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01 · ABSTRACT

Abstract

Heart rhythm decreases and alterations depend on aging and correlate with lifestyle and metabolic alterations like obesity, dyslipidemia, and chronic inflammation; these alterations may also produce ventricular hypertrophy and atrial fibrillation, increasing lethal arrhythmias. The high sucrose diet in young adult Wistar rats produces metabolic syndrome from the eighth week that continues twenty-six weeks later. In this work, we analyzed the changes presented by the heart during six months of metabolic syndrome.

After this period, the rats were anesthetized, and the electrocardiogram was recorded. We observed that metabolic syndrome produced bradycardia and arrhythmias. The electrocardiogram showed an 18 % decrease in the heart rate in rats with metabolic syndrome and a decreased ability to regulate heart rate variability using the p-p interval Poincare graph. The electrical activity recorded in the sinus node showed alteration in the morphology and propagation of the action potential, therefore, a dysfunction in the pacemaker and supraventricular arrhythmias. This data correlated with the increase in the collagen and lipid area in the pacemaker that produced unexcitable segments, which induced lethal arrhythmias by alterations in electrical activity and premature aging and frailty, like those described in humans. We proposed that the changes in electrical and morphological alterations in the sinus node that are associated with metabolic syndrome are the cause of cardiovascular frailty and premature aging of the heart.

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02 · PUBLICATION RECORD

Article details

JournalMedical Research Archives
IssueVol 12 No 10 (2024): October Issue, Issue 10, VOl.12
SectionResearch Articles
Published22 October 2024
DOI10.18103/mra.v12i10.5939
ISSN2375-1924
03 · RIGHTS & REUSE

Rights & reuse

This article is published under a Creative Commons Attribution License (CC BY 3.0) and may be shared or distributed by anyone as long as attribution is given to the journal.

Authors & affiliations

AA

Alondra Albarado-Ibañez

Laboratorio de Fisiopatología Cardiovascular. Centro de Investigación en Fisicoquímica de Materiales, Instituto de Ciencias, Benemérita Universidad Autónoma de Puebla

JT

Julian Torres-Jacome

Laboratorio de Fisiopatología Cardiovascular. Centro de Investigación en Fisicoquímica de Materiales, Instituto de Ciencias, Benemérita Universidad Autónoma de Puebla

MH

Marcia Hiriart

Neuroscience Division, Cognitive Neuroscience Department, Instituto de Fisiología Celular, Universidad Nacional Autónoma de México UNAM.

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