Table 1.
Characteristics of included study.
| # | Reference | Sample | Control group | Nicotine | Length of exposure | Overall risk of bias/quality∗ | Result | |
|---|---|---|---|---|---|---|---|---|
| Characteristics | Total number of electronic cigarette population | |||||||
| Human studies | ||||||||
| Randomized controlled trial (RCT) | ||||||||
| 1 | George et al. [11] | Smokers | 74 | N/A | 16 mg/mL | Chronic (1 month) | Some concerns | Switching from conventional cigarette to electronic cigarette improves endothelial function and vascular stiffness marker. |
| 2 | Ikonomidis et al. [12] | Smokers | 40 | N/A | 12 mg/mL | Chronic (4 months) | Some concerns | Switching from conventional cigarette to electronic cigarette improves arterial stiffness and oxidative stress. |
| 3 | Ikonomidis et al. [13] | Smokers | 70 | Tobacco smokers | 0.12 mg/mL | Chronic (1 month) | High risk | Replacing conventional cigarette with electronic cigarette results in reduced systolic and oxidative stress. |
| Observational; cross-sectional | ||||||||
| 4 | Bricknell et al. [14] | Nonsmokers and smokers | 74,013 | N/A | N/A | Observational study | Fair | ENDS (including electronic cigarette) use is associated with stroke. |
| 5 | Fetterman et al. [15] | Nonsmokers and smokers | 36 | N/A | N/A | Observational study | Good | Electronic cigarette use is associated with elevated augmentation index (AIx, arterial stiffness marker) and an indication of endothelial dysfunction. |
| 6 | Oliveri et al. [16] | Smokers | 144 | Tobacco smokers | N/A | Observational study | Good | Electronic cigarette users show lower levels of biomarkers of exposure (NNK, nicotine, acrolein, and carbon monoxide) and biomarkers of potential harm (platelet activation, oxidative stress, and endothelial function) than cigarette smokers |
| 7 | Podzolkov et al. [17] | Nonsmokers and smokers | 2 | N/A | N/A | Observational study | Fair | Smoking traditional and electronic cigarette are related to albuminuria and an increase in the augmentation index (arterial stiffness marker). |
| 8 | Rader et al. [18] | Nonsmokers and smokers | 35 | N/A | N/A | Observational study | Poor | Electronic cigarette users show more pronounced impaired coronary microvascular endothelial function than chronic conventional cigarette users. |
| 9 | Sahota et al. [19] | Nonsmokers and smokers | 20 | N/A | 4-36 mg/mL | Observational study | Fair | Electronic cigarette users develop more carotid plaque burden than nonsmokers |
| 10 | Vindhyal et al. [20] | Nonsmokers and smokers | 401 and 2,240 dual users | N/A | N/A | Observational study | Poor | Electronic cigarette users are associated with an increased risk of myocardial infarction than nonsmokers |
| Animal studies | ||||||||
| 1 | El-Mahdy et al. [21] | Animal (mice C57BL/6 J) | 100 | Air | 0, 6, or 24 mg/mL | 60 weeks | Electronic cigarette can induce cardiovascular disease similar to conventional cigarette smoking. The severity of toxicity increases with exposure duration and nicotine content. | |
| 2 | Espinoza-Derout et al. [22] | Animals (ApoE–/– mice) | 5/test group | EC without nicotine/saline aerosol | 2.40% | 12 weeks | Electronic cigarette with nicotine induce an abnormal increase in ROS levels and mitochondrial DNA mutations associated with cardiac dysfunction and atherogenesis. Electronic cigarette without nicotine did not produce significant effect. |
|
| 3 | Kuntic et al. [23] | Animal (C57BL/6 and NOX2 null mice) | 151 | Air | 12 mg/ml | 5 days | Electronic cigarette vapor increases vascular, cerebral, and pulmonary oxidative stress via a NOX-2-dependent mechanism. The adverse effect is more pronounced with nicotine than without nicotine. | |
| 4 | Li et al. [24] | Animal (mice) | 5-10/test group | Air | 2.40% | 16 weeks | Electronic cigarette increases the level of mitochondrial DNA damage in blood and expression of TLR9 and induces the development of atherosclerosis. | |
| 5 | Olfert et al. [25] | Animal (mice C57BL/6 J) | 15 | Air | 18 mg/mL | 32 weeks | Electronic cigarette vapor accelerates arterial stiffness and impairs aortic endothelial function. | |
| 6 | Szostak et al. [26] | Animals (ApoE–/– mice) | 309 (10-16/test group) | Air | 4% | 24 weeks | Electronic cigarette vapor shows small or completely absent effects on systolic and diastolic functions of the heart, atherosclerotic progression, altered lipid profiles, and alteration of the heart ventricle and aorta transcriptomes compare to 3R4F conventional cigarette smoke. | |
Notes: (∗) The SYRCLE's RoB for animal intervention does not provide overall risk of bias.