The effect of electronic cigarettes on young versus old normal hearts and pathologic hearts

电子烟对年轻与老年正常心脏和病理心脏的影响

• 批准号: 10240296
• 负责人: Robert A Kloner
• 金额: $ 45.3万
• 依托单位: HUNTINGTON MEDICAL RESEARCH INSTITUTES
• 依托单位国家: 美国
• 财政年份: 2018
• 资助国家: 美国
• 起止时间: 2018-09-14 至 2023-08-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/10240296
• 关键词: Acrolein; Acute; Adolescent; Adrenergic beta-Antagonists; Adult; Age; Air; Aldehydes; Antioxidants; Apoptosis; Arrhythmia; Arteries; Atherosclerosis; Biochemical; Blood Pressure; Cardiac; Cardiac Catheterization Procedures; Cardiovascular Diseases; Cardiovascular Pathology; Cardiovascular Physiology; Cardiovascular system; Cells; Chemicals; Chronic; Cicatrix; Cigarette; Controlled Study; Dangerousness; Data; Deterioration; Dilatation - action; Disease model; Dose; Echocardiography; Electrocardiogram; Electronic cigarette; Endothelium; Exposure to; Female; Fibrosis; Flavoring; Functional disorder; Gene Expression; Genotype; Glycerol; Goals; Head; Heart; Heart Diseases; Heart Rate; Heart failure; Histologic; Human; Hypertrophy; Individual; Infarction; Inflammation; Injury; Knowledge; Laboratories; Left; Left Ventricular Dysfunction; Left Ventricular Function; Left Ventricular Hypertrophy; Left Ventricular Remodeling; Long-Term Effects; Lung; Measures; Mediating; Mitochondria; Modeling; Morphology; Myocardial Infarction; Nicotine; Outcome; Particle Size; Particulate; Pathologic; Phenotype; Pilot Projects; Pollution; Propylene Glycols; Rattus; Reactive Oxygen Species; Risk; Rodent; Rodent Model; Smoke; Stretching; Structure; Sympathetic Nervous System; System; Tars; Testing; Thinness; Time; Tobacco; Toxic effect; Vasodilation; Ventricular; aged; cigarette smoke; cigarette smoking; effective therapy; electronic cigarette use; endothelial dysfunction; experience; heart function; heart rate variability; in vivo; male; mortality; sex; vaping; vapor

Project Summary/Abstract E-cigarettes (E-C) continue to gain popularity, but the effects of E-C on the cardiovascular (CV) system of either normal individuals or those with heart disease are unknown. Cigarette smoke can increase heart rate, blood pressure, worsen endothelial dysfunction, and accelerate atherosclerosis. Some suggest that substituting E-C could be a safer approach to reduce cigarette smoking risks as they lack tar and some of the other noxious chemicals associated with cigarette smoke. However, E-C can still deliver nicotine and other potentially dangerous chemicals such as acrolein, propylene glycol, glycerol, aldehydes, and flavorings. In addition, the small particle size that may result from E-C vaping could result in increased toxicity to the lungs and cardiovascular system. There is a large knowledge gap in that there are no studies that have examined the effect of chronic exposure to E-C on the CV system in otherwise healthy young individuals where there has been a rapid increase in E-C use versus older individuals who may be turning to E-C as a way to quit standard cigarettes. In addition there is not data on the long-term effect of E-C on subjects with known CV disease. Thus, before suggesting that individuals can feel safe that their use of E-C is not going to cause or exacerbate CV disease, rigorous controlled studies are needed to assess the effect of E-C on CV phenotype and genotype. Our goal will be to determine the acute and chronic effects that E-C has in comparison to standard cigarette smoke on the young versus the old CV system and on the diseased CV system, including left ventricular (LV) dysfunction due to previous myocardial infarction (MI). We will determine whether E-C are safer, equally safe or less safe for subjects who have these underlying CV conditions versus standard cigarettes. We hypothesize that E-C, especially if they carry nicotine, will contribute to adverse LV remodeling post myocardial infarction, worsen heart failure, and endothelial dysfunction. We will determine whether these effects will be lessened if E-C does not contain nicotine, and whether certain therapies can reverse the effects. A well-established rodent model of MI will be used and there will be collaborative effort between a laboratory that has extensive experience subjecting rodents to exposure to smoke and pollution with a laboratory that has extensive experience with analyzing the pathophysiology of in vivo cardiac disease models including assessment by echocardiography, cardiac catheterization, detailed histologic and histochemical analyses, biochemical analyses, assessment of endothelial function, assessment of mitochondrial function, ultrastructural analysis, and assessment of gene expression.

项目总结/摘要 电子烟（E-C）继续受到欢迎，但E-C对心血管（CV）系统的影响 正常人或心脏病患者的死亡率尚不清楚。吸烟会增加 心率、血压、恶化内皮功能障碍和加速动脉粥样硬化。一些 这表明，替代E-C可能是一种更安全的方法，以减少吸烟的风险，因为他们缺乏 焦油和其他一些与香烟烟雾有关的有毒化学物质。然而，E-C仍然可以 释放尼古丁和其他潜在危险的化学物质，如丙烯醛，丙二醇，甘油， 醛和调味剂。此外，可能由E-C蒸汽烟产生的小颗粒尺寸可能会导致 导致对肺和心血管系统的毒性增加。知识差距很大， 没有研究检查长期暴露于E-C对CV系统的影响， 其他方面健康的年轻人，与老年人相比， 那些可能转向E-C作为戒烟方法的人。此外，没有数据 E-C对已知CV疾病受试者的长期影响。因此，在建议 个人可以感到安全，他们使用E-C不会导致或加重CV疾病，严格 需要对照研究来评估E-C对CV表型和基因型的影响。我们的目标将 确定与标准香烟烟雾相比，E-C的急性和慢性影响 年轻与老年CV系统以及病变CV系统（包括左心室（LV）） 由于先前的心肌梗死（MI）导致的功能障碍。我们将确定E-C是否更安全， 对于患有这些基础CV疾病的受试者，与标准治疗相比，安全性相同或较低 香烟我们假设，E-C，特别是如果它们携带尼古丁，将有助于不利的左心室 心肌梗死后重塑，加重心力衰竭和内皮功能障碍。我们将 确定如果E-C不含尼古丁，这些影响是否会减轻，以及某些 治疗可以逆转这种影响。将使用完善的MI啮齿动物模型， 实验室之间的合作努力，具有丰富的经验，使啮齿动物暴露于 烟雾和污染与实验室，有丰富的经验，分析 体内心脏病模型的病理生理学，包括通过超声心动图、心脏 导管插入术，详细的组织学和组织化学分析，生化分析， 内皮功能、线粒体功能评估、超微结构分析和 基因表达。

项目成果

Marijuana and electronic cigarettes on cardiac arrhythmias.

大麻和电子烟对心律失常的影响。

• DOI: 10.1016/j.hrthm.2022.09.022
• 发表时间: 2023
• 期刊: Heart rhythm
• 影响因子: 5.5
• 作者: Kloner,RobertA

E-cigarette or Vaping Product Use-Associated Lung Injury Produced in an Animal Model From Electronic Cigarette Vapor Exposure Without Tetrahydrocannabinol or Vitamin E Oil.

• DOI: 10.1161/jaha.120.017368
• 发表时间: 2020-09-15
• 期刊: Journal of the American Heart Association
• 影响因子: 5.4
• 作者: Kleinman MT;Arechavala RJ;Herman D;Shi J;Hasen I;Ting A;Dai W;Carreno J;Chavez J;Zhao L;Kloner RA
• 通讯作者: Kloner RA

One Acute Exposure to E-Cigarette Smoke Using Various Heating Elements and Power Levels Induces Pulmonary Inflammation.

• DOI: 10.14740/cr1425
• 发表时间: 2022-12
• 期刊: Cardiology research
• 影响因子: 1.9