Chronic Metabolic Syndrome develops a frailty of cardiac rhythm similar to aging in rats
Main Article Content
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.
Article Details
The Medical Research Archives grants authors the right to publish and reproduce the unrevised contribution in whole or in part at any time and in any form for any scholarly non-commercial purpose with the condition that all publications of the contribution include a full citation to the journal as published by the Medical Research Archives.
References
2. Ajoolabady A, Pratico D, Vinciguerra M, Lip GYH, Franceschi C, Ren J. Inflammaging: mechanisms and role in the cardiac and vasculature. Trends Endocrinol Metab. 2023;34(6):373-87.
3. Islam MS. Islets of Langerhans. 2nd edition. ed. New York: Springer; 2014. pages cm p.
4. Lakatta EG. Arterial and cardiac aging: major shareholders in cardiovascular disease enterprises: Part III: cellular and molecular clues to heart and arterial aging. Circulation. 2003;107(3):490-7.
5. Lakatta EG, Levy D. Arterial and cardiac aging: major shareholders in cardiovascular disease enterprises: Part I: aging arteries: a "set up" for vascular disease. Circulation. 2003;107(1):139-46.
6. Wang M, Kim SH, Monticone RE, Lakatta EG. Matrix metalloproteinases promote arterial remodeling in aging, hypertension, and atherosclerosis. Hypertension. 2015;65(4):698-703.
7. Gencer B, Butler J, Bauer DC, Auer R, Kalogeropoulos A, Marques-Vidal P, et al. Association of electrocardiogram abnormalities and incident heart failure events. Am Heart J. 2014;167(6):869-75 e3.
8. Jones SA. Ageing to arrhythmias: conundrums of connections in the ageing heart. J Pharm Pharmacol. 2006;58(12):1571-6.
9. Arroyo-Carmona RE, Mitre-Velasco Y, Martinez-Laguna Y, Torres-Jacome J, Albarado-Ibanez A. A maternal diet high in carbohydrates causes bradyarrhythmias and changes in heart rate variability in the offspring sex-dependent in mice. Lab Anim Res. 2024;40(1):34.
10. D'Souza A, Trussell T, Morris GM, Dobrzynski H, Boyett MR. Supraventricular Arrhythmias in Athletes: Basic Mechanisms and New Directions. Physiology (Bethesda). 2019;34(5):314-26.
11. Singh D, Vinod K, Saxena SC, Deepak KK.
Effects of RR segment duration on HRV spectrum estimation. Physiol Meas. 2004;25(3):721-35.
12. Sharma RK, Deepak KK, Bijlani RL, Rao PS. Short-term physical training alters cardiovascular autonomic response amplitude and latencies. Indian J Physiol Pharmacol. 2004;48(2):165-73.
13. Larson ED, St Clair JR, Sumner WA, Bannister RA, Proenza C. Depressed pacemaker activity of sinoatrial node myocytes contributes to the age-dependent decline in maximum heart rate. Proc Natl Acad Sci U S A. 2013;110(44):18011-6.
14. Albarado-Ibanez A, Avelino-Cruz JE, Velasco M, Torres-Jacome J, Hiriart M. Metabolic syndrome remodels electrical activity of the sinoatrial node and produces arrhythmias in rats. PLoS One. 2013;8(11):e76534.
15. Boyett MR, Honjo H, Yamamoto M, Nikmaram MR, Niwa R, Kodama I. Regional differences in effects of 4-aminopyridine within the sinoatrial node. Am J Physiol. 1998;275(4):H1158-68.
16. Arroyo-Carmona RE, Lopez-Serrano AL, Albarado-Ibanez A, Mendoza-Lucero FM, Medel-Cajica D, Lopez-Mayorga RM, et al. Heart Rate Variability as Early Biomarker for the Evaluation of Diabetes Mellitus Progress. J Diabetes Res. 2016; 2016:8483537.
17. Guerra F, Mancinelli L, Angelini L, Fortunati M, Rappelli A, Dessi-Fulgheri P, et al. The association of left ventricular hypertrophy with metabolic syndrome is dependent on body mass index in hypertensive overweight or obese patients. PLoS One. 2011;6(1):e16630.
18. Lauer MS, Larson MG, Evans JC, Levy D. Association of left ventricular dilatation and hypertrophy with chronotropic incompetence in the Framingham Heart Study. Am Heart J. 1999; 137(5):903-9.
19. Hashem MS, Kalashyan H, Choy J, Chiew SK, Shawki AH, Dawood AH, et al. Left ventricular relative wall thickness versus left ventricular mass index in non-cardioembolic stroke patients. Medicine (Baltimore). 2015;94(20):e872.
20. Movahed MR, Bates S, Strootman D, Sattur S. Obesity in adolescence is associated with left ventricular hypertrophy and hypertension. Echocardiography. 2011;28(2):150-3.
21. Sengupta P. The Laboratory Rat: Relating Its Age With Human's. Int J Prev Med. 2013;4(6):62 4-30.
22. Bisset ES, Howlett SE. The biology of frailty in humans and animals: Understanding frailty and promoting translation. Aging Med (Milton). 2019;2 (1):27-34.
23. Budelli R, Torres J, Catsigeras E, Enrich H. Two-neurons network. I. Integrate and fire pacemaker models. Biol Cybern. 1991;66(2):95-101.