Table 5.

Acute and chronic effects of e-cigarettes as a possible risk factor and trigger for stroke.

Acute Direct Effect
Kuntic et al. [35]	E-cigarette product acrolein (reactive aldehydes) mediated NOX-2-driven oxidative stress and cerebrovascular inflammation
Caporale et al. [43]	Transient impairment of cerebrovascular reactivity and endothelial function
Sifat et al. [8]	Induces a state of glucose deprivation at the neurovascular unit, leading to enhanced ischemic brain injury and/or stroke risk
Acute Indirect Effect
Antoniewicz et al., Mitchelle et al. [44,45]	Increased HR; increased arterial stiffness is an independent risk factor for cardio and cerebrovascular events such as myocardial infarctions and stroke
Nocella et al. [46]	Increase the soluble CD40L and P-selectin; enhance platelet aggregation
Boas et al. [47]	Activation of splenocardiac axis (increase oxidative stress and increase sympathetic activity)
Carnevale et al. [40]	Increase oxidative stress and endothelial dysfunction by increasing soluble NOX-mediated peptides and decreasing NO bioavailability and vitamin E
Chronic Direct Effect
Kuntic et al. [35]	Endothelial dysfunction and narrowing of vessels
Kaisar et al. [25]	Alter blood-brain barrier (BBB) permeability and vascular inflammation
Qasim et al. [48]	In mice, alter physiological hemostasis and increase the risk of thrombogenic events; platelet activation
Chronic Indirect Effect
Alzahrani et al. [49]	Increased odds of having myocardial infarction (OR = 1.79, 95% CI = 1.20, 2.66, p = 0.004)
Moheimani et al. [50]	Increases in cardiac sympathetic activity and oxidative stress, both of which increase the risk of vascular disease
Frederik Franzen et al. [51]	Increase peripheral and central blood pressure and pulse wave velocity
Vlachopoulos et al. [52]	Increase aortic stiffness and increase blood pressure