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Published on: February 10, 2013
Nicotine and novel tobacco products drive adverse cardiac remodeling and dysfunction in preclinical studies
Nicholas D Fried1, Joshua M Oakes1, Anna K Whitehead1
1Department of Physiology, Louisiana State University Health Sciences Center, New Orleans, LA, United States.
Insights
Nicotine exposure alters heart structure in mice under stress, potentially worsening heart failure. Emerging tobacco products may pose risks for cardiac remodeling and heart failure.
Area of Science:
- Cardiovascular Science
- Toxicology
Background:
- Cardiac remodeling is a key factor in heart failure (HF) development.
- Cigarette smoking is linked to cardiac remodeling, but the impact of nicotine and novel tobacco products remains unclear.
- Understanding these effects is crucial given declining cigarette use and rising popularity of alternatives.
Purpose of the Study:
- To investigate the effects of chronic nicotine exposure on cardiac remodeling under hemodynamic stress.
- To review preclinical evidence on nicotine and novel tobacco products in cardiac dysfunction.
Main Methods:
- Adult male mice were exposed to inhaled nicotine for 8 weeks.
- Hemodynamic stress was induced using angiotensin (Ang)-II infusion in a subset of mice.
- Left ventricular structure and function were evaluated using echocardiography.
Main Results:
- Nicotine exposure prevented Ang-II-induced left ventricular posterior wall thickening.
- Nicotine-exposed mice showed reduced relative wall thickness.
- Ang-II increased left ventricular mass index in both air- and nicotine-exposed groups.
Conclusions:
- Nicotine exposure may shift cardiac remodeling from concentric to eccentric hypertrophy under stress, potentially contributing to HF.
- Findings align with other studies on nicotine and electronic cigarette exposure.
- Clinicians and researchers should consider novel tobacco products as potential risk factors for cardiac remodeling and HF.
Background:
The 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.
Methods:
Adult, 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.
Results:
Chronic, 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.
Conclusions:
These 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.
