. With cilnidipine therapy, dogs with 1-week AF showed significantly reduced autonomic changes reflected by heart rate variability (decreases in RMSSD and pNN50) and plasma norepinephrine concentrations. In addition, cilnidipine-treated dogs had decreased extracellular matrix gene expression vs. nifedipine-dogs. As in previous work, atrial fibrosis had not yet developed after 1-week AF, so three additional groups were studied under longer-term AF (21 days): (i) Shams, instrumented without tachypacing or drug therapy (n = 8); (ii) a placebo group, tachypaced while receiving placebo (n = 8); (iii) a cilnidipine group, subjected to tachypacing during treatment with cilnidipine (10 mg twice-daily; n = 8). Cilnidipine attenuated 3-week AF effects on AF duration and atrial conduction, and suppressed AF-induced increases in fibrous-tissue content, decreases in connexin-43 expression and reductions in sodium-channel expression.
conclusionsCilnidipine, a commercially available NTCC-blocking drug, prevents AF-induced autonomic, electrical and structural remodelling, along with associated AF promotion.
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