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Catheter Ablation in Combination With Left Atrial Appendage Closure for Atrial Fibrillation
28:13

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Published on: February 26, 2013

The isoprenoid pathway in lone atrial fibrillation with embolic stroke

A Ravikumar1, P A Kurup

  • 1Department of Medicine, Medical College Hospital, University of Kerala, Trivandrum.

Indian Heart Journal
|June 29, 2001
PubMed

Insights

Lone atrial fibrillation with embolic stroke involves an upregulated isoprenoid pathway and increased digoxin secretion, particularly in individuals with right-hemispheric dominance. This pathway dysregulation is linked to stroke pathogenesis.

Area of Science:

  • Biochemistry
  • Neuroscience
  • Cardiology

Background:

  • Investigated the isoprenoid pathway in lone atrial fibrillation (AF) patients with embolic stroke.
  • Compared these patients with individuals exhibiting right, left, or bihemispheric dominance.

Purpose of the Study:

  • To determine the role of hemispheric dominance in the pathogenesis of lone AF with embolic stroke.
  • To elucidate the specific biochemical alterations in the isoprenoid pathway.

Main Methods:

  • Measured hydroxyl methyl glutaryl-CoA reductase and RBC sodium-potasium ATPase activity.
  • Assessed serum levels of magnesium, digoxin, dolichol, and ubiquinone.
  • Analyzed tyrosine/tryptophan catabolites, glycoconjugate metabolism, free radical levels, and RBC membrane composition.

Main Results:

  • Lone AF with embolic stroke showed elevated digoxin, dolichol, and free radicals, with low ubiquinone.
  • Observed increased tryptophan catabolites and altered tyrosine catabolites.
  • Right-hemispheric dominance mirrored these biochemical patterns, while left-hemispheric dominance showed reversed patterns.

Conclusions:

  • Lone AF with embolic stroke is linked to an upregulated isoprenoid pathway and hypothalamic digoxin secretion.
  • This dysregulation is specifically observed in right-hemisphere dominant individuals.
  • Suggests hemispheric dominance influences stroke pathogenesis via isoprenoid pathway modulation.
Abstract

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