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[Pathogenetic characteristics of the development of arrhythmia in patients with ischemic heart disease]
Insights
Lipid peroxidation activation and its products cause cardiac arrhythmia in coronary patients. Correcting arrhythmia may involve managing lipid peroxidation levels.
Area of Science:
- Biochemistry
- Cardiology
- Physiology
Context:
- Investigated 93 coronary patients without myocardial infarction.
- Examined patients with and without cardiac arrhythmia.
- Assessed ACTH, hydrocortisone, cyclic nucleotides, beta-receptors, lipid peroxidation, antioxidant system, and hemodynamics.
Purpose:
- To determine the role of lipid peroxidation (LPO) in the emergence of cardiac arrhythmia.
- To explore the underlying mechanisms of LPO-induced arrhythmia.
Summary:
- Clinical findings suggest LPO activation and excessive LPO product accumulation in blood are primary causes of arrhythmia.
- Experimental data indicate LPO products can induce arrhythmia by increasing Na-Ca channel density and inhibiting Ca-dependent ATPase activity.
Impact:
- Highlights the critical role of lipid peroxidation in cardiac arrhythmia development.
- Suggests potential therapeutic targets for managing arrhythmia by controlling LPO.
Abstract:
ACTH, hydrocortisone and cyclic nucleotides levels, beta-receptors sensitivity, lipid peroxidation (LPO), antioxidant system, hemodynamics were investigated in 93 coronary patients without myocardial infarction in the presence of cardiac arrhythmia and after its correction. The clinical and laboratory findings indicate that it is primarily LPO activation and LPO products excessive accumulation in the blood that are responsible for arrhythmia emergence. Experimental data support these results by showing possibility of cardiac arrhythmia onset due to LPO products which raise the density of Na-Ca channels and inhibit the activity of Ca-dependent ATPase.