Nicotine and novel tobacco products drive adverse cardiac remodeling and dysfunction in preclinical studies
BackgroundThe heart undergoes structural and functional changes in response to injury and hemodynamic stress known as cardiac remodeling. Cardiac remodeling often decompensates causing dysfunction and heart failure (HF). Cardiac remodeling and dysfunction are significantly associated with cigarette...
| Main Authors: | , , , , , |
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| Format: | Article |
| Language: | English |
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Frontiers Media S.A.
2022-10-01
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| Series: | Frontiers in Cardiovascular Medicine |
| Subjects: | |
| Online Access: | https://www.frontiersin.org/articles/10.3389/fcvm.2022.993617/full |
| _version_ | 1797997198167769088 |
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| author | Nicholas D. Fried Joshua M. Oakes Anna K. Whitehead Eric Lazartigues Eric Lazartigues Eric Lazartigues Eric Lazartigues Xinping Yue Jason D. Gardner |
| author_facet | Nicholas D. Fried Joshua M. Oakes Anna K. Whitehead Eric Lazartigues Eric Lazartigues Eric Lazartigues Eric Lazartigues Xinping Yue Jason D. Gardner |
| author_sort | Nicholas D. Fried |
| collection | DOAJ |
| description | BackgroundThe heart undergoes structural and functional changes in response to injury and hemodynamic stress known as cardiac remodeling. Cardiac remodeling often decompensates causing dysfunction and heart failure (HF). Cardiac remodeling and dysfunction are significantly associated with cigarette smoking. Although cigarette smoking has declined, the roles of nicotine and novel tobacco products (including electronic cigarettes and heat-not-burn tobacco) in cardiac remodeling are unclear. In this perspective, we present evidence demonstrating maladaptive cardiac remodeling in nicotine-exposed mice undergoing hemodynamic stress with angiotensin (Ang)-II infusion and review preclinical literature linking nicotine and novel tobacco products with cardiac remodeling and dysfunction.MethodsAdult, male C57BL/6J mice were exposed to room air or chronic, inhaled nicotine for 8 weeks. A subset of mice was infused with Ang-II via subcutaneous osmotic mini-pumps during the final 4 weeks of exposure. Left ventricular structure and function were assessed with echocardiography.ResultsChronic, inhaled nicotine abrogated Ang-II-induced thickening of the left ventricular posterior wall, leading to reduced relative wall thickness. Ang-II infusion was associated with increased left ventricular mass index in both air- and nicotine-exposed mice.ConclusionsThese changes suggest a phenotypic shift from concentric hypertrophy to eccentric hypertrophy in nicotine-exposed, hemodynamically-stressed mice which could drive HF pathogenesis. These findings join a growing body of animal studies demonstrating cardiac remodeling and dysfunction following nicotine and electronic cigarette exposure. Further exploration is necessary; however, clinicians and researchers should not overlook these emerging products as potential risk factors in the pathogenesis of cardiac remodeling and associated diseases including HF. |
| first_indexed | 2024-04-11T10:29:20Z |
| format | Article |
| id | doaj.art-7cff00d530d54c5c8d2679ad9ca5356b |
| institution | Directory Open Access Journal |
| issn | 2297-055X |
| language | English |
| last_indexed | 2024-04-11T10:29:20Z |
| publishDate | 2022-10-01 |
| publisher | Frontiers Media S.A. |
| record_format | Article |
| series | Frontiers in Cardiovascular Medicine |
| spelling | doaj.art-7cff00d530d54c5c8d2679ad9ca5356b2022-12-22T04:29:28ZengFrontiers Media S.A.Frontiers in Cardiovascular Medicine2297-055X2022-10-01910.3389/fcvm.2022.993617993617Nicotine and novel tobacco products drive adverse cardiac remodeling and dysfunction in preclinical studiesNicholas D. Fried0Joshua M. Oakes1Anna K. Whitehead2Eric Lazartigues3Eric Lazartigues4Eric Lazartigues5Eric Lazartigues6Xinping Yue7Jason D. Gardner8Department of Physiology, Louisiana State University Health Sciences Center, New Orleans, LA, United StatesDepartment of Physiology, Louisiana State University Health Sciences Center, New Orleans, LA, United StatesDepartment of Physiology, Louisiana State University Health Sciences Center, New Orleans, LA, United StatesDepartment of Pharmacology & Experimental Therapeutics, Louisiana State University Health Sciences Center, New Orleans, LA, United StatesCardiovascular Center of Excellence, New Orleans, LA, United StatesNeuroscience center of Excellence, Louisiana State University Health Sciences Center, New Orleans, LA, United StatesSoutheast Louisiana Veterans Health Care Systems, New Orleans, LA, United StatesDepartment of Physiology, Louisiana State University Health Sciences Center, New Orleans, LA, United StatesDepartment of Physiology, Louisiana State University Health Sciences Center, New Orleans, LA, United StatesBackgroundThe heart undergoes structural and functional changes in response to injury and hemodynamic stress known as cardiac remodeling. Cardiac remodeling often decompensates causing dysfunction and heart failure (HF). Cardiac remodeling and dysfunction are significantly associated with cigarette smoking. Although cigarette smoking has declined, the roles of nicotine and novel tobacco products (including electronic cigarettes and heat-not-burn tobacco) in cardiac remodeling are unclear. In this perspective, we present evidence demonstrating maladaptive cardiac remodeling in nicotine-exposed mice undergoing hemodynamic stress with angiotensin (Ang)-II infusion and review preclinical literature linking nicotine and novel tobacco products with cardiac remodeling and dysfunction.MethodsAdult, male C57BL/6J mice were exposed to room air or chronic, inhaled nicotine for 8 weeks. A subset of mice was infused with Ang-II via subcutaneous osmotic mini-pumps during the final 4 weeks of exposure. Left ventricular structure and function were assessed with echocardiography.ResultsChronic, inhaled nicotine abrogated Ang-II-induced thickening of the left ventricular posterior wall, leading to reduced relative wall thickness. Ang-II infusion was associated with increased left ventricular mass index in both air- and nicotine-exposed mice.ConclusionsThese changes suggest a phenotypic shift from concentric hypertrophy to eccentric hypertrophy in nicotine-exposed, hemodynamically-stressed mice which could drive HF pathogenesis. These findings join a growing body of animal studies demonstrating cardiac remodeling and dysfunction following nicotine and electronic cigarette exposure. Further exploration is necessary; however, clinicians and researchers should not overlook these emerging products as potential risk factors in the pathogenesis of cardiac remodeling and associated diseases including HF.https://www.frontiersin.org/articles/10.3389/fcvm.2022.993617/fullnicotineelectronic cigarettes (E-cigarettes)heat-not-burn (HNB)cardiac remodelingnovel tobacco products |
| spellingShingle | Nicholas D. Fried Joshua M. Oakes Anna K. Whitehead Eric Lazartigues Eric Lazartigues Eric Lazartigues Eric Lazartigues Xinping Yue Jason D. Gardner Nicotine and novel tobacco products drive adverse cardiac remodeling and dysfunction in preclinical studies Frontiers in Cardiovascular Medicine nicotine electronic cigarettes (E-cigarettes) heat-not-burn (HNB) cardiac remodeling novel tobacco products |
| title | Nicotine and novel tobacco products drive adverse cardiac remodeling and dysfunction in preclinical studies |
| title_full | Nicotine and novel tobacco products drive adverse cardiac remodeling and dysfunction in preclinical studies |
| title_fullStr | Nicotine and novel tobacco products drive adverse cardiac remodeling and dysfunction in preclinical studies |
| title_full_unstemmed | Nicotine and novel tobacco products drive adverse cardiac remodeling and dysfunction in preclinical studies |
| title_short | Nicotine and novel tobacco products drive adverse cardiac remodeling and dysfunction in preclinical studies |
| title_sort | nicotine and novel tobacco products drive adverse cardiac remodeling and dysfunction in preclinical studies |
| topic | nicotine electronic cigarettes (E-cigarettes) heat-not-burn (HNB) cardiac remodeling novel tobacco products |
| url | https://www.frontiersin.org/articles/10.3389/fcvm.2022.993617/full |
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