Publications by authors named "Jan W Fiolet"

Article Synopsis
  • Empagliflozin (EMPA) is a medication for type 2 diabetes that reduces cardiovascular death risk, but its exact mechanism is unclear.
  • The study measured sodium and calcium levels in heart cells from rabbits and rats, finding that EMPA lowers sodium and calcium levels while increasing mitochondrial calcium.
  • Results suggest that EMPA directly affects heart cell chemistry by inhibiting the sodium/hydrogen exchanger (NHE), which lowers sodium and calcium levels independently of its glucose-lowering effects.
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Background: Atrial fibrosis is an important component of the arrhythmogenic substrate in patients with atrial fibrillation (AF). We studied the effect of interstitial fibrosis on conduction velocity (CV) in the left atrial appendage of patients with AF.

Methods And Results: Thirty-five left atrial appendages were obtained during AF surgery.

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Aims: Transgenic mice are frequently used to investigate the role of genes involved in cardiac conduction. The QRS duration calculated from the electrocardiogram (ECG) is a commonly used measure for ventricular conduction time. However, the relation between ventricular activation and QRS duration calculated from a mouse surface ECG is not well understood.

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Objective: Metabolic inhibition causes a decline in mechanical performance and, if prolonged, myocardial contracture and cell death. The decline in mechanical performance is mainly due to altered intracellular calcium handling, which is under control of the Na(+)/Ca(2+)-exchanger (NCX) The driving force of the NCX (ΔG(ncx)) determines the activity of NCX. The aim of this study was to describe the relation between ΔG(ncx) and calcium homeostasis during metabolic inhibition.

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Background: Fish oil reduces sudden death in patients with prior myocardial infarction. Sudden death in heart failure may be due to triggered activity based on disturbed calcium handling. We hypothesized that superfusion with omega3-polyunsaturated fatty acids (omega3-PUFAs) from fish inhibits triggered activity in heart failure.

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Background: Fish oil reduces the incidence of sudden cardiac death in postmyocardial infarction patients. Triggered activity is the principal mechanism of arrhythmogenesis under these conditions.

Objective: The purpose of this study was to test whether dietary fish oil in pigs inhibits Ca2+ overload-induced triggered activity.

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Background: Omega-3 polyunsaturated fatty acids (omega3-PUFAs) from fish oil reduce the risk of sudden death presumably by preventing life-threatening arrhythmias. Acutely administered omega3-PUFAs modulate the activity of several cardiac ion channels, but the chronic effects of a diet enriched with fish oil leading to omega3-PUFA-incorporation into the sarcolemma on membrane currents are unknown.

Methods: Pigs received a diet either rich in omega3-PUFAs or in omega9-fatty acids for 8 weeks.

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Article Synopsis
  • - The study investigates the impact of chronic Na(+)/H(+)-exchanger (NHE-1) inhibition on heart disease progression in rabbits, proposing that blocking NHE-1 may prevent hypertrophy and heart failure (HF) due to improved calcium handling.
  • - Rabbits were divided into control and cariporide-treated groups, with the latter showing minimal hypertrophy and no signs of heart failure after three months, suggesting effective prevention of disease progression.
  • - Results indicated that cariporide treatment maintained normal cellular structure and function, preserving action potentials and calcium handling in cardiac cells, highlighting NHE-1's role in heart health.
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Objective: Myocardial ischemia and ventricular arrhythmias often complicate congestive heart failure. Ischemia-induced dispersion in repolarization is an important arrhythmogenic factor that might be caused by intrinsic cellular differences in response to simulated ischemia (SI) or by changed coupling of myocytes. We hypothesized that intrinsic heterogeneity in action potential duration (APD) or the occurrence of rigor is larger in failing than in normal rabbit myocytes during SI.

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Objective: After-depolarization associated arrhythmias are frequently observed in heart failure and associated with spontaneous calcium release from sarcoplasmic reticulum (SR), calcium after-transients. We hypothesize that disturbed SR calcium handling underlies calcium after-transients in heart failure (HF).

Methods: We measured the stimulation rate dependence (0.

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