A Pilot Study on the <sup>1</sup>H-NMR Serum Metabolic Profile of Takotsubo Patients Reveals Systemic Response to Oxidative Stress
Takotsubo syndrome (TTS) presents as an acute coronary syndrome characterized by severe left ventricular (LV) dysfunction and non-obstructive coronary artery disease that typically shows spontaneous recovery within days or weeks. The mechanisms behind TTS are mainly related to beta-adrenergic overst...
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2021-12-01
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author | Domitilla Vanni Nicola Viceconte Greta Petrella Flavio Giuseppe Biccirè Francesco Pelliccia Gaetano Tanzilli Daniel Oscar Cicero |
author_facet | Domitilla Vanni Nicola Viceconte Greta Petrella Flavio Giuseppe Biccirè Francesco Pelliccia Gaetano Tanzilli Daniel Oscar Cicero |
author_sort | Domitilla Vanni |
collection | DOAJ |
description | Takotsubo syndrome (TTS) presents as an acute coronary syndrome characterized by severe left ventricular (LV) dysfunction and non-obstructive coronary artery disease that typically shows spontaneous recovery within days or weeks. The mechanisms behind TTS are mainly related to beta-adrenergic overstimulation and acute endogenous catecholamine surge, both of which could increase oxidative status that may induce further deterioration of cardiac function. Although several studies reported evidence of inflammation and oxidative stress overload in myocardial tissue of TTS models, systemic biochemical evidence of augmented oxidant activity in patients with TTS is lacking. In this study, serum samples of ten TTS patients and ten controls have been analyzed using <sup>1</sup>H-NMR spectroscopy. The results of this pilot study show a marked alteration in the systemic metabolic profile of TTS patients, mainly characterized by significant elevation of ketone bodies, 2-hydroxybutyrate, acetyl-L-carnitine, and glutamate levels, in contrast with a decrease of several amino acid levels. The overall metabolic fingerprint reflects a systemic response to oxidative stress caused by the stressor that triggered the syndrome’s onset. |
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language | English |
last_indexed | 2024-03-10T04:38:51Z |
publishDate | 2021-12-01 |
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series | Antioxidants |
spelling | doaj.art-adedadc641c0473786fd559f187d2e9a2023-11-23T03:33:53ZengMDPI AGAntioxidants2076-39212021-12-011012198210.3390/antiox10121982A Pilot Study on the <sup>1</sup>H-NMR Serum Metabolic Profile of Takotsubo Patients Reveals Systemic Response to Oxidative StressDomitilla Vanni0Nicola Viceconte1Greta Petrella2Flavio Giuseppe Biccirè3Francesco Pelliccia4Gaetano Tanzilli5Daniel Oscar Cicero6Department of Chemical Science and Technology, University of Rome “Tor Vergata”, 00133 Rome, ItalyDepartment of Internal Medicine, Anesthesiologic and Cardiovascular Sciences, Sapienza University of Rome, Policlinic Umberto I, 00161 Rome, ItalyDepartment of Chemical Science and Technology, University of Rome “Tor Vergata”, 00133 Rome, ItalyDepartment of Internal Medicine, Anesthesiologic and Cardiovascular Sciences, Sapienza University of Rome, Policlinic Umberto I, 00161 Rome, ItalyDepartment of Internal Medicine, Anesthesiologic and Cardiovascular Sciences, Sapienza University of Rome, Policlinic Umberto I, 00161 Rome, ItalyDepartment of Internal Medicine, Anesthesiologic and Cardiovascular Sciences, Sapienza University of Rome, Policlinic Umberto I, 00161 Rome, ItalyDepartment of Chemical Science and Technology, University of Rome “Tor Vergata”, 00133 Rome, ItalyTakotsubo syndrome (TTS) presents as an acute coronary syndrome characterized by severe left ventricular (LV) dysfunction and non-obstructive coronary artery disease that typically shows spontaneous recovery within days or weeks. The mechanisms behind TTS are mainly related to beta-adrenergic overstimulation and acute endogenous catecholamine surge, both of which could increase oxidative status that may induce further deterioration of cardiac function. Although several studies reported evidence of inflammation and oxidative stress overload in myocardial tissue of TTS models, systemic biochemical evidence of augmented oxidant activity in patients with TTS is lacking. In this study, serum samples of ten TTS patients and ten controls have been analyzed using <sup>1</sup>H-NMR spectroscopy. The results of this pilot study show a marked alteration in the systemic metabolic profile of TTS patients, mainly characterized by significant elevation of ketone bodies, 2-hydroxybutyrate, acetyl-L-carnitine, and glutamate levels, in contrast with a decrease of several amino acid levels. The overall metabolic fingerprint reflects a systemic response to oxidative stress caused by the stressor that triggered the syndrome’s onset.https://www.mdpi.com/2076-3921/10/12/1982Takotsubo syndromemetabolomics<sup>1</sup>H-NMRsystemic stressor response |
spellingShingle | Domitilla Vanni Nicola Viceconte Greta Petrella Flavio Giuseppe Biccirè Francesco Pelliccia Gaetano Tanzilli Daniel Oscar Cicero A Pilot Study on the <sup>1</sup>H-NMR Serum Metabolic Profile of Takotsubo Patients Reveals Systemic Response to Oxidative Stress Antioxidants Takotsubo syndrome metabolomics <sup>1</sup>H-NMR systemic stressor response |
title | A Pilot Study on the <sup>1</sup>H-NMR Serum Metabolic Profile of Takotsubo Patients Reveals Systemic Response to Oxidative Stress |
title_full | A Pilot Study on the <sup>1</sup>H-NMR Serum Metabolic Profile of Takotsubo Patients Reveals Systemic Response to Oxidative Stress |
title_fullStr | A Pilot Study on the <sup>1</sup>H-NMR Serum Metabolic Profile of Takotsubo Patients Reveals Systemic Response to Oxidative Stress |
title_full_unstemmed | A Pilot Study on the <sup>1</sup>H-NMR Serum Metabolic Profile of Takotsubo Patients Reveals Systemic Response to Oxidative Stress |
title_short | A Pilot Study on the <sup>1</sup>H-NMR Serum Metabolic Profile of Takotsubo Patients Reveals Systemic Response to Oxidative Stress |
title_sort | pilot study on the sup 1 sup h nmr serum metabolic profile of takotsubo patients reveals systemic response to oxidative stress |
topic | Takotsubo syndrome metabolomics <sup>1</sup>H-NMR systemic stressor response |
url | https://www.mdpi.com/2076-3921/10/12/1982 |
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