ArticleHeart rhythm2009
Effects of simvastatin on cardiac neural and electrophysiologic remodeling in rabbits with hypercholesterolemia.
Article in Heart rhythm, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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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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Who cites it
8 citing papers in PubMed, 27 citations in OpenAlex.
- Effects of Statin on Arrhythmia and Heart Rate Variability in Healthy Persons With 48-Hour Sleep Deprivation.Journal of the American Heart Association · 2016Trial
- The role of metabolic syndrome in sudden cardiac death risk: Recent evidence and future directions.European journal of clinical investigation · 2022Review
- Mechanisms Underlying Antiarrhythmic Properties of Cardioprotective Agents Impacting Inflammation and Oxidative Stress.International journal of molecular sciences · 2022Review
- TdP Incidence in Methoxamine-Sensitized Rabbit Model Is Reduced With Age but Not Influenced by Hypercholesterolemia.Frontiers in physiology · 2021Article
- Effects of rosuvastatin on atrial nerve sprouting and electrical remodeling in rabbits with myocardial infarction.International journal of clinical and experimental medicine · 2015Article
- Article
- Association of statin therapy with ventricular arrhythmias among patients with acute coronary syndrome.Heart Asia · 2013Article
- Simvastatin modulates remodeling of Kv4.3 expression in rat hypertrophied cardiomyocytes.International journal of biological sciences · 2012Article
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
Abstract
backgroundSignificant cardiac neural and electrophysiologic remodeling occurs with hypercholesterolemia (HC). Whether simvastatin can reverse HC-induced remodeling is unclear.
objectiveThe purpose of this study was to determine the mechanisms underlying the antiarrhythmic effects of statins.
methodsRabbits (N = 38) were fed HC chow (HC), standard chow (Control), HC chow followed by standard chow (Withdrawal), or HC chow and simvastatin (Statin) for 8 weeks. The hearts then were Langendorff-perfused for electrophysiologic studies. Nerves were identified by immunostaining of growth-associated protein-43 (GAP43) and tyrosine hydroxylase (TH). Action potential duration (APD) restitution in normal hearts with (N = 5) and without (N = 5) simvastatin therapy also was studied.
resultsSerum cholesterol levels (mg/dL) were 1,855 +/- 533 in HC, 50 +/- 21 in Control, 570 +/- 115 in Withdrawal, and 873 +/- 112 in Statin groups (P <.001). Compared with HC (16,700 +/- 5,342; 12,200 +/- 3,878 microm(2)/mm(2)), the Statin group had significantly reduced GAP43-positive (10,289 +/- 3,393 microm(2)/mm(2), P = .03) and TH-positive (7,685 +/- 2,959 microm(2)/mm(2), P = .04) nerve density, respectively. APD was longer in HC rabbits than in controls (192 +/- 20 ms vs 174 +/- 17 ms; P <.03). Withdrawal and Statin groups had less APD prolongation than HC group. Statin group has less repolarization heterogeneity than HC group (P <.01). Statin therapy flattened the slope of APD restitution in normal hearts. Ventricular fibrillation was either induced or occurred spontaneously in 79% of hearts in HC, 20% in Control, and 66% in Withdrawal groups. However, there was no VF in hearts of Statin group (P <.001).
conclusionSimvastatin significantly reduced vulnerability to ventricular fibrillation via the mechanism of reduction of HC-induced neural and electrophysiologic remodeling.
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